Ignet

Gene Information

Gene symbol: TGFB2

Gene name: transforming growth factor, beta 2

HGNC ID: 11768

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	AGT	1 hits
3	BMP2	1 hits
4	BMP4	1 hits
5	CASP3	1 hits
6	COL1A1	1 hits
7	COL1AR	1 hits
8	COL4A4	1 hits
9	CTGF	1 hits
10	EGR1	1 hits
11	GAD2	1 hits
12	HGF	1 hits
13	HSD17B4	1 hits
14	IDDM2	1 hits
15	IFNA1	1 hits
16	IGF1	1 hits
17	IL10	1 hits
18	IL12A	1 hits
19	IL2	1 hits
20	IL4	1 hits
21	IL6	1 hits
22	LTA	1 hits
23	MAPK14	1 hits
24	MMP9	1 hits
25	NGF	1 hits
26	NUDT6	1 hits
27	PDGFB	1 hits
28	PRRX1	1 hits
29	RHOD	1 hits
30	RNF138	1 hits
31	SMAD4	1 hits
32	SPHK1	1 hits
33	TGFA	1 hits
34	TGFB1	1 hits
35	TGFB3	1 hits
36	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	8760354	Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation.
2	8760354	A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD).
3	8760354	Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67.
4	8760354	Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content.
5	8760354	Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis.
6	8760354	Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA).
7	8760354	Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA.
8	8760354	Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription.
9	8760354	As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM.
10	9639441	Transforming growth factor beta2 in the vitreous in proliferative diabetic retinopathy.
11	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
12	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
13	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
14	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
15	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
16	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
17	10600222	There was no correlation between the levels of NGF and TGF-beta2.
18	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
19	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
20	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
21	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
22	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
23	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
24	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
25	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
26	10600222	There was no correlation between the levels of NGF and TGF-beta2.
27	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
28	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
29	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
30	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
31	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
32	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
33	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
34	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
35	10600222	There was no correlation between the levels of NGF and TGF-beta2.
36	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
37	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
38	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
39	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
40	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
41	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
42	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
43	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
44	10600222	There was no correlation between the levels of NGF and TGF-beta2.
45	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
46	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
47	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
48	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
49	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
50	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
51	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
52	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
53	10600222	There was no correlation between the levels of NGF and TGF-beta2.
54	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
55	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
56	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
57	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
58	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
59	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
60	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
61	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
62	10600222	There was no correlation between the levels of NGF and TGF-beta2.
63	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
64	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
65	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
66	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
67	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
68	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
69	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
70	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
71	10600222	There was no correlation between the levels of NGF and TGF-beta2.
72	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
73	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
74	10600222	Altered plasma levels of nerve growth factor and transforming growth factor-beta2 in type-1 diabetes mellitus.
75	10600222	Nerve growth factor (NGF) and transforming growth factor-beta2 (TGF-beta2) are cytokines which have known immunological effects.
76	10600222	An elevated level of NGF has been reported in certain autoimmune diseases, whereas TGF-beta2 is an immunosuppressor which is known to play a role in regulating cell proliferation.
77	10600222	In this study we measured the levels of NGF and TGF-beta2 in the sera of patients with IDDM (n = 26) and values were compared to those of age-matched normal subjects (n = 27) and also to patients with type-2 diabetes mellitus (NIDDM) (n = 26) with similar HbA1c levels and an equal duration of diabetes.
78	10600222	Serum NGF levels were significantly elevated in IDDM patients compared to those of age-matched controls (p <.001) and NIDDM controls (p <.01).
79	10600222	TGF-beta2 levels were lower in IDDM patients when compared with the healthy control (p <.001) and the NIDDM control (p <.05).
80	10600222	There was no correlation between the levels of NGF and TGF-beta2.
81	10600222	The duration of diabetes and the level of HbA1c did not affect the NGF and TGF-beta2 levels in the IDDM patients.
82	10600222	We conclude that an increase in NGF and a suppression in TGF-beta2 levels are present in patients with type-1 diabetes mellitus and that both cytokines may play independent roles in the pathogenesis of this disease.
83	10600653	We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR.
84	10600653	Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production.
85	10600653	A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous.
86	10600653	We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR.
87	10600653	Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production.
88	10600653	A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous.
89	10600653	We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR.
90	10600653	Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production.
91	10600653	A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous.
92	10698197	TGF-beta1, TGF-beta2, and receptor mRNA and protein were detected in the control nondiabetic kidney.
93	10698197	It was found that dramatic and dynamic changes occur in all parts of the renal TGF-beta axis in both models of experimental diabetes, but TGF-beta2 and TGF-betaRII proteins were the predominant responsive element, particularly during the acute phase of disease.
94	10698197	TGF-beta1, TGF-beta2, and receptor mRNA and protein were detected in the control nondiabetic kidney.
95	10698197	It was found that dramatic and dynamic changes occur in all parts of the renal TGF-beta axis in both models of experimental diabetes, but TGF-beta2 and TGF-betaRII proteins were the predominant responsive element, particularly during the acute phase of disease.
96	11446768	Total RNA was isolated from normal and diseased corneas. cDNA was synthesized from individual corneas and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed with primers to IL-1alpha, 1IL-8, PDGF-B, BMP-2, BMP-4, IGF-I, TGF-beta2, FGF-2, and VEGF.
97	11446768	Antibodies to IGF-I, BMP-2, VEGF and TGF-beta2 were used for immunohistochemistry.
98	11446768	IGF-I and BMP-4 RNA levels were increased in PBK/ABK.
99	11446768	In contrast, PBK/ABK corneas had specific significant elevations of BMP-4 and IGF-I.
100	11446768	Total RNA was isolated from normal and diseased corneas. cDNA was synthesized from individual corneas and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed with primers to IL-1alpha, 1IL-8, PDGF-B, BMP-2, BMP-4, IGF-I, TGF-beta2, FGF-2, and VEGF.
101	11446768	Antibodies to IGF-I, BMP-2, VEGF and TGF-beta2 were used for immunohistochemistry.
102	11446768	IGF-I and BMP-4 RNA levels were increased in PBK/ABK.
103	11446768	In contrast, PBK/ABK corneas had specific significant elevations of BMP-4 and IGF-I.
104	11524245	Transforming growth factor-beta2 antibody attenuates fibrosis in the experimental diabetic rat kidney.
105	11524245	The transforming growth factor-betas (TGF-betas) have been shown to play a major role in fibrosis and we have shown that TGF-beta2, in particular, increases co-ordinately with fibrogenesis in the diabetic kidney.
106	11524245	Transforming growth factor-beta2 antibody attenuates fibrosis in the experimental diabetic rat kidney.
107	11524245	The transforming growth factor-betas (TGF-betas) have been shown to play a major role in fibrosis and we have shown that TGF-beta2, in particular, increases co-ordinately with fibrogenesis in the diabetic kidney.
108	11754388	Transforming Growth Factor-beta2 (TGF-beta2) has been shown to be essential for embryonic development and survival.
109	12876066	We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels.
110	12876066	The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2.
111	12876066	In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta.
112	12876066	Impaired vascular dysfunction may be partly due to decreased inositol 1,4,5-trisphosphate receptor (IP3R), as reduced type I IP3R expression was found in diabetic aorta and restored by anti-TGF-beta antibodies.
113	12876066	We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels.
114	12876066	The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2.
115	12876066	In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta.
116	12876066	Impaired vascular dysfunction may be partly due to decreased inositol 1,4,5-trisphosphate receptor (IP3R), as reduced type I IP3R expression was found in diabetic aorta and restored by anti-TGF-beta antibodies.
117	14550911	We analyzed the expression pattern of transforming growth factor-beta isoforms (TGF-beta1, TGF-beta2 and TGF-beta3) in the developing brain of embryos derived from the normal and diabetic mice exposed to cyclophosphamide (CP), a cytotoxic teratogen.
118	14550911	The CP-treated diabetic embryos showed significantly more TGF-beta1 and TGF-beta2 immunoreactive cells in the regions of telencephalon and diencephalon in comparison to that of CP-treated non-diabetic embryos.
119	14550911	We analyzed the expression pattern of transforming growth factor-beta isoforms (TGF-beta1, TGF-beta2 and TGF-beta3) in the developing brain of embryos derived from the normal and diabetic mice exposed to cyclophosphamide (CP), a cytotoxic teratogen.
120	14550911	The CP-treated diabetic embryos showed significantly more TGF-beta1 and TGF-beta2 immunoreactive cells in the regions of telencephalon and diencephalon in comparison to that of CP-treated non-diabetic embryos.
121	15637419	Concentration of transforming growth factor beta2 in aqueous humor.
122	15637419	It was found that the total TGF-beta(2) concentration (1) decreases with age, (2) shows slight changes with axial length, (3) has slight changes with difference of localization of opacification, (4) is significantly high in patients with concurrent open-angle glaucoma (p < 0.05), (5) is high in patients with complicating diabetes who have undergone panretinal photocoagulation for diabetic retinopathy (p < 0.05) and (6) is low in patients with atopic cataracts.
123	15637419	These findings provide useful information on the intraocular activity of TGF-beta(2).
124	15637419	Concentration of transforming growth factor beta2 in aqueous humor.
125	15637419	It was found that the total TGF-beta(2) concentration (1) decreases with age, (2) shows slight changes with axial length, (3) has slight changes with difference of localization of opacification, (4) is significantly high in patients with concurrent open-angle glaucoma (p < 0.05), (5) is high in patients with complicating diabetes who have undergone panretinal photocoagulation for diabetic retinopathy (p < 0.05) and (6) is low in patients with atopic cataracts.
126	15637419	These findings provide useful information on the intraocular activity of TGF-beta(2).
127	15637419	Concentration of transforming growth factor beta2 in aqueous humor.
128	15637419	It was found that the total TGF-beta(2) concentration (1) decreases with age, (2) shows slight changes with axial length, (3) has slight changes with difference of localization of opacification, (4) is significantly high in patients with concurrent open-angle glaucoma (p < 0.05), (5) is high in patients with complicating diabetes who have undergone panretinal photocoagulation for diabetic retinopathy (p < 0.05) and (6) is low in patients with atopic cataracts.
129	15637419	These findings provide useful information on the intraocular activity of TGF-beta(2).
130	15953049	When exposed to transforming growth factor-beta2 (1-10,000 pg/ml) and platelet-derived growth factor-BB (0.5-500 ng/ml) under both normo- and hyperglycemic conditions, there was a dose-related increase in proliferation of both diabetic and nondiabetic controls.
131	15953049	Western blot analysis did not show any apparent difference in the expression of platelet-derived growth factor receptor alpha, mitogen-activated protein kinase/ERK2, or transforming growth factor-beta receptor II to account for the reduced proliferation of diabetic hTCF.
132	16954341	Betaglycan potentiates TGF-beta; however, soluble betaglycan, which is produced by the shedding of the membrane-bound receptor, is a potent antagonist of TGF-beta.
133	16954341	These effects were associated with lower kidney levels of mRNAs encoding TGF-beta1, TGF-beta2, TGF-beta3, collagen IV, collagen I, fibronectin, and serum glucocorticoid kinase as well as a reduction in the immunostaining of collagen IV and fibronectin.
134	16954341	Because SBG has a high affinity for all TGF-beta isoforms, in particular TGF-beta2, it is found naturally in serum and tissues and its shedding may be regulated.
135	16954341	Betaglycan potentiates TGF-beta; however, soluble betaglycan, which is produced by the shedding of the membrane-bound receptor, is a potent antagonist of TGF-beta.
136	16954341	These effects were associated with lower kidney levels of mRNAs encoding TGF-beta1, TGF-beta2, TGF-beta3, collagen IV, collagen I, fibronectin, and serum glucocorticoid kinase as well as a reduction in the immunostaining of collagen IV and fibronectin.
137	16954341	Because SBG has a high affinity for all TGF-beta isoforms, in particular TGF-beta2, it is found naturally in serum and tissues and its shedding may be regulated.
138	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
139	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
140	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
141	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
142	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
143	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
144	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
145	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
146	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
147	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
148	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
149	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
150	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
151	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
152	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
153	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
154	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
155	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
156	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
157	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
158	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
159	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
160	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
161	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
162	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
163	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
164	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
165	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
166	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
167	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
168	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
169	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
170	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
171	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
172	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
173	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
174	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
175	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
176	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
177	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
178	17192487	Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor.
179	17192487	The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified.
180	17192487	In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes.
181	17192487	Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01).
182	17192487	Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4.
183	17192487	TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase.
184	17192487	Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression.
185	17192487	In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases.
186	17389681	In post-OF diabetic mice, mRNA abundance of early growth response-1 (Egr-1), collagen-4alpha1, and matrix metalloproteinase-9 were increased and 3beta-hydroxysteroid dehydrogenase 4 (3beta-HSD4) and transforming growth factor-beta(2) (TGF-beta(2)) were decreased compared with cycling diabetic mice.
187	17389681	In peri-OF diabetic mice, mRNA abundance of Egr-1 and 3beta-HSD4 were increased, and TGF-beta(2) was decreased compared with cycling diabetic mice.
188	17389681	In post-OF diabetic mice, mRNA abundance of early growth response-1 (Egr-1), collagen-4alpha1, and matrix metalloproteinase-9 were increased and 3beta-hydroxysteroid dehydrogenase 4 (3beta-HSD4) and transforming growth factor-beta(2) (TGF-beta(2)) were decreased compared with cycling diabetic mice.
189	17389681	In peri-OF diabetic mice, mRNA abundance of Egr-1 and 3beta-HSD4 were increased, and TGF-beta(2) was decreased compared with cycling diabetic mice.
190	18406405	Transforming growth factor-beta1 (TGF-beta1) has been associated with diabetic nephropathy and retinopathy but not neuropathy.
191	18406405	In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-beta1 and TGF-beta2 mRNA, but not TGF-beta3, was increased at 4 and 12 weeks.
192	18406405	In high glucose conditions, combination with TGF-beta2>beta1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-beta neutralizing antibody inhibits this increase.
193	18406405	Transforming growth factor-beta1 (TGF-beta1) has been associated with diabetic nephropathy and retinopathy but not neuropathy.
194	18406405	In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-beta1 and TGF-beta2 mRNA, but not TGF-beta3, was increased at 4 and 12 weeks.
195	18406405	In high glucose conditions, combination with TGF-beta2>beta1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-beta neutralizing antibody inhibits this increase.
196	19390543	Myocardial expressions of collagen III, transforming growth factor-beta2, angiotensin-converting enzyme (ACE), angiotensin II type-1 receptor and myocardial oxidative stress (evaluated by 4-hydroxy-2-nonenal-modified protein) were mostly enhanced in the HT+DM group.
197	19657322	Transforming growth factor-beta2 upregulates sphingosine kinase-1 activity, which in turn attenuates the fibrotic response to TGF-beta2 by impeding CTGF expression.
198	19657322	Transforming growth factor-beta2 (TGF-beta2) stimulates the expression of pro-fibrotic connective tissue growth factor (CTGF) during the course of renal disease.
199	19657322	Because sphingosine kinase-1 (SK-1) activity is also upregulated by TGF-beta, we studied its effect on CTGF expression and on the development of renal fibrosis.
200	19657322	Over-expression of SK-1 reduced CTGF induction, an effect mediated by intracellular sphingosine-1-phosphate.
201	19657322	Similarly, in a mouse model of streptozotocin-induced diabetic nephropathy, SK-1 and CTGF were upregulated in podocytes.
202	19657322	Transforming growth factor-beta2 upregulates sphingosine kinase-1 activity, which in turn attenuates the fibrotic response to TGF-beta2 by impeding CTGF expression.
203	19657322	Transforming growth factor-beta2 (TGF-beta2) stimulates the expression of pro-fibrotic connective tissue growth factor (CTGF) during the course of renal disease.
204	19657322	Because sphingosine kinase-1 (SK-1) activity is also upregulated by TGF-beta, we studied its effect on CTGF expression and on the development of renal fibrosis.
205	19657322	Over-expression of SK-1 reduced CTGF induction, an effect mediated by intracellular sphingosine-1-phosphate.
206	19657322	Similarly, in a mouse model of streptozotocin-induced diabetic nephropathy, SK-1 and CTGF were upregulated in podocytes.
207	23250756	The transcription factor paired-related homeobox 1 (Prrx1) inhibits adipogenesis by activating transforming growth factor-β (TGFβ) signaling.
208	23250756	Stable knockdown of Prrx1a/b enhances adipogenesis, with increased expression of peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein-α and FABP4 and increased secretion of the adipokines adiponectin and chemerin.
209	23250756	Prrx1 knockdown decreases expression of Tgfb2 and Tgfb3, and inhibition of TGFβ signaling during adipogenesis mimics the effects of Prrx1 knockdown.
210	23250756	These observations suggest that increased Prrx1 expression may promote TGFβ activity in adipose tissue and thereby contribute to aberrant adipocyte function during obesity.