Ignet

Gene Information

Gene symbol: TEK

Gene name: TEK tyrosine kinase, endothelial

HGNC ID: 11724

Synonyms: TIE2, TIE-2, VMCM1, CD202b

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	ANGPT1	1 hits
4	ANGPT2	1 hits
5	APLN	1 hits
6	CASP3	1 hits
7	FLT1	1 hits
8	ICAM1	1 hits
9	IGF1R	1 hits
10	INS	1 hits
11	KDR	1 hits
12	MAPK3	1 hits
13	NOS2A	1 hits
14	NOS3	1 hits
15	PDGFB	1 hits
16	PECAM1	1 hits
17	PGF	1 hits
18	PPP1R3C	1 hits
19	PTPN13	1 hits
20	PTPN6	1 hits
21	S100A4	1 hits
22	STAT1	1 hits
23	STAT5A	1 hits
24	TIE1	1 hits
25	TM7SF2	1 hits
26	TNF	1 hits
27	VCAM1	1 hits
28	VEGFA	1 hits
29	VWF	1 hits
30	WNT7B	1 hits

Related Sentences

#	PMID	Sentence
1	6839921	We evaluated the performance of 50 insulin-dependent diabetic patients in the measurement of their own capillary blood glucose concentrations using Chemstrip bG, Dextrostix-Dextrometer, and Stat Tek systems.
2	6839921	The percentage of patient determinations that differed from the laboratory value by more than 20% was 37%, 30%, and 14% for the Chemstrip bG, Dextrostix-Dextrometer, and Stat Tek systems, respectively.
3	6839921	We evaluated the performance of 50 insulin-dependent diabetic patients in the measurement of their own capillary blood glucose concentrations using Chemstrip bG, Dextrostix-Dextrometer, and Stat Tek systems.
4	6839921	The percentage of patient determinations that differed from the laboratory value by more than 20% was 37%, 30%, and 14% for the Chemstrip bG, Dextrostix-Dextrometer, and Stat Tek systems, respectively.
5	7096867	Data presented in this study indicates that the following systems; Eyetone-Ames, Dextrometer-Ames, Chemstrip bG-BioDynamics, and Stat Tek-BioDynamics, perform with accuracy in the estimation of blood glucose as compared to the results of the Beckman Auto-Analyzer.
6	11289054	Angiotensin II induces expression of the Tie2 receptor ligand, angiopoietin-2, in bovine retinal endothelial cells.
7	11289054	In this study, we investigated the effect of angiotensin II (AII) on Ang1 and Ang2 expression in cultured bovine retinal endothelial cells (BRECs).
8	11289054	AII stimulated Ang2 but not Ang1 mRNA expression in a dose- and time-dependent manner.
9	11289054	Protein kinase C (PKC) inhibitor completely inhibited AII-induced Ang2 expression, and the mitogen-activated protein kinase (MAPK) inhibitor also inhibited it by 69.4+/-15.6%.
10	11289054	These data suggest that AII stimulates Ang2 expression through AT1 receptor-mediated PKC and MAPK pathways in BREC, and AII may play a novel role in retinal neovascularization.
11	11310829	Expressional regulation of angiopoietin-1 and -2 and the tie-1 and -2 receptor tyrosine kinases during cutaneous wound healing: a comparative study of normal and impaired repair.
12	11310829	As angiogenesis is central to a normal wound-healing process, we investigated the regulation of Ang-1 and -2 and the related tyrosine kinase with immunoglobulin and epidermal growth factor homology (Tie)-1 and -2 receptors during normal repair in Balb/c mice and diabetes-impaired wound healing conditions in genetically diabetic (db/db) mice.
13	11310829	For both normal and impaired healing conditions, we observed a constitutive expression of Ang-1, which was paralleled by an increase of Ang-2 upon injury.
14	11310829	Furthermore, Tie-1 was strongly induced during repair with a prolonged expression in diabetic mice, whereas Tie-2 expression was constitutive during normal repair but completely absent in diabetes-impaired healing.
15	11310829	The overexpression of Ang-2 in the presence of markedly reduced VEGF in wounds of diabetic mice was associated with a dramatic decrease in endothelial cell numbers compared with normal healing as assessed by analysis of the endothelium-specific markers CD31 and von Willebrand factor, whereas the lymphatic endothelium remained stable as determined by expression of VEGF receptor-3 (VEGFR-3/Flt-4).
16	11310829	Expressional regulation of angiopoietin-1 and -2 and the tie-1 and -2 receptor tyrosine kinases during cutaneous wound healing: a comparative study of normal and impaired repair.
17	11310829	As angiogenesis is central to a normal wound-healing process, we investigated the regulation of Ang-1 and -2 and the related tyrosine kinase with immunoglobulin and epidermal growth factor homology (Tie)-1 and -2 receptors during normal repair in Balb/c mice and diabetes-impaired wound healing conditions in genetically diabetic (db/db) mice.
18	11310829	For both normal and impaired healing conditions, we observed a constitutive expression of Ang-1, which was paralleled by an increase of Ang-2 upon injury.
19	11310829	Furthermore, Tie-1 was strongly induced during repair with a prolonged expression in diabetic mice, whereas Tie-2 expression was constitutive during normal repair but completely absent in diabetes-impaired healing.
20	11310829	The overexpression of Ang-2 in the presence of markedly reduced VEGF in wounds of diabetic mice was associated with a dramatic decrease in endothelial cell numbers compared with normal healing as assessed by analysis of the endothelium-specific markers CD31 and von Willebrand factor, whereas the lymphatic endothelium remained stable as determined by expression of VEGF receptor-3 (VEGFR-3/Flt-4).
21	11564813	To establish a model of continuous endothelial activation and to elucidate the role of endothelial derived TNF in vivo, we generated transgenic mice expressing a noncleavable transmembrane form of TNF under the control of the endothelial-specific tie2 promoter.
22	11564813	Adult tie2-transmembrane TNF-transgenic mice developed chronic inflammatory pathology in kidney and liver, characterized by perivascular infiltration of mononuclear cells into these organs.
23	11564813	Along with the infiltrate, an up-regulation of the adhesion molecules ICAM-1 and VCAM-1, but not E-selectin, in the endothelium was observed.
24	11564813	Although the blood levels of soluble TNF and IFN-gamma were increased in transgenic animals after challenge with Con A, no damage of hepatocytes could be detected, as assessed by the lack of increase in plasma transaminase activities and the absence of TUNEL staining in the liver.
25	11564813	To establish a model of continuous endothelial activation and to elucidate the role of endothelial derived TNF in vivo, we generated transgenic mice expressing a noncleavable transmembrane form of TNF under the control of the endothelial-specific tie2 promoter.
26	11564813	Adult tie2-transmembrane TNF-transgenic mice developed chronic inflammatory pathology in kidney and liver, characterized by perivascular infiltration of mononuclear cells into these organs.
27	11564813	Along with the infiltrate, an up-regulation of the adhesion molecules ICAM-1 and VCAM-1, but not E-selectin, in the endothelium was observed.
28	11564813	Although the blood levels of soluble TNF and IFN-gamma were increased in transgenic animals after challenge with Con A, no damage of hepatocytes could be detected, as assessed by the lack of increase in plasma transaminase activities and the absence of TUNEL staining in the liver.
29	11978069	Using an ovine model of PI-IUGR we have observed changes in the expression of vascular endothelial growth factor, placental growth factor, their common receptors, as well as angiopoietin 2 and its receptor, Tie 2.
30	14638905	Increased renal vascular endothelial growth factor and angiopoietins by angiotensin II infusion is mediated by both AT1 and AT2 receptors.
31	14638905	Angiotensin II-infused rats received no treatment, an AT(1) receptor antagonist valsartan (30 mg/kg per d), or an AT(2) receptor antagonist PD123319 (830 ng/min).
32	14638905	Gene expression of vascular endothelial growth factor (VEGF) and receptor VEGF-R2, as well as Tie-2 and its ligands angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) were assessed by reverse transcription-PCR.
33	14638905	Gene and protein expression of VEGF, Ang-1, and Ang-2 were increased by angiotensin II infusion.
34	14638905	Valsartan and PD123319 attenuated angiotensin II-associated increases in VEGF gene and protein expression.
35	14638905	Ang-1 and Ang-2 gene but not protein expression were reduced by both treatments.
36	14638905	In situ hybridization and immunohistochemical studies localized VEGF, Ang-1, and Ang-2 expression to the epithelial cells of the glomerulus, and VEGF-R2 and Tie-2 receptors to the endothelial cells of the kidney.
37	14638905	These findings extend the increasing evidence that the AT(2) receptor, in addition to the AT(1) receptor subtype, plays an important role in mediating the proliferative actions of angiotensin II in the kidney.
38	14638905	Increased renal vascular endothelial growth factor and angiopoietins by angiotensin II infusion is mediated by both AT1 and AT2 receptors.
39	14638905	Angiotensin II-infused rats received no treatment, an AT(1) receptor antagonist valsartan (30 mg/kg per d), or an AT(2) receptor antagonist PD123319 (830 ng/min).
40	14638905	Gene expression of vascular endothelial growth factor (VEGF) and receptor VEGF-R2, as well as Tie-2 and its ligands angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) were assessed by reverse transcription-PCR.
41	14638905	Gene and protein expression of VEGF, Ang-1, and Ang-2 were increased by angiotensin II infusion.
42	14638905	Valsartan and PD123319 attenuated angiotensin II-associated increases in VEGF gene and protein expression.
43	14638905	Ang-1 and Ang-2 gene but not protein expression were reduced by both treatments.
44	14638905	In situ hybridization and immunohistochemical studies localized VEGF, Ang-1, and Ang-2 expression to the epithelial cells of the glomerulus, and VEGF-R2 and Tie-2 receptors to the endothelial cells of the kidney.
45	14638905	These findings extend the increasing evidence that the AT(2) receptor, in addition to the AT(1) receptor subtype, plays an important role in mediating the proliferative actions of angiotensin II in the kidney.
46	15047628	Because pericyte recruitment and endothelial cell survival are controlled, in part, by the angiopoietin/Tie2 ligand/receptor system, we studied the expression of angiopoietin-2 and -1 in relation to the evolution of pericyte loss in diabetic rat retinae, using quantitative retinal morphometry, and in retinae from mice with heterozygous angiopoietin deficiency (Ang-2 LacZ knock-in mice).
47	15161630	Analysis of gene expression by real-time reverse transcriptase-polymerase chain reaction demonstrates a significant up-regulation of platelet-derived growth factor-B and fibroblast growth factor-2 in VEGF-treated wounds, which corresponds with the increased granulation tissue in these wounds.
48	15161630	We observed increased numbers of circulating VEGFR2(+)/CD11b(-) cells in the VEGF-treated mice by fluorescence-activated cell sorting analysis, which likely represent an endothelial precursor population.
49	15161630	In diabetic mice with bone marrow replaced by that of tie2/lacZ mice we demonstrate that the local recruitment of bone marrow-derived endothelial lineage lacZ+ cells was augmented by topical VEGF.
50	15335307	Members of the vascular endothelial growth factor (VEGF) family are key stimulators that interact with two tyrosine kinase receptors, VEGF receptor (VEGFR)1 and 2; binding to two other receptors that lack tyrosine kinase activity, the neuropilins, is also important.
51	15335307	Signalling through the VEGF pathway is modulated by the Tie2 receptor and its binding partners, the angiopoietins.
52	15548809	Plasma vascular endothelial growth factor, angiopoietin-2, and soluble angiopoietin receptor tie-2 in diabetic retinopathy: effects of laser photocoagulation and angiotensin receptor blockade.
53	15918158	Transplanted LSEC were distinct from Kupffer cells with expression of Tie-2 promoter-driven GFP and of CD31, without F4/80 reactivity.
54	16543381	Angiopoietin-1 (Ang1) is a specific growth factor functioning to generate a stable and functional vasculature through the Tie2 and Tie1 receptors.
55	16543381	Here we determined the effectiveness of cartilage oligomeric matrix protein (COMP)-Ang1, a soluble, stable, and potent form of Ang1, on promotion of healing in cutaneous wounds of diabetic mice.
56	16625496	Alterations in the placental bed expression of VEGFR-1, VEGFR -2, and Tie-1, but not of VEGF and Tie-2, may be associated with PE, IUGR, or DM.
57	17941874	Several factors are contemplated to be engaged in pericyte conscription including angiopoietin-1 and its receptor tyrosine kinase Tie-2, vascular endothelial growth factor-A and its receptor flk-1 and the platelet-derived growth factor PDGF-B/PDGF-beta system.
58	18408125	Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) are the two ligands of the Tie-2 receptor, a receptor tyrosine kinase that is expressed on the endothelium.
59	18408125	In control mice, myocardial ischemia increased expression of both Ang-2 and Tie-2.
60	18408125	In STZ mice, Ang-2 expression was elevated, whereas Tie-2 expression was reduced, and neither was significantly altered by ischemia.
61	18408125	Using in vivo administration of an adenovirus containing Ang-1 or Ang-2, we found that shifting the Ang-2-to-Ang-1 ratio to favor Ang-1 reduced myocardial apoptosis and infarct size in STZ mice, while shifting the Ang-2-to-Ang-1 ratio to favor Ang-2 resulted in a significant increase in myocardial infarct size and apoptosis in control mice.
62	18408125	Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) are the two ligands of the Tie-2 receptor, a receptor tyrosine kinase that is expressed on the endothelium.
63	18408125	In control mice, myocardial ischemia increased expression of both Ang-2 and Tie-2.
64	18408125	In STZ mice, Ang-2 expression was elevated, whereas Tie-2 expression was reduced, and neither was significantly altered by ischemia.
65	18408125	Using in vivo administration of an adenovirus containing Ang-1 or Ang-2, we found that shifting the Ang-2-to-Ang-1 ratio to favor Ang-1 reduced myocardial apoptosis and infarct size in STZ mice, while shifting the Ang-2-to-Ang-1 ratio to favor Ang-2 resulted in a significant increase in myocardial infarct size and apoptosis in control mice.
66	18408125	Angiopoietin-1 (Ang-1) and angiopoietin-2 (Ang-2) are the two ligands of the Tie-2 receptor, a receptor tyrosine kinase that is expressed on the endothelium.
67	18408125	In control mice, myocardial ischemia increased expression of both Ang-2 and Tie-2.
68	18408125	In STZ mice, Ang-2 expression was elevated, whereas Tie-2 expression was reduced, and neither was significantly altered by ischemia.
69	18408125	Using in vivo administration of an adenovirus containing Ang-1 or Ang-2, we found that shifting the Ang-2-to-Ang-1 ratio to favor Ang-1 reduced myocardial apoptosis and infarct size in STZ mice, while shifting the Ang-2-to-Ang-1 ratio to favor Ang-2 resulted in a significant increase in myocardial infarct size and apoptosis in control mice.
70	18552213	To study the function of STAT5A/B in vivo, we deleted the floxed Stat5a/b locus in hematopoietic cells with a Tie2-Cre transgene.
71	18552213	We detected STAT5A/B binding sites in the first intron of the Tfr1 gene and found that expression of constitutively active STAT5A in an erythroid cell line increased Tfr1 levels.
72	18552213	We conclude that STAT5A/B is an important regulator of iron update in erythroid progenitor cells via its control of Tfr1 transcription.
73	18556567	Disruption of Ang-1/Tie-2 signaling contributes to the impaired myocardial vascular maturation and angiogenesis in type II diabetic mice.
74	18670619	Here, we tested the hypothesis that the response to pro-angiogenic molecules such as angiotensin-converting enzyme (ACE), endothelin-1 (ET-1), and vascular endothelial growth factor-A (VEGF) is altered by hyperglycemia.
75	18670619	Transfected (Chinese hamster ovary [CHO] or human embryonic kidney [HEK]) cells overexpressing ACE, ET-1, or VEGF were deposed onto the CAM of hyperglycemic or control embryos.
76	18670619	Only VEGF overexpression evoked a proangiogenic response in the CAM from hyperglycemic embryos, upregulating the expression of endogenous VEGF, VEGF-R2, and Tie-2, all of them related to activation of endothelial cells.
77	20079751	Incubation with 30 mM glucose caused 50% suppression in the ability of Ang1 to activate Tie2-receptor phosphorylation without any decrease in Tie2 expression or increased internalization in microvascular endothelial cells.
78	20079751	By contrast, Ang1 activation of Erk1/2 signaling was not affected by hyperglycemia.
79	20079751	Incubation of microvascular endothelial cells with 200 microM palmitic acid significantly inhibited Ang1-dependent Akt phosphorylation without affecting phosphorylation of the Tie-2 receptor or of ERK1/2.
80	20079751	Incubation with 30 mM glucose caused 50% suppression in the ability of Ang1 to activate Tie2-receptor phosphorylation without any decrease in Tie2 expression or increased internalization in microvascular endothelial cells.
81	20079751	By contrast, Ang1 activation of Erk1/2 signaling was not affected by hyperglycemia.
82	20079751	Incubation of microvascular endothelial cells with 200 microM palmitic acid significantly inhibited Ang1-dependent Akt phosphorylation without affecting phosphorylation of the Tie-2 receptor or of ERK1/2.
83	20348331	Clinical and genetic correlates of circulating angiopoietin-2 and soluble Tie-2 in the community.
84	20940700	This review provides an overview of molecular mechanisms of angiopoietin-1/-2 and Tie2 signaling in regard to the endothelial activation status in health and disease.
85	21515377	T2DM-mice also exhibited increased blood-brain barrier leakage and concomitantly, increased Angiopoietin2, but decreased Angiopoietin1, Tie2 and tight junction protein expression in the ischemic brain.
86	21515377	Therefore, decreased Angiopoietin1/Tie2 and increased Angiopoietin2 expression may contribute to diabetes-induced vascular damage after stroke.
87	21515377	T2DM-mice also exhibited increased blood-brain barrier leakage and concomitantly, increased Angiopoietin2, but decreased Angiopoietin1, Tie2 and tight junction protein expression in the ischemic brain.
88	21515377	Therefore, decreased Angiopoietin1/Tie2 and increased Angiopoietin2 expression may contribute to diabetes-induced vascular damage after stroke.
89	21570988	Our results indicate that mDMECs isolated from mouse tails expressed most of the characteristic EC markers such as von Willebrand Factor (vWF), CD31, Tie1, Tie2, ANGPT1, ANGPT2, FLK-1, FLT-1, and VEGF-A.
90	21570988	Further characterization demonstrated that these cells also expressed proteins involved in organogenesis such as bone morphogenetic proteins-2, -4 (BMP-2/-4), and their receptor (BMPR1A).
91	21570988	Surprisingly, higher expression of vWF, ANGPT1, and BMP-2 was observed in mDMECs compared to EOMA cells.
92	21606590	Angiopoietin-1/Tek signaling is a critical regulator of blood vessel development, with conventional knockout of angiopoietin-1 or Tek in mice being embryonically lethal due to vascular defects.
93	22180648	The functional role of angiopoietin-2 (Ang-2) in the regulation of angiogenesis is dependent on other growth factors such as VEGF and a given physiopathological conditions.
94	22180648	The levels of Tie-2, VEGF, caspase-3, Wnt7b, fibroblast-specific protein-1 (FSP-1), and adhesion molecules (ICAM-1 and VCAM-1) expression were measured.
95	22180648	Overexpression of Ang-2 suppressed Tie-2 and VEGF expression in db/db mouse hearts together with significant upregulation of Wnt7b expression.
96	22180648	Overexpression of Ang-2 also sensitizes ICAM-1 and VCAM-1 expression in db/db mouse hearts.
97	22180648	Exposure of MHMEC to Ang-2 resulted in increased caspase-3 activity and endothelial apoptosis.
98	22180648	Further, counterbalance of Ang-2 by overexpression of Ang-1 reversed loss of capillary density and fibrosis formation in db/db mouse hearts.
99	22180648	The functional role of angiopoietin-2 (Ang-2) in the regulation of angiogenesis is dependent on other growth factors such as VEGF and a given physiopathological conditions.
100	22180648	The levels of Tie-2, VEGF, caspase-3, Wnt7b, fibroblast-specific protein-1 (FSP-1), and adhesion molecules (ICAM-1 and VCAM-1) expression were measured.
101	22180648	Overexpression of Ang-2 suppressed Tie-2 and VEGF expression in db/db mouse hearts together with significant upregulation of Wnt7b expression.
102	22180648	Overexpression of Ang-2 also sensitizes ICAM-1 and VCAM-1 expression in db/db mouse hearts.
103	22180648	Exposure of MHMEC to Ang-2 resulted in increased caspase-3 activity and endothelial apoptosis.
104	22180648	Further, counterbalance of Ang-2 by overexpression of Ang-1 reversed loss of capillary density and fibrosis formation in db/db mouse hearts.
105	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
106	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
107	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
108	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
109	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
110	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
111	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
112	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
113	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
114	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
115	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
116	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
117	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
118	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
119	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
120	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
121	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
122	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
123	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
124	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
125	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
126	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
127	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
128	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
129	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
130	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
131	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
132	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
133	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
134	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
135	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
136	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
137	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
138	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
139	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
140	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
141	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
142	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
143	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
144	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
145	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
146	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
147	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
148	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
149	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
150	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
151	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
152	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
153	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
154	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
155	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
156	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
157	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
158	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
159	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
160	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
161	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
162	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
163	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
164	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
165	22454630	Inhibition of protein tyrosine phosphatase improves angiogenesis via enhancing Ang-1/Tie-2 signaling in diabetes.
166	22454630	Our previous studies demonstrate that disruption of Angiopoietin-1 (Ang-1)/Tie-2 signaling pathway contributes to the diabetes-associated impairment of angiogenesis.
167	22454630	Protein tyrosine phosphatase (PTP) has a critical role in the regulation of insulin signal by inhibition of tyrosine kinase phosphorylation.
168	22454630	In present study, we examined the role of protein tyrosine phosphatase-1 (SHP-1) in diabetes-associated impairment of Ang-1/Tie-2 angiogenic signaling and angiogenesis.
169	22454630	Furthermore, SHP-1 bond to Tie-2 receptor and stimulation with Ang-1 led to SHP-1 dissociation from Tie-2 in mouse heart microvascular endothelial cell (MHMEC).
170	22454630	Exposure of MHMEC to high glucose (HG, 30 mmol/L) increased SHP-1/Tie-2 association accompanied by a significant reduction of Tie-2 phosphorylation.
171	22454630	Exposure of MHMEC to HG also blunted Ang-1-mediated SHP-1/Tie-2 dissociation.
172	22454630	Knockdown of SHP-1 significantly attenuated HG-induced caspase-3 activation and apoptosis in MHMEC.
173	22454630	Treatment with PTP inhibitors restored Ang-1-induced Akt/eNOS phosphorylation and angiogenesis.
174	22454630	Our data implicate a critical role of SHP-1 in diabetes-associated vascular complications, and that upregulation of Ang-1/Tie-2 signaling by targeting SHP-1 should be considered as a new therapeutic strategy for the treatment of diabetes-associated impairment of angiogenesis.
175	22733797	We recently demonstrated that reducing IGF-1 receptor (IGF-1R) numbers in the endothelium enhances nitric oxide (NO) bioavailability and endothelial cell insulin sensitivity.
176	22733797	To examine the effect of increasing IGF-1R in the endothelium, we generated mice overexpressing human IGF-1R in the endothelium (human IGF-1R endothelium-overexpressing mice [hIGFREO]) under direction of the Tie2 promoter enhancer. hIGFREO aorta had reduced basal NO bioavailability (percent constriction to N(G)-monomethyl-l-arginine [mean (SEM) wild type 106% (30%); hIGFREO 48% (10%)]; P < 0.05).
177	22814286	Tissular hypoxia and its impact were quantified using pimonidazole immunostaining and mRNA of hypoxic inducible factor, vascular endothelial growth factor receptors 1 and 2, Tie-2, endothelial nitric oxide synthase, and inducible nitric oxide synthase.
178	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
179	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
180	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
181	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
182	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
183	23577111	Apelin receptor (APLNR) and the endogenous ligand of APLNR, apelin, induce the sprouting of endothelial cells in an autocrine or paracrine manner, which may be one of the mechanisms of DN.
184	23577111	Therefore, we observed apelin/APLNR expression in kidneys from patients with type 2 diabetes as well as the correlation between albuminuria and serum apelin in patients with type 2 diabetes.
185	23577111	The results showed that serum apelin was significantly higher in the patients with type 2 diabetes compared to healthy people (p<0.05, Fig. 1B) and that urinary albumin was positively correlated with serum apelin (R = 0.78, p<0.05).
186	23577111	Apelin also promoted the permeability of glomerular endothelial cells (p<0.05) and upregulated the expression of VEGFR2 and Tie2 in glomerular endothelial cells (p<0.05).
187	23577111	These results indicated that upregulated apelin in type 2 diabetes, which may be attributed to increased fat mass, promotes angiogenesis in glomeruli to form abnormal vessels and that enhanced apelin increases permeability via upregulating the expression of VEGFR2 and Tie2 in glomerular endothelial cells.
188	23904052	Isoxanthohumol modulates angiogenesis and inflammation via vascular endothelial growth factor receptor, tumor necrosis factor alpha and nuclear factor kappa B pathways.
189	23904052	Angiogenic regulators, including vascular endothelial growth factor receptor 2 (HUVEC, 55%), angiopoietins 1 (HUVEC, 39%; HASMC, 35%), angiopoietin 2 (HUVEC, 38%), and Tie2 (HUVEC, 56%) were also inhibited by 10 µM of IXN treatments.