Ignet

Gene Information

Gene symbol: BGN

Gene name: biglycan

HGNC ID: 1044

Synonyms: DSPG1, SLRR1A

Related Genes

#	Gene Symbol	Number of hits
1	ACAN	1 hits
2	ACE	1 hits
3	AKT1	1 hits
4	APOB	1 hits
5	CD36	1 hits
6	COL1A1	1 hits
7	COL1AR	1 hits
8	COL4A4	1 hits
9	DCN	1 hits
10	EDN1	1 hits
11	ELN	1 hits
12	FMOD	1 hits
13	LDLR	1 hits
14	LUM	1 hits
15	MAPK1	1 hits
16	MAPK10	1 hits
17	MAPK3	1 hits
18	MAPK8	1 hits
19	MET	1 hits
20	MMP13	1 hits
21	MMP3	1 hits
22	PDGFA	1 hits
23	SAA	1 hits
24	SMAD2	1 hits
25	TGFA	1 hits
26	TGFB1	1 hits
27	VCAN	1 hits

Related Sentences

#	PMID	Sentence
1	7593228	Biglycan but not decorin mRNAs were detected by Northern analysis and by PCR.
2	8479121	In mesangial cells continuously grown on filters, the levels of messenger RNA for collagen types I and IV, biglycan and TGF-beta were not different in cells grown at elevated or standard glucose concentrations for two and four weeks.
3	8645702	It is possible that the two proteoglycans represent two populations, one with two dermatan sulfate side chains (120 kDa) and the other with only one side chain (85 kDa), presumably fitting in the decorin/biglycan family of small proteoglycans.
4	9162605	Patients with insulin-dependent diabetes mellitus (IDDM) and albuminuria are at high risk for severe micro- and macrovascular complications.
5	9162605	Diabetic vascular complications are characterized by structural alterations of extracellular matrix (ECM) components in glomeruli and large vessel walls, namely, accumulation of collagen IV, collagen VI and fibronectin and relative decrease of heparan sulphate proteoglycan (HSPG).
6	9162605	TGF-beta stimulates production of ECM components such as collagen IV, fibronectin, proteoglycans (decorin and biglycan) without increasing HSPG.
7	9162605	TGF-beta antagonists, such as decorin, betaglycan, and possibly also heparin, might be potential candidates for future therapy to prevent diabetic vascular disease.
8	10390922	In the initial phase of disease the morphologic aspect showed an increased accumulation of proteoglycan biglycan, laminin, fibronectin and type IV collagen.
9	10652025	Expression of decorin, biglycan, and collagen type I in human renal fibrosing disease.
10	10812497	Aberrant proteolytic digestion of biglycan and decorin by saliva and exocrine gland lysates from the NOD mouse model for autoimmune exocrinopathy.
11	11259366	Small proteoglycans in human diabetic nephropathy: discrepancy between glomerular expression and protein accumulation of decorin, biglycan, lumican, and fibromodulin.
12	11259366	Small leucine-rich proteoglycans (SLRPs), for example, decorin, biglycan, fibromodulin, and lumican, are extracellular matrix organizers and binding partners of TGF-b.
13	11259366	Biglycan was expressed by glomerular endothelial cells and, together with fibromodulin, by distal tubular cells and in collecting ducts.
14	11259366	Decorin and lumican became expressed in tubuli.
15	11259366	In severe glomerulosclerosis, increased decorin concentrations were found in plasma and urine, and urinary TGF-b/decorin complexes could be demonstrated indirectly.
16	11259366	Small proteoglycans in human diabetic nephropathy: discrepancy between glomerular expression and protein accumulation of decorin, biglycan, lumican, and fibromodulin.
17	11259366	Small leucine-rich proteoglycans (SLRPs), for example, decorin, biglycan, fibromodulin, and lumican, are extracellular matrix organizers and binding partners of TGF-b.
18	11259366	Biglycan was expressed by glomerular endothelial cells and, together with fibromodulin, by distal tubular cells and in collecting ducts.
19	11259366	Decorin and lumican became expressed in tubuli.
20	11259366	In severe glomerulosclerosis, increased decorin concentrations were found in plasma and urine, and urinary TGF-b/decorin complexes could be demonstrated indirectly.
21	11259366	Small proteoglycans in human diabetic nephropathy: discrepancy between glomerular expression and protein accumulation of decorin, biglycan, lumican, and fibromodulin.
22	11259366	Small leucine-rich proteoglycans (SLRPs), for example, decorin, biglycan, fibromodulin, and lumican, are extracellular matrix organizers and binding partners of TGF-b.
23	11259366	Biglycan was expressed by glomerular endothelial cells and, together with fibromodulin, by distal tubular cells and in collecting ducts.
24	11259366	Decorin and lumican became expressed in tubuli.
25	11259366	In severe glomerulosclerosis, increased decorin concentrations were found in plasma and urine, and urinary TGF-b/decorin complexes could be demonstrated indirectly.
26	11561166	The three principal CSPGs in the arterial wall are versican, which is part of the hyalectan gene family; and decorin and biglycan, which are members of a separate gene family, the small leucine-rich proteoglycans.
27	11788619	Thus, we were unable to confirm previous reports that TG-rich lipoproteins from subjects with diabetes are enriched in apo E compared with age-matched controls, consistent with the lack of difference in binding of these lipoproteins to either biglycan or the low-density lipoprotein receptor.
28	14521940	DNA sequencing revealed that CDK4 represents the rat beta defensin-1 gene (rBD-1). rBD-1 mRNA was detected in rat kidney, heart, lung, and skeletal muscle using RT-PCR.
29	14521940	Biglycan and TGF-beta1 mRNAs were significantly up-regulated in kidneys of GK rats at 26 weeks compared to 16 and 6 weeks, showing that the kidneys of GK rats mimic the gene expression pattern described for human and experimental DN.
30	15661861	Dihydrotestosterone (10 nm) and testosterone (100 nm) treatment of VSMCs resulted in the synthesis of biglycan and decorin that showed reduced electrophoretic mobility by SDS-PAGE, indicating an increase in GAG length.
31	16630654	Immunohistochemistry indicated intensive staining of decorin and biglycan in the diabetic placenta with different localizations.
32	16630654	Additionally, the basement membrane HSPG, perlecan was found to contain both CS/DS and HS in GDM placentas and plain HS in controls.
33	17652266	Because arterial extracellular matrix contains several molecules, including biglycan, versican, hyaluronan, and elastin, that may affect plaque lipid retention and stability, we determined whether diabetes affects plaque content of these molecules in a porcine model of hyperlipidemia and diabetes.
34	17652266	Hyaluronan, biglycan, versican, and apolipoprotein B (apoB) were detected with monospecific peptides or antisera, and elastin with Movat's pentachrome stain, and contents of each were quantified by computer-assisted morphometry.
35	17652266	In the hyperlipidemic groups, diabetes was associated with a 4-fold increase in intimal area, with strong correlations between intimal area and immunostained areas for hyaluronan (R(2) = 0.83, p<0.0001), biglycan (R(2) = 0.72, p<0.0001), and apoB (R(2) = 0.23, p=0.0069).
36	17652266	Because arterial extracellular matrix contains several molecules, including biglycan, versican, hyaluronan, and elastin, that may affect plaque lipid retention and stability, we determined whether diabetes affects plaque content of these molecules in a porcine model of hyperlipidemia and diabetes.
37	17652266	Hyaluronan, biglycan, versican, and apolipoprotein B (apoB) were detected with monospecific peptides or antisera, and elastin with Movat's pentachrome stain, and contents of each were quantified by computer-assisted morphometry.
38	17652266	In the hyperlipidemic groups, diabetes was associated with a 4-fold increase in intimal area, with strong correlations between intimal area and immunostained areas for hyaluronan (R(2) = 0.83, p<0.0001), biglycan (R(2) = 0.72, p<0.0001), and apoB (R(2) = 0.23, p=0.0069).
39	17652266	Because arterial extracellular matrix contains several molecules, including biglycan, versican, hyaluronan, and elastin, that may affect plaque lipid retention and stability, we determined whether diabetes affects plaque content of these molecules in a porcine model of hyperlipidemia and diabetes.
40	17652266	Hyaluronan, biglycan, versican, and apolipoprotein B (apoB) were detected with monospecific peptides or antisera, and elastin with Movat's pentachrome stain, and contents of each were quantified by computer-assisted morphometry.
41	17652266	In the hyperlipidemic groups, diabetes was associated with a 4-fold increase in intimal area, with strong correlations between intimal area and immunostained areas for hyaluronan (R(2) = 0.83, p<0.0001), biglycan (R(2) = 0.72, p<0.0001), and apoB (R(2) = 0.23, p=0.0069).
42	18348167	By affinity coelectrophoresis (ACE), we found reduced affinities of heparin and KSPGs for glycated but not normal collagen, whereas the dermatan sulfate (DS)PGs decorin and biglycan bound similarly to both, and that the affinity of heparin for normal collagen decreased with increasing pH.
43	18348167	B-cells expressing the cell surface heparan sulfate PG syndecan-1 adhered well to normal but not glycated collagen, and endothelial cell migration was delayed on glycated collagen.
44	18484279	All agents decreased (35)S-SO(4) incorporation and reduced the size of the proteoglycans, decorin and biglycan as assessed by SDS-PAGE.
45	19238187	The major chondroitin sulfate (CS) and dermatan sulfate (DS) proteoglycans are aggrecan, versican, biglycan and decorin.
46	19498343	Plasma concentrations of the acute-phase reactant serum amyloid A (SAA) are elevated in both obesity and cardiovascular disease.
47	19498343	Moreover, SAA was localized with apoB-containing lipoproteins and biglycan in the vascular wall.
48	19498343	Taken together, these data suggest male apoE-deficient mice are a model of metabolic syndrome and that chronic low level inflammation associated with increased SAA concentrations may mediate atherosclerotic lesion formation.
49	20083846	We discovered that streptozotocin-induced diabetes in Dcn(-/-) mice led to increased proteinuria associated with enhanced cyclin-dependent kinase inhibitor p27Kip1 in podocytes and tubular epithelial cells.
50	20083846	Notably, diabetic Dcn(-/-) kidneys revealed marked upregulation of the proinflammatory proteoglycan biglycan and enhanced infiltration of mononuclear cells.
51	20213272	TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2.
52	20213272	Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains.
53	20213272	TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L).
54	20213272	Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect.
55	20213272	Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L.
56	20213272	Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells.
57	20213272	TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2.
58	20213272	Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains.
59	20213272	TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L).
60	20213272	Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect.
61	20213272	Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L.
62	20213272	Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells.
63	20213272	TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2.
64	20213272	Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains.
65	20213272	TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L).
66	20213272	Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect.
67	20213272	Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L.
68	20213272	Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells.
69	20213272	TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2.
70	20213272	Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains.
71	20213272	TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L).
72	20213272	Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect.
73	20213272	Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L.
74	20213272	Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells.
75	20610572	PDGF beta-receptor kinase activity and ERK1/2 mediate glycosaminoglycan elongation on biglycan and increases binding to LDL.
76	20610572	Structural characteristics of glycosaminoglycan (GAG) chains on PGs influence lipoprotein binding and are altered adversely by platelet-derived growth factor (PDGF).
77	20610572	The signaling pathway for PDGF-mediated GAG elongation via the PDGF receptor (PDGFR) was investigated.
78	20610572	Knockdown of PDGFRbeta using small interfering RNA demonstrated that PDGF mediated changes in PGs via PDGFRbeta.
79	20610572	Downstream signaling to GAG hyperelongation was mediated through ERK MAPK and not phosphatidylinositol-3 kinase or phospholipase Cgamma.
80	20610572	In high-fat-fed apolipoprotein E(-/-) mice, inhibition of PDGFRbeta activity by imatinib reduced aortic total lipid staining area by 35% (P < 0.05).
81	20625315	Endothelin-1 stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by endothelin receptor transactivation of the transforming growth factor-[beta] type I receptor.
82	20625315	The effect of endothelin-1 to stimulate an increase in glycosaminoglycan size on biglycan was also blocked in a concentration-dependent manner by SB431542.
83	21723246	The renal proteoglycans biglycan and decorin were detectable in glomeruli, with a significant increase in renal biglycan content in diabetic mice on the high-cholesterol diet.
84	21723246	Renal biglycan and renal apolipoprotein B were colocalized, and regression analyses showed a significant relation between renal biglycan and renal apolipoprotein B content.
85	21723246	The renal proteoglycans biglycan and decorin were detectable in glomeruli, with a significant increase in renal biglycan content in diabetic mice on the high-cholesterol diet.
86	21723246	Renal biglycan and renal apolipoprotein B were colocalized, and regression analyses showed a significant relation between renal biglycan and renal apolipoprotein B content.
87	21913799	TGF-β stimulates biglycan core protein synthesis but not glycosaminoglycan chain elongation via Akt phosphorylation in vascular smooth muscle.
88	21913799	We investigated whether TGF-β-mediated proteoglycan synthesis is via PI3K/Akt.
89	21913799	Akt phosphorylation was blocked by Akt1/2 inhibitor SN30978; however, it did not block Smad2 phosphorylation at either the carboxy or linker regions indicating that TGF-β-mediated Akt phosphorylation is independent of Smad2 signalling.
90	21913799	Treatment with SN30978 showed a concentration-dependent decrease in TGF-β-mediated [(35)S]-sulphate and [(35)S]-Met/Cys incorporation into secreted proteoglycans; however, SDS-PAGE showed no change in biglycan size.
91	21913799	Our findings demonstrate that Akt is a downstream signalling component of TGF-β-mediated biglycan core protein synthesis but not glycosaminoglycan chain hyper-elongation in VSM.
92	21913799	TGF-β stimulates biglycan core protein synthesis but not glycosaminoglycan chain elongation via Akt phosphorylation in vascular smooth muscle.
93	21913799	We investigated whether TGF-β-mediated proteoglycan synthesis is via PI3K/Akt.
94	21913799	Akt phosphorylation was blocked by Akt1/2 inhibitor SN30978; however, it did not block Smad2 phosphorylation at either the carboxy or linker regions indicating that TGF-β-mediated Akt phosphorylation is independent of Smad2 signalling.
95	21913799	Treatment with SN30978 showed a concentration-dependent decrease in TGF-β-mediated [(35)S]-sulphate and [(35)S]-Met/Cys incorporation into secreted proteoglycans; however, SDS-PAGE showed no change in biglycan size.
96	21913799	Our findings demonstrate that Akt is a downstream signalling component of TGF-β-mediated biglycan core protein synthesis but not glycosaminoglycan chain hyper-elongation in VSM.
97	21913799	TGF-β stimulates biglycan core protein synthesis but not glycosaminoglycan chain elongation via Akt phosphorylation in vascular smooth muscle.
98	21913799	We investigated whether TGF-β-mediated proteoglycan synthesis is via PI3K/Akt.
99	21913799	Akt phosphorylation was blocked by Akt1/2 inhibitor SN30978; however, it did not block Smad2 phosphorylation at either the carboxy or linker regions indicating that TGF-β-mediated Akt phosphorylation is independent of Smad2 signalling.
100	21913799	Treatment with SN30978 showed a concentration-dependent decrease in TGF-β-mediated [(35)S]-sulphate and [(35)S]-Met/Cys incorporation into secreted proteoglycans; however, SDS-PAGE showed no change in biglycan size.
101	21913799	Our findings demonstrate that Akt is a downstream signalling component of TGF-β-mediated biglycan core protein synthesis but not glycosaminoglycan chain hyper-elongation in VSM.
102	22532774	Biglycan is highly similar in structure to decorin, therefore we hypothesized it would have a similar expression profile and role to decorin in adipose tissue.
103	22532774	Collectively, our data suggest that the small leucine-rich proteoglycan family proteins biglycan and decorin may play a role in the development of obesity and T2D, possibly by facilitating expansion of adipose tissue mass.
104	22532774	Biglycan is highly similar in structure to decorin, therefore we hypothesized it would have a similar expression profile and role to decorin in adipose tissue.
105	22532774	Collectively, our data suggest that the small leucine-rich proteoglycan family proteins biglycan and decorin may play a role in the development of obesity and T2D, possibly by facilitating expansion of adipose tissue mass.
106	23042903	The gene expression of collagen I and III, biglycan, versican, MMP-13, and MMP-3 was measured by quantitative RT-PCR, and their protein distribution was studied by immunohistochemistry.
107	23042903	This correlated with impaired structural organization of collagen fibers and a reduced expression of collagen I and III in the injured tendons of the diabetic GK compared with Wistar control.