Ignet

Gene Information

Gene symbol: HSPG2

Gene name: heparan sulfate proteoglycan 2

HGNC ID: 5273

Synonyms: perlecan, PRCAN

Related Genes

#	Gene Symbol	Number of hits
1	ANGPTL3	1 hits
2	APOE	1 hits
3	BGN	1 hits
4	CD36	1 hits
5	CD44	1 hits
6	COL1A1	1 hits
7	COL4A4	1 hits
8	DCN	1 hits
9	DMD	1 hits
10	FBN1	1 hits
11	GPC1	1 hits
12	IL7	1 hits
13	JUP	1 hits
14	NID1	1 hits
15	NPHS1	1 hits
16	NPHS2	1 hits
17	PRKCA	1 hits
18	PRKCB1	1 hits
19	SDC1	1 hits
20	SDC4	1 hits
21	SMC3	1 hits
22	TGFA	1 hits
23	TGFB1	1 hits
24	TJP1	1 hits
25	UTRN	1 hits
26	VCAN	1 hits

Related Sentences

#	PMID	Sentence
1	9176840	Mouse glomerular epithelial cells in culture with features of podocytes in vivo express aminopeptidase A and angiotensinogen but not other components of the renin-angiotensin system.
2	9176840	By indirect immunofluorescence, the cells were positive for cytokeratin, vimentin, desmin, and the ZO-1 protein, a component of the tight junction complex.
3	9176840	The mRNA expression of several components of the renin-angiotensin system was also examined, and some factors indirectly coupled to the renin-angiotensin system component angiotensin II in this podocytic culture by RT-PCR analysis. mRNA Expression for the angiotensin II degrading hydrolase aminopeptidase A and angiotensinogen was found, but this was not found for any other component of this system, such as renin, angiotensin-converting enzyme, or the angiotensin II receptors AT1a, AT1b, and AT2.
4	9176840	In addition, expression of the growth factors transforming growth factor-beta and interleukin-7, and the extracellular matrix components fibronectin, laminin B2, perlecan, and collagen IV alpha 1, was observed.
5	9434070	Syndecan-4, glypican-1 and biglycan were all expressed in normal glomeruli, whereas syndecan-1, perlecan and versican mRNAs were confined to the papillary area.
6	9434070	By hybridizing adjacent sections with a probe for the podocyte-specific PTPase GLEPP-1, the glomerular cells containing mRNA for syndecan-4 and glypican-1 could be identified as podocytes, whereas the cells expressing biglycan were identified as mesangial cells.
7	9434070	The constitutive expression of syndecan-4, glypican-1 and biglycan in glomerular cells points to a role for these polyanionic molecules in maintaining the integrity of the glomerular filtration barrier.
8	10703664	Because the major DG binding partners in the GBM (laminin, agrin, perlecan), and the intracellular dystrophin analogue utrophin are also present in glomeruli, it appears that podocytes adhere to the GBM via DG complexes, similar to muscle fibers in which actin is linked via dystrophin and DG to the extracellular matrix.
9	15585670	The HGECs express several PGs: syndecan, versican, glypican, perlecan, decorin, and biglycan, which may contribute to the glomerular charge barrier.
10	16622173	We found that podocytes produce versican, syndecan-1, decorin, and biglycan together with the previously known PG syndecan-4, glypican, and perlecan.
11	16622173	PAN treatment downregulated the mRNA and the protein expression of both versican (by 24 +/- 6%, P < 0.01, for mRNA and by 50% for protein) and perlecan (by 14 +/- 5%, P < 0.05, for mRNA and by 50% for protein).
12	16622173	Steroid treatment decreased perlecan (by 24 +/- 3%, P < 0.01) and syndecan-1 expression (by 30 +/- 4%, P < 0.01) but increased the expression of decorin 2.5-fold.
13	16622173	We found that podocytes produce versican, syndecan-1, decorin, and biglycan together with the previously known PG syndecan-4, glypican, and perlecan.
14	16622173	PAN treatment downregulated the mRNA and the protein expression of both versican (by 24 +/- 6%, P < 0.01, for mRNA and by 50% for protein) and perlecan (by 14 +/- 5%, P < 0.05, for mRNA and by 50% for protein).
15	16622173	Steroid treatment decreased perlecan (by 24 +/- 3%, P < 0.01) and syndecan-1 expression (by 30 +/- 4%, P < 0.01) but increased the expression of decorin 2.5-fold.
16	16622173	We found that podocytes produce versican, syndecan-1, decorin, and biglycan together with the previously known PG syndecan-4, glypican, and perlecan.
17	16622173	PAN treatment downregulated the mRNA and the protein expression of both versican (by 24 +/- 6%, P < 0.01, for mRNA and by 50% for protein) and perlecan (by 14 +/- 5%, P < 0.05, for mRNA and by 50% for protein).
18	16622173	Steroid treatment decreased perlecan (by 24 +/- 3%, P < 0.01) and syndecan-1 expression (by 30 +/- 4%, P < 0.01) but increased the expression of decorin 2.5-fold.
19	17259378	The protein kinase C (PKC)-beta isoform has been implicated to play a pivotal role in the development of diabetic kidney disease.
20	17259378	After 8 weeks of diabetes, the high-glucose-induced renal and glomerular hypertrophy, as well as the increased expression of extracellular matrix proteins such as collagen and fibronectin, was reduced in PKC-beta(-/-) mice.
21	17259378	Furthermore, the high-glucose-induced expression of the profibrotic cytokine transforming growth factor (TGF)-beta1 and connective tissue growth factor were significantly diminished in the diabetic PKC-beta(-/-) mice compared with diabetic wild-type mice, suggesting a role of the PKC-beta isoform in the regulation of renal hypertrophy.
22	17259378	Notably, increased urinary albumin-to-creatinine ratio persisted in the diabetic PKC-beta(-/-) mice.
23	17259378	The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-beta(-/-) mice as previously demonstrated in the nonalbuminuric diabetic PKC-alpha(-/-) mice.
24	17259378	In summary, the differential effects of PKC-beta deficiency on diabetes-induced renal hypertrophy and albuminuria suggest that PKC-beta contributes to high-glucose-induced TGF-beta1 expression and renal fibrosis, whereas perlecan, as well as nephrin, expression and albuminuria is regulated by other signaling pathways.
25	17259378	The protein kinase C (PKC)-beta isoform has been implicated to play a pivotal role in the development of diabetic kidney disease.
26	17259378	After 8 weeks of diabetes, the high-glucose-induced renal and glomerular hypertrophy, as well as the increased expression of extracellular matrix proteins such as collagen and fibronectin, was reduced in PKC-beta(-/-) mice.
27	17259378	Furthermore, the high-glucose-induced expression of the profibrotic cytokine transforming growth factor (TGF)-beta1 and connective tissue growth factor were significantly diminished in the diabetic PKC-beta(-/-) mice compared with diabetic wild-type mice, suggesting a role of the PKC-beta isoform in the regulation of renal hypertrophy.
28	17259378	Notably, increased urinary albumin-to-creatinine ratio persisted in the diabetic PKC-beta(-/-) mice.
29	17259378	The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-beta(-/-) mice as previously demonstrated in the nonalbuminuric diabetic PKC-alpha(-/-) mice.
30	17259378	In summary, the differential effects of PKC-beta deficiency on diabetes-induced renal hypertrophy and albuminuria suggest that PKC-beta contributes to high-glucose-induced TGF-beta1 expression and renal fibrosis, whereas perlecan, as well as nephrin, expression and albuminuria is regulated by other signaling pathways.
31	19553347	Renal tissue from Tg26 mice not only showed decreased apoE expression but also displayed downregulation of perlecan mRNA expression.
32	19553347	Moreover, nef transgenic mice showed a decrease in renal tissue expression of both apoE and perlecan.
33	19553347	These findings suggest that HIV-1-induced reduction in podocyte apoE expression and associated downregulation of podocyte perlecan might be contributing to mesangial cell (MC) phenotype in HIVAN.
34	19553347	Renal tissue from Tg26 mice not only showed decreased apoE expression but also displayed downregulation of perlecan mRNA expression.
35	19553347	Moreover, nef transgenic mice showed a decrease in renal tissue expression of both apoE and perlecan.
36	19553347	These findings suggest that HIV-1-induced reduction in podocyte apoE expression and associated downregulation of podocyte perlecan might be contributing to mesangial cell (MC) phenotype in HIVAN.
37	19553347	Renal tissue from Tg26 mice not only showed decreased apoE expression but also displayed downregulation of perlecan mRNA expression.
38	19553347	Moreover, nef transgenic mice showed a decrease in renal tissue expression of both apoE and perlecan.
39	19553347	These findings suggest that HIV-1-induced reduction in podocyte apoE expression and associated downregulation of podocyte perlecan might be contributing to mesangial cell (MC) phenotype in HIVAN.
40	20424482	Puromycin-induced injury of cultured podocytes showed a time-dependent upregulation of ANGPTL3 accompanied by a time-dependent downregulation of perlecan and agrin by Western blot and RT-PCR analysis.
41	20424482	In addition, the increased expression of ANGPTL3 following gene transfection upregulated the expression of perlecan and agrin in podocytes.
42	20424482	Double immunolabeling demonstrated colocalization of perlecan and ANGPTL3 on podocytes following pcDNA3.1-ANGPTL3 transfection.
43	20424482	In conclusion, ANGPTL3 expression is upregulated in puromycin-induced podocyte damage and is associated with the reduction of perlecan and agrin expression.
44	20424482	Puromycin-induced injury of cultured podocytes showed a time-dependent upregulation of ANGPTL3 accompanied by a time-dependent downregulation of perlecan and agrin by Western blot and RT-PCR analysis.
45	20424482	In addition, the increased expression of ANGPTL3 following gene transfection upregulated the expression of perlecan and agrin in podocytes.
46	20424482	Double immunolabeling demonstrated colocalization of perlecan and ANGPTL3 on podocytes following pcDNA3.1-ANGPTL3 transfection.
47	20424482	In conclusion, ANGPTL3 expression is upregulated in puromycin-induced podocyte damage and is associated with the reduction of perlecan and agrin expression.
48	20424482	Puromycin-induced injury of cultured podocytes showed a time-dependent upregulation of ANGPTL3 accompanied by a time-dependent downregulation of perlecan and agrin by Western blot and RT-PCR analysis.
49	20424482	In addition, the increased expression of ANGPTL3 following gene transfection upregulated the expression of perlecan and agrin in podocytes.
50	20424482	Double immunolabeling demonstrated colocalization of perlecan and ANGPTL3 on podocytes following pcDNA3.1-ANGPTL3 transfection.
51	20424482	In conclusion, ANGPTL3 expression is upregulated in puromycin-induced podocyte damage and is associated with the reduction of perlecan and agrin expression.
52	20424482	Puromycin-induced injury of cultured podocytes showed a time-dependent upregulation of ANGPTL3 accompanied by a time-dependent downregulation of perlecan and agrin by Western blot and RT-PCR analysis.
53	20424482	In addition, the increased expression of ANGPTL3 following gene transfection upregulated the expression of perlecan and agrin in podocytes.
54	20424482	Double immunolabeling demonstrated colocalization of perlecan and ANGPTL3 on podocytes following pcDNA3.1-ANGPTL3 transfection.
55	20424482	In conclusion, ANGPTL3 expression is upregulated in puromycin-induced podocyte damage and is associated with the reduction of perlecan and agrin expression.
56	24190885	Retinal pigmented epithelial (RPE) cells that expressed high levels of E-cadherin and had cell-cell junctions rich in zona occludens (ZO)-1, β-catenin and heparan sulfate, required syndecan-4 but not fibronectin or protein kinase C α (PKCα) to assemble extracellular matrix (fibrillin microfibrils and perlecan).
57	24190885	In contrast, RPE cells that strongly expressed mesenchymal smooth muscle α-actin but little ZO-1 or E-cadherin, required fibronectin (like fibroblasts) and PKCα, but not syndecan-4.
58	24190885	TGFβ, which stimulates epithelial-mesenchymal transition, altered gene expression and overcame the dependency on syndecan-4 for microfibril deposition in epithelial RPE cells, whereas blocking cadherin interactions disrupted microfibril deposition.
59	24190885	Renal podocytes had a transitional phenotype with pericellular β-catenin but little ZO-1; they required syndecan-4 and fibronectin for efficient microfibril deposition.
60	25531564	In vitro, short-term exposure of human PECs to hyperglycemic conditions (30 mM glucose) advanced glycation end products (100 μg/ml) or transforming growth factor-β1 (TGF-β1; 5 ng/ml) increased the mRNA expression of collagen type I α-1, collagen type IV (all six α-chains), bamacan, nidogen 1, laminin α-1, and perlecan.
61	28228399	Light, electron microscopic, immunofluorescence, and in situ hybridization studies clearly show that the thickening of the GBM is due not only to overproduction of components of the mature GBM (α3 and α5 chains of collagen IV and agrin) by podocytes but also to resumed increased synthesis of the α1 chain of collagen IV and of perlecan by endothelial cells usually seen during embryonic development.
62	31200942	These cells co-expressed the podocyte markers podocin, nephrin, p57 and VEGF164, but not markers of endothelial (ERG) or mesangial (Perlecan) cells.
63	31630546	In healthy glomeruli, parietal epithelial cell (PEC)-derived extracellular matrix (ECM) proteins include laminin-β₁, perlecan, and collagen type IV-α₂ and podocyte-specific ECM proteins include laminin-β₂, agrin, and collagen type IV-α₄.
64	31630546	To determine the role of CD44, FSGS was induced in CD44^-/- and CD44^+/+ mice.
65	31630546	PEC staining for perlecan, collagen type IV-α₂, laminin-β₂, and agrin were significantly lower in diseased CD44^-/- mice compared with diseased CD44^+/+ mice.
66	31630546	In healthy glomeruli, parietal epithelial cell (PEC)-derived extracellular matrix (ECM) proteins include laminin-β₁, perlecan, and collagen type IV-α₂ and podocyte-specific ECM proteins include laminin-β₂, agrin, and collagen type IV-α₄.
67	31630546	To determine the role of CD44, FSGS was induced in CD44^-/- and CD44^+/+ mice.
68	31630546	PEC staining for perlecan, collagen type IV-α₂, laminin-β₂, and agrin were significantly lower in diseased CD44^-/- mice compared with diseased CD44^+/+ mice.
69	32858527	PECs differentiated to a podocyte fate had ultrastructural features of podocytes and co-expressed the podocyte markers podocin, nephrin, p57 and VEGF164, but not markers of mesangial (Perlecan) or endothelial (ERG) cells.