Ignet

Gene Information

Gene symbol: PDGFB

Gene name: platelet-derived growth factor beta polypeptide

HGNC ID: 8800

Synonyms: SSV

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	AXL	1 hits
3	CD2AP	1 hits
4	CD44	1 hits
5	COL1A1	1 hits
6	COL4A4	1 hits
7	CYR61	1 hits
8	EDN1	1 hits
9	EGF	1 hits
10	FGF2	1 hits
11	FGF4	1 hits
12	HGF	1 hits
13	IFNG	1 hits
14	INS	1 hits
15	ITGAV	1 hits
16	ITGB1	1 hits
17	MIB1	1 hits
18	MIF	1 hits
19	MSN	1 hits
20	NOTCH3	1 hits
21	NOV	1 hits
22	NPHS2	1 hits
23	PDGFA	1 hits
24	PDGFC	1 hits
25	PDGFD	1 hits
26	PDGFRA	1 hits
27	RDX	1 hits
28	TGFA	1 hits
29	TGFB1	1 hits
30	THY1	1 hits
31	TJP1	1 hits
32	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	34939009	Mesangioproliferative Kidney Diseases and Platelet-Derived Growth Factor-Mediated AXL Phosphorylation.
2	27440779	Additionally, markers of epithelial-to-mesenchymal transition (platelet-derived growth factor receptor-β, α-smooth muscle actin, Notch-3) and PEC activation (CD44, collagen IV) were further increased by mTOR reduction.
3	25411387	PDGFB/PDGFRβ is a major mediator for GEC and mesangial cell cross talk, while vascular endothelial growth factor (VEGF), angiopoietins, and endothelin-1 are the major mediators for GEC and podocyte communication.
4	21866094	Induction of progressive glomerulonephritis by podocyte-specific overexpression of platelet-derived growth factor-D.
5	21866094	Induction of progressive glomerulonephritis by podocyte-specific overexpression of platelet-derived growth factor-D.
6	21866094	Platelet-derived growth factor-D (PDGF-D), normally expressed in podocytes, mediates mesangial cell proliferation in vivo.
7	21866094	Platelet-derived growth factor-D (PDGF-D), normally expressed in podocytes, mediates mesangial cell proliferation in vivo.
8	21866094	Renal mRNA expression of podocin and nephrin, as well as the number of glomerular WT-1-positive cells, were significantly reduced in hemizygous compared to wild-type mice, indicating loss and/or dedifferentation of podocytes.
9	21866094	Renal mRNA expression of podocin and nephrin, as well as the number of glomerular WT-1-positive cells, were significantly reduced in hemizygous compared to wild-type mice, indicating loss and/or dedifferentation of podocytes.
10	21866094	PDGF-A, -B, and both PDGF receptor chain mRNAs, fibronectin, type IV collagen, RANTES, MCP-1, and CCR-2 mRNAs were all increased in the renal cortex of PDGF-D transgenic mice.
11	21866094	PDGF-A, -B, and both PDGF receptor chain mRNAs, fibronectin, type IV collagen, RANTES, MCP-1, and CCR-2 mRNAs were all increased in the renal cortex of PDGF-D transgenic mice.
12	20031026	This study demonstrates that the expression of the mesenchymal markers CD29 and CD44, the epithelial markers CD51 and ZO-1 and the podocyte markers CD2AP and NPHS2 can be induced in these cells via incubation with epidermal growth factor/platelet-derived growth factor BB and fibroblast growth factor 4/hepatocyte growth factor, respectively.
13	20020158	The levels of the proliferation marker, mindbomb homolog 1 and the major MC mitogen, platelet-derived growth factor, and its receptors, however, were quite normal.
14	20020158	Only a small number of cells were positive for CD68 (marker for phagocytic cells) and CD34 (marker for mesenchymal precursor cells) in the NPHS1 mesangium.
15	20020158	The expression levels of the profibrotic mediators osteopontin and transforming growth factor beta were up-regulated in NPHS1 glomeruli by 3.2 and 1.6-fold, respectively, compared to the controls.
16	20020158	The synthesis by MCs of the typical fibroblast products collagen I, fibronectin, and tenascin, however, was low, and the extracellular matrix increase was caused by the accumulation of a normal MC product, collagen IV.
17	17914348	CCN3 is a novel endogenous PDGF-regulated inhibitor of glomerular cell proliferation.
18	17914348	CCN3 is a novel endogenous PDGF-regulated inhibitor of glomerular cell proliferation.
19	17914348	We identified CCN3 as a suppressed gene following platelet-derived growth factor (PDGF)-BB or -DD stimulation in a cDNA-array analysis of mesangial cells.
20	17914348	We identified CCN3 as a suppressed gene following platelet-derived growth factor (PDGF)-BB or -DD stimulation in a cDNA-array analysis of mesangial cells.
21	17914348	Induction of mesangial cell proliferation by PDGF-BB or the specific PDGF beta-receptor ligand PDGF-DD led to downregulation of CCN3 mRNA, confirming the array study.
22	17914348	Induction of mesangial cell proliferation by PDGF-BB or the specific PDGF beta-receptor ligand PDGF-DD led to downregulation of CCN3 mRNA, confirming the array study.
23	17914348	Inhibition of PDGF-B in mesangioproliferative disease led to overexpression of glomerular CCN3 mRNA.
24	17914348	Inhibition of PDGF-B in mesangioproliferative disease led to overexpression of glomerular CCN3 mRNA.
25	17914348	Our study identifies CCN3 as an endogenous inhibitor of mesangial cell growth and a modulator of PDGF-induced mitogenesis.
26	17914348	Our study identifies CCN3 as an endogenous inhibitor of mesangial cell growth and a modulator of PDGF-induced mitogenesis.
27	12845621	These include increased synthesis of type IV collagen following hyperglycaemia-induced alteration of the pattern of podocyte-integrin expression, decreased expression of matrix metalloproteinases (MMP-2 and 3), and increased expression of tissue inhibitor of metalloproteinase (TIMP).
28	12845621	Other factors which may contribute to renal matrix accumulation include vascular endothelial growth factor (VEGF), since treatment with anti-VEGF antibodies attenuates glomerular basement membrane thickening, platelet-derived growth factor (PDGF) (B chain) and its receptor, which appear to be highly expressed in mesangial and visceral epithelial cells and might play a role in the development of diabetic nephropathy.
29	12707386	By Northern blot analysis, Cyr61 mRNA was markedly upregulated in glomeruli of Thy-1 GN from day 3 through day 7, when mesangial cell migration was most prominent.
30	12707386	By in situ hybridization and immunohistochemistry, Cyr61 mRNA and protein were expressed by proximal straight tubules and afferent and efferent arterioles in normal rat kidneys and were intensely upregulated at podocytes in Thy-1 GN.
31	12707386	Platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta1 (TGF-beta1), of which the gene expression in the glomeruli of Thy-1 GN was upregulated in similar time course as Cyr61, induced Cyr61 mRNA expression in cultured podocytes.
32	12707386	In conclusion, it is shown that Cyr61 is strongly upregulated at podocytes in Thy-1 GN possibly by PDGF and TGF-beta.
33	12138258	These include platelet-derived growth factor (PDGF), a central mediator of mesangial cell proliferation and matrix synthesis, vascular endothelial growth factor (VEGF), a central angiogenic mediator regulating endothelial cell proliferation and survival and finally hepatocyte growth factor (HGF), an angiogenic growth factor with additional pronounced activity at the tubulointerstitial level.
34	11912250	Expression of a novel PDGF isoform, PDGF-C, in normal and diseased rat kidney.
35	11912250	Expression of a novel PDGF isoform, PDGF-C, in normal and diseased rat kidney.
36	11912250	Expression of a novel PDGF isoform, PDGF-C, in normal and diseased rat kidney.
37	11912250	Platelet-derived growth factor-C (PDGF-C) is a new member of the PDGF family.
38	11912250	Platelet-derived growth factor-C (PDGF-C) is a new member of the PDGF family.
39	11912250	Platelet-derived growth factor-C (PDGF-C) is a new member of the PDGF family.
40	11912250	PDGF-C expression was also studied in anti-Thy 1.1 rats treated with PDGF-B aptamer antagonists (n = 5) or irrelevant control aptamers (n = 5).
41	11912250	PDGF-C expression was also studied in anti-Thy 1.1 rats treated with PDGF-B aptamer antagonists (n = 5) or irrelevant control aptamers (n = 5).
42	11912250	PDGF-C expression was also studied in anti-Thy 1.1 rats treated with PDGF-B aptamer antagonists (n = 5) or irrelevant control aptamers (n = 5).
43	11912250	Inhibition of PDGF-B via specific aptamers reduced the injury in anti-Thy 1.1 nephritis but did not affect the glomerular PDGF-C overexpression or the mitogenicity of PDGF-CC in vitro.
44	11912250	Inhibition of PDGF-B via specific aptamers reduced the injury in anti-Thy 1.1 nephritis but did not affect the glomerular PDGF-C overexpression or the mitogenicity of PDGF-CC in vitro.
45	11912250	Inhibition of PDGF-B via specific aptamers reduced the injury in anti-Thy 1.1 nephritis but did not affect the glomerular PDGF-C overexpression or the mitogenicity of PDGF-CC in vitro.
46	10482316	Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes.
47	10482316	Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes.
48	10482316	Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously.
49	10482316	Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously.
50	10482316	The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin.
51	10482316	The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin.
52	9513903	Six-hour stimulation of mesangial cells with interferon-gamma or platelet-derived growth factor significantly increased MIF mRNA levels.
53	9513903	However, the addition of recombinant MIF to mesangial cells did not affect mesangial cell proliferation or constitutive transforming growth factor-beta mRNA expression, nor did MIF induce monocyte chemoattractant protein-1 mRNA expression.
54	9371576	In the above cells, persistent infection induced the de novo synthesis of platelet-derived growth factor A/B and enhanced the release of transforming growth factor beta1/2.
55	8647942	The cytoskeletal linking proteins, moesin and radixin, are upregulated by platelet-derived growth factor, but not basic fibroblast growth factor in experimental mesangial proliferative glomerulonephritis.
56	8647942	The expression of the two cytoskeletal linking proteins, moesin and radixin, was examined in experimental mesangial proliferative nephritis in rats (anti-Thy1 model).
57	8647942	Moesin and radixin mRNA and protein are constitutively expressed in all cell types of normal rat glomeruli, except podocytes.
58	8647942	In the anti-Thy1 model the expression of moesin and radixin was increased in infiltrating macrophages and in activated, alpha-smooth muscle actin-positive mesangial cells and was concentrated in the cellular extensions of mesangial cells in areas of glomerular remodelling.
59	8647942	Studies using neutralizing antibodies demonstrated that the increase in moesin and radixin expression by mesangial cells is mediated by PDGF, but not bFGF.
60	8647942	The increase in these cytoskeletal proteins appears to be regulated primarily (radixin) or partially (moesin) posttranscriptionally.
61	8647942	The data suggest that PDGF mediated upregulation of the cytoskeletal proteins, moesin and radixin, is important for cell migration and other changes that accompany the coordinated restoration of glomerular architecture after injury.