Ignet

Gene Information

Gene symbol: COL1AR

Gene name: collagen, type I, alpha, receptor

HGNC ID: 2199

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	ACTN4	1 hits
3	AGRN	1 hits
4	BMP7	1 hits
5	COL1A1	1 hits
6	COL4A4	1 hits
7	CTGF	1 hits
8	DES	1 hits
9	HK2	1 hits
10	MALAT1	1 hits
11	MAPK1	1 hits
12	NDST1	1 hits
13	NES	1 hits
14	NOV	1 hits
15	NPHS1	1 hits
16	NPHS2	1 hits
17	POSTN	1 hits
18	PTK2	1 hits
19	SERPINE1	1 hits
20	SYNPO	1 hits
21	TGFA	1 hits
22	TGFB1	1 hits

Related Sentences

#	PMID	Sentence
1	34197715	Overexpression of mm9_circ_013935 alleviates renal inflammation and fibrosis in diabetic nephropathy via the miR-153-3p/NFIC axis.
2	34197715	The expression of proteins related to fibrosis (collagen I, collagen III, fibronectin) was detected using Western blot.
3	34197715	The concentration of inflammation cytokines (tumor necrosis factor α, interleukin 1β (IL-1β), IL-8) in mouse podocytes was assessed by ELISA.
4	34197715	The miR-153-3p was revealed to bind with circ-RBM4 and directly targeted nuclear factor I/C (NFIC) in mouse podocytes.
5	34197715	Rescue assays indicated that circ-RBM4 attenuated HG-induced fibrosis and inflammation response in mouse podocytes by inhibiting miR-153-3p expression or upregulating NFIC expression.
6	34197715	Circ-RBM4 alleviated the renal inflammation and renal fibrosis in DN by targeting the miR-153-3p/NFIC axis.
7	33995063	lncRNA MALAT1 Promotes Renal Fibrosis in Diabetic Nephropathy by Targeting the miR-2355-3p/IL6ST Axis.
8	33995063	MALAT1 overexpression aggravated protein levels of collagen I (col I), collagen IV (col IV), fibronectin (FN), and laminin (LN) in HK-2 cells, while MALAT1 knockdown exerted the opposite effect.
9	33995063	In addition, miR-2355-3p overexpression attenuated fibrosis-related gene levels in HG-treated cells by inhibiting IL6ST expression and inactivating the recombinant signal transducer and activator of the transcription 3 (STAT3) signaling pathway.
10	33995063	Knockdown of miR-2355-3p reversed the inhibitory effect of MALAT1 knockdown on IL6ST, col I, col IV, FN, and LN protein levels in HG-induced cells.
11	33995063	Overexpression of MALAT1 aggravated cell damage in HG-induced cells via the miR-2355-3p/IL6ST/STAT3 signaling pathway.
12	33995063	In conclusion, MALAT1 overexpression may enhance renal fibrosis in diabetic rats and cell damage in HG-induced HK-2 cells via the miR-2355-3p/IL6ST axis, which provides a new perspective of DN treatment.
13	33137336	Nep25 mice, which express the human CD25 receptor on podocytes under control of the nephrin promotor and develop glomerulosclerosis when a specific toxin is administered were used.
14	33137336	At week six tubular injury markers normalized but with patchy collagen I and interstitial fibrosis.
15	32691413	Thus, in this study, the role of miR-27a-3p-prohibitin/TMBIM6 signaling axis in the progression of DN was elucidated.
16	32691413	Our results showed that miR-27a-3p was upregulated and prohibitin or transmembrane BAX inhibitor motif containing 6 (TMBIM6) was downregulated in the kidney tissues of db/db mice and HG-treated HK-2 cells.
17	32691413	Silencing miR-27a-3p enhanced the expression of prohibitin and TMBIM6 in the kidney tissues and HK-2 cells.
18	32691413	MiR-27a-3p silencing ameliorated renal fibrosis, reflected by reduced profibrogenic genes (e.g., transforming growth factor β1, fibronectin, collagen I and III, and α-smooth muscle actin).
19	32691413	In addition, miR-27a-3p silencing attenuated endoplasmic reticulum (ER) stress, reflected by reduced expression of p-IRE1α, p-eIF2α, XBP1s, and CHOP.
20	32691413	Mechanically, we identified prohibitin and TMBIM6 as direct targets of miR-27a-3p.
21	32691413	Inhibition of miR-27a-3p protected HG-treated HK-2 cells from apoptosis, extracellular matrix accumulation, mitochondrial dysfunction, and ER stress by regulating prohibitin or TMBIM6.
22	32691413	Taken together, we reveal that miR-27a-3p-prohibitin/TMBIM6 signaling axis regulates the progression of DN, which can be a potential therapeutic target.
23	31816967	Embryonic SCs and inducible pluripotent SCs are the most frequently used cell types, but autologous patient-derived renal SCs, such as human CD133+CD24+ renal progenitor cells (RPCs), represent a preferable option.
24	31816967	We employed collagen I-coated hydrogels with variable stiffness to modulate the mechanical environment of RPCs and found that their morphology, proliferation, migration, and differentiation toward the podocyte lineage were highly dependent on mechanical stiffness.
25	29552824	Secondly, the protein expression levels of the epithelial markers in podocytes such as nephrin and podocin, the mesenchymal markers such as desmin and collagen Ⅰ and the EMT-related mediators such as snail were detected respectively.
26	29552824	The results indicated that, HG could cause the low protein expression levels of nephrin and podocin and the high protein expression levels of desmin, collagen Ⅰ and snail in podocytes, and inducing podocyte EMT.
27	29552824	In addition, L-TP had no effect on the activation of podocyte proliferation, the co-treatment of L-TP and HG could significantly recover the protein expression levels of nephrin and podocin, inhibit the protein expression levels of desmin, collagen I and snail in podocytes, thus, further improving podocyte EMT.
28	29506630	In this study for the first time, we have investigated the responses of human podocytes cultured on different composition of GBM proteins which are cellular Fn (EDA+), plasma Fn (EDA-) and collagen IV.
29	29506630	Conditionally immortalised human podocyte were grown on the dishes coated with different matrices; collagen IV (Col IV), cellular fibronectin (CFn) containing the EDA Exon, plasma fibronectin (PFn), which lacks the EDA Exon (EDA-Fn).
30	29506630	CFn downregulated gene expression of synaptopodin and increased gene expression of collagen I and Fn.
31	29506624	CCN3, a key matricellular protein, distinctly inhibits TGFβ1-mediated Smad1/5/8 signalling in human podocyte culture.
32	29506624	CCN3, a key matricellular protein, distinctly inhibits TGFβ1-mediated Smad1/5/8 signalling in human podocyte culture.
33	29506624	CCN3 is a member of CCN family which also comprises CCN1 (CYR61), CCN2 (CTGF), CCN4 (WISP-1), CCN5 (WISP-2) and CCN6 (WISP-3).
34	29506624	CCN3 is a member of CCN family which also comprises CCN1 (CYR61), CCN2 (CTGF), CCN4 (WISP-1), CCN5 (WISP-2) and CCN6 (WISP-3).
35	29506624	CCN3 has been shown to antagonise CTGF.
36	29506624	CCN3 has been shown to antagonise CTGF.
37	29506624	Real time PCR was performed to look for gene expression of Fn and collagen IV and collagen I.
38	29506624	Real time PCR was performed to look for gene expression of Fn and collagen IV and collagen I.
39	29506624	TGFβ1 induced the Smad1/5/8, Smad3 and p38 phosphorylation and CCN3 downregulated the TGFβ1 induced Smad1/5/8 phosphorylation and did not affect Smad3 and p38 phosphorylation.
40	29506624	TGFβ1 induced the Smad1/5/8, Smad3 and p38 phosphorylation and CCN3 downregulated the TGFβ1 induced Smad1/5/8 phosphorylation and did not affect Smad3 and p38 phosphorylation.
41	29506624	CCN3 also induced collagen IV, Collagen I and Fn gene expression.
42	29506624	CCN3 also induced collagen IV, Collagen I and Fn gene expression.
43	29506624	This is the first evidence of downregulation of TGFβ-mediated activation of a Smad1/5/8 signalling pathway by CCN3 in human podocytes and in any cell type.
44	29506624	This is the first evidence of downregulation of TGFβ-mediated activation of a Smad1/5/8 signalling pathway by CCN3 in human podocytes and in any cell type.
45	29383936	Novel RAS Inhibitors Poricoic Acid ZG and Poricoic Acid ZH Attenuate Renal Fibrosis via a Wnt/β-Catenin Pathway and Targeted Phosphorylation of smad3 Signaling.
46	29383936	TGF-β1 upregulated the collagen I protein expression in HK-2 cells, and PZG and PZH treatment significantly inhibited the upregulated collagen I expression (TGF group 0.59 ± 0.08 vs TGF+PZG group 0.36 ± 0.08, P < 0.01; TGF+PZH group 0.39 ± 0.12, P < 0.01).
47	29330473	In addition, the expression of the podocyte damage marker desmin was significantly higher in the Ndst1 ^f/f Tie2Cre ^- group compared to the Ndst1 ^f/f Tie2Cre ⁺ animals (p < 0.001), although both groups had comparable numbers of podocytes.
48	29330473	Diabetic Ndst1 ^f/f Tie2Cre ⁺ animals also showed reduced interstitial fibrosis as evidenced by reduced density of αSMA-positive myofibroblasts (p < 0.01), diminished collagen III deposition (p < 0.001) and reduced mRNA expression of collagen I (p < 0.001) and fibronectin (p < 0.001).
49	28739650	We examined whether BMS002, a novel dual LPAR1 and LPAR3 antagonist, affects development of DN in endothelial nitric oxide synthase-knockout db/db mice.
50	28739650	LPAR inhibition also reduced histologic glomerular injury; decreased the expression of profibrotic and fibrotic components, including fibronectin, α-smooth muscle actin, connective tissue growth factor, collagen I, and TGF-β; and reduced renal macrophage infiltration and oxidative stress.
51	24578131	Furthermore, treatment of these cells with periostin increased the expression of collagen I and stimulated the phosphorylation of FAK, p38, and ERK 42/44.
52	23223090	The maximally effective dose of valsartan was determined to be 1000 mg/l, which reduced proteinuria by 80% and maximally reduced glomerular matrix expansion, fibronectin, collagen I and collagen III staining and glomerular mRNAs for TGFß1, PAI-1, FN and collagen I.
53	23223090	Notably, valsartan given at this dose prevented podocyte dysfunction by preserving expression of podocin and nephrin and the counter-regulating molecule B7-1 that is involved in podocyte injury.
54	21734098	We show that treatment with AGE-BSA significantly reduced podocyte adhesion to collagen IV, laminin, and fibronectin compared with Co-BSA (nonglycated BSA)-incubated cells, which was further augmented by transient inhibition of NRP1 expression using NRP1 short interference (si) RNA.
55	21734098	No changes were observed when podocyte adhesion to collagen I was assayed.
56	21734098	In addition, AGE-BSA or suppression of NRP1 both reduced the phosphorylation of focal adhesion kinase (FAK) and Erk1/2 in PMA-stimulated differentiated podocytes.
57	21734098	Analysis of RhoA family GTPase activity demonstrated that treatment with AGE-BSA or NRP1 depletion inhibited as well the activation of the Rac-1 and Cdc42 but did not affect RhoA activity.
58	21734098	Our study demonstrates that AGEs, in part via suppression of NRP1 expression, decreased podocyte adhesion and contribute to reduction of Rac-1 and Cdc42 GTPase activity.
59	21731625	This consists of a nanofibre membrane containing collagen I, electrospun directly onto a micro-photoelectroformed fine nickel supporting mesh.
60	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.
61	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.
62	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.
63	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.
64	19581826	Immunohistochemistry provided a profile of podocyte differentiation with metanephric mesenchyme and developing podocytes nestin positive and synaptopodin negative, whereas mature podocytes were positive for both markers.
65	19581826	Immunohistochemistry provided a profile of podocyte differentiation with metanephric mesenchyme and developing podocytes nestin positive and synaptopodin negative, whereas mature podocytes were positive for both markers.
66	19581826	Further investigation of individual components of ECM (laminin, fibronectin, collagen I, or collagen IV) indicated that collagen I supported the greatest proliferation similar to renal ECM, whereas a greater number of mature podocytes (nestin+/synaptopodin+) were observed on fibronectin.
67	19581826	Further investigation of individual components of ECM (laminin, fibronectin, collagen I, or collagen IV) indicated that collagen I supported the greatest proliferation similar to renal ECM, whereas a greater number of mature podocytes (nestin+/synaptopodin+) were observed on fibronectin.
68	19581826	These results suggest that (1) culture of fetal monkey podocytes can be accomplished, (2) renal ECM and collagen I can support renal cortical cells in vitro, which may recapitulate the developing kidney in vivo, and (3) fibronectin can support podocyte differentiation in vitro.
69	19581826	These results suggest that (1) culture of fetal monkey podocytes can be accomplished, (2) renal ECM and collagen I can support renal cortical cells in vitro, which may recapitulate the developing kidney in vivo, and (3) fibronectin can support podocyte differentiation in vitro.
70	18202193	TGF-beta1 suppressed the slit diaphragm-associated protein P-cadherin, zonula occludens-1, and nephrin, a change consistent with loss of the epithelial feature.
71	18202193	Meanwhile, TGF-beta1 induced the expression of the intermediate filament protein desmin and interstitial matrix components fibronectin and collagen I.
72	18202193	Furthermore, TGF-beta1 promoted the expression and secretion of matrix metalloproteinase-9 by podocytes.
73	18202193	Functionally, TGF-beta1 increased albumin permeability across podocyte monolayers, as demonstrated by a paracellular albumin influx assay.
74	18202193	The expression of Snail, a key transcriptional factor that has been implicated in initiating epithelial-to-mesenchymal transition, was induced by TGF-beta1, and ectopic expression of Snail suppressed P-cadherin and nephrin in podocytes.
75	18202193	In vivo, in addition to loss of nephrin and zonula occludens-1, mesenchymal markers such as desmin, fibroblast-specific protein-1, and matrix metalloproteinase-9 could be observed in glomerular podocytes of diabetic nephropathy.
76	17768702	Diabetic, but not non-diabetic, MHS rats showed significantly reduced synaptopodin and nephrin expression, though to a lesser extent than non-diabetic and diabetic MNS rats, together with unchanged podocyte number, density and structure and no proteinuria.
77	17768702	Agrin expression was significantly altered in diabetic versus non-diabetic MHS animals, whereas collagen I was expressed only in diabetic MHS rats and collagen IV content did not change significantly between the two groups.
78	16899516	Transgenic expression of BMP-7 in glomerular podocytes and proximal tubules prevents podocyte dropout and reductions in nephrin levels in diabetic mice.
79	16899516	Maintenance of BMP-7 also reduces glomerular fibrosis and interstitial collagen accumulation as well as collagen I and fibronectin expression.
80	16837921	Both wild-type and K256E alpha-actinin-4-expressing podocytes adhered equally to an extracellular matrix (collagen-I).
81	16837921	Both wild-type and K256E alpha-actinin-4-expressing podocytes adhered equally to an extracellular matrix (collagen-I).
82	16837921	However, podocytes expressing K256E alpha-actinin-4 showed a reduced ability to spread and migrate on collagen-I.
83	16837921	However, podocytes expressing K256E alpha-actinin-4 showed a reduced ability to spread and migrate on collagen-I.
84	8169750	Using reagents directed against the alpha 1/alpha 2 and alpha 3 chains of type IV collagen [alpha 1/alpha 2(IV), alpha 3(IV)], laminin, heparan sulphate proteoglycan (HPG), fibronectin, collagen I, and collagen III, we investigated the modifications of the glomerular matrix components in several human glomerular lesions compared with normal kidney.