Effects of aminoguanidine and vitamin C on collagen type IV in diabetic nephropathy rats

Endocrine ◽  
2010 ◽  
Vol 39 (3) ◽  
pp. 251-258 ◽  
Author(s):  
Qiangxiang Li ◽  
Xiang Ao ◽  
Youhong Du ◽  
Yang Li ◽  
Yangshi Ou ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Vitamin C ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Type Iv

scholarly journals Differential expression of parietal epithelial cell and podocyte extracellular matrix proteins in focal segmental glomerulosclerosis and diabetic nephropathy

2019 ◽  
Vol 317 (6) ◽  
pp. F1680-F1694 ◽  
Author(s):  
Gek Cher Chan ◽  
Diana G. Eng ◽  
Jeffrey H. Miner ◽  
Charles E. Alpers ◽  
Kelly Hudkins ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Diabetic Nephropathy ◽  
Epithelial Cell ◽  
Focal Segmental Glomerulosclerosis ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Ecm Proteins ◽  
Segmental Glomerulosclerosis ◽  
Parietal Epithelial Cell

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. This study aimed to define individual ECM protein isoform expression by PECs in both experimental and human focal segmental glomerulosclerosis (FSGS) and diabetic nephropathy (DN) and to determine if changes were CD44 dependent. In experimental FSGS induced with a cytotoxic podocyte antibody and in the BTBR ob/ob mouse model of DN, PEC-derived protein staining was significantly increased in PECs. Dual staining also showed de novo expression of the podocyte-specific ECM proteins laminin-β2 and agrin in PECs. Similar findings were observed in biopsies from patients with FSGS and DN. Increases in individual ECM proteins colocalized with CD44 in PECs in disease. To determine the role of CD44, FSGS was induced in CD44−/− and CD44+/+ mice. PEC staining for perlecan, collagen type IV-α2, laminin-β2, and agrin were significantly lower in diseased CD44−/− mice compared with diseased CD44+/+ mice. These results show that in experimental and human FSGS and DN, PECs typically in an activated state, produce both PEC-derived and podocyte-specific ECM protein isoforms, and that the majority of these changes were dependent on CD44.

scholarly journals Serum anti-collagen type IV IgM antibodies and development of diabetic nephropathy in diabetics with essential hypertension

2016 ◽  
Vol 1 ◽  
pp. 86-92 ◽  
Author(s):  
Asparuh Nikolov ◽  
Ivan Tsinlikov ◽  
Ivanka Tsinlikova ◽  
George Nicoloff ◽  
Alexander Blazhev ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Essential Hypertension ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Igm Antibodies ◽  
Type Iv

Camel milk attenuates the biochemical and morphological features of diabetic nephropathy: Inhibition of Smad1 and collagen type IV synthesis

2015 ◽  
Vol 229 ◽  
pp. 100-108 ◽  
Author(s):  
Aida A. Korish ◽  
Abdel Galil Abdel Gader ◽  
Hesham M. Korashy ◽  
Abdul Majeed Al-Drees ◽  
Abdulqader A. Alhaider ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Collagen Type ◽  
Morphological Features ◽  
Camel Milk ◽  
Collagen Type Iv ◽  
Type Iv

scholarly journals Liraglutide suppresses production of extracellular matrix proteins and ameliorates renal injury of diabetic nephropathy by enhancing Wnt/β-catenin signaling

2020 ◽  
Vol 319 (3) ◽  
pp. F458-F468 ◽  
Author(s):  
Linjing Huang ◽  
Tingting Lin ◽  
Meizhen Shi ◽  
Xiuqing Chen ◽  
Peiwen Wu
Keyword(s):  
Diabetic Nephropathy ◽  
Collagen Type ◽  
Mesangial Cells ◽  
Smooth Muscle Actin ◽  
Diabetic Rats ◽  
Collagen Type Iv ◽  
Signaling Proteins ◽  
Muscle Actin ◽  
Type Iv

The Wnt/β-catenin signaling pathway is involved in production of the extracellular matrix (ECM) by mesangial cells (MCs). Recent studies by us and others have demonstrated that glucagon-like peptide-1 receptor agonists (GLP-1RAs) have protective effects against diabetic nephropathy. The purpose of the present study was to investigate whether the Wnt/β-catenin signaling in MCs contributes to GLP-1RA-induced inhibition of ECM accumulation and mitigation of glomerular injury in diabetic nephropathy. In cultured human mesangial cells, liraglutide (a GLP-1RA) treatment significantly reduced high glucose (HG)-stimulated production of fibronectin, collagen type IV, and α-smooth muscle actin, and the liraglutide effects were significantly attenuated by XAV-939, a selective inhibitor of Wnt/β-catenin signaling. Furthermore, HG treatment significantly decreased protein abundance of Wnt4, Wnt5a, phospho-glycogen synthase kinase-3β, and β-catenin. These HG effects on Wnt/β-catenin signaling proteins were significantly blunted by liraglutide treatment. For in vivo experiments, we administered liraglutide (200 μg·kg−1·12 h−1) by subcutaneous injection to streptozocin-induced type 1 diabetic rats for 8 wk. Administration of liraglutide significantly improved elevated blood urine nitrogen, serum creatinine, and urinary albumin excretion rate and alleviated renal hypertrophy, mesangial expansion, and glomerular fibrosis in type 1 diabetic rats, whereas blood glucose level and body weight did not have significant changes. Consistent with the in vitro experiments, liraglutide treatment significantly reduced the diabetes-induced increases in glomerular fibronectin, collagen type IV, and α-smooth muscle actin and decreases in glomerular Wnt/β-catenin signaling proteins. These results suggest that liraglutide alleviated glomerular ECM accumulation and renal injury in diabetic nephropathy by enhancing Wnt/β-catenin signaling.

THE ROLE OF DETERMINING THE LEVELS OF SERUM COLLAGEN TYPE IV IN DIAGNOSING EARLY DIABETIC NEPHROPATHY

Renal Failure ◽  
2002 ◽  
Vol 24 (6) ◽  
pp. 747-753 ◽  
Author(s):  
Xunhui Xu ◽  
Zhaolong Wu ◽  
Qin Zhou ◽  
Yiwen Zhang ◽  
Dan Wu
Keyword(s):  
Diabetic Nephropathy ◽  
Collagen Type ◽  
Collagen Type Iv ◽  
Type Iv ◽  
Serum Collagen ◽  
Early Diabetic Nephropathy

scholarly journals Tribbles 3 Regulates the Fibrosis Cytokine TGF-β1 through ERK1/2-MAPK Signaling Pathway in Diabetic Nephropathy

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Luwei Zhang ◽  
Jinhang Zhang ◽  
Xinnong Liu ◽  
Shengli Liu ◽  
Jun Tian
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
High Glucose ◽  
Collagen Type ◽  
Mesangial Cells ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Collagen Type Iv ◽  
Diabetic Mice ◽  
Type Iv

To reveal the expression and possible role of tribbles homolog 3 (TRB3) in the incidence of type 2 diabetic nephropathy, we used immunohistochemistry, real-time quantitative PCR, western blot analysis, and enzyme-linked immunosorbent assay (ELISA) to study the expression of TRB3, extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (ERK1/2 MAPK), transforming growth factorβ1 (TGF-β1), and collagen type IV in kidneys of db/db diabetic mice and in murine renal mesangial cells stimulated with high glucose. The expression of TRB3, TGF-β1, and collagen type IV was increased in kidneys of db/db diabetic mice. TGF-β1 and collagen type IV regulated by high glucose through ERK1/2 MAPK were downregulated by silencing TRB3 in renal mesangial cells. TRB3 may be involved in diabetic nephropathy by regulating the fibrosis cytokine TGF-β1 and collagen type IV through the ERK1/2 MAPK signaling pathway.

Release of collagen type IV degrading activity from C6 astrocytoma cells and cell density

1996 ◽  
Vol 84 (6) ◽  
pp. 1013-1019 ◽  
Author(s):  
Masashi Tamaki ◽  
Warren McDonald ◽  
Rolando F. Del Maestro
Keyword(s):  
Cell Density ◽  
Collagen Type ◽  
Cell Communication ◽  
Collagen Type Iv ◽  
Major Protein ◽  
Content Type ◽  
Type Iv ◽  
Astrocytoma Cells ◽  
C6 Astrocytoma

✓ Type IV collagen is a major protein component of the vascular basement membrane and its degradation is crucial to the initiation of tumor-associated angiogenesis. The authors have investigated the influence of cell density on the release of collagen type IV degrading activity by C6 astrocytoma cells in monolayer culture. The release of collagen type IV degrading activity was assessed biochemically, immunocytochemically, and by Western blot analysis. The results demonstrate that increasing plating density and increasing cell density are associated with decreased collagen type IV degrading activity released per tumor cell. These findings indicate the existence of regulatory mechanisms dependent on cell—cell communication, which modulate release of collagen type IV degrading activity. The extrapolation of these results to the in vivo tumor microenvironment would suggest that individual and/or small groups of invading tumor cells, distant from the main tumor mass, would release substantial collagen type IV degrading activity, which may be crucial to their continued invasion and to angiogenesis.

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