scholarly journals Inactivation of AMPK Mediates High Phosphate-Induced Extracellular Matrix Accumulation via NOX4/TGFß-1 Signaling in Human Mesangial Cells

2014 ◽  
Vol 34 (4) ◽  
pp. 1260-1272 ◽  
Author(s):  
Alexandros Papadimitriou ◽  
Elisa B.M.I. Peixoto ◽  
Kamila C. Silva ◽  
Jacqueline M. Lopes de Faria ◽  
José B. Lopes de Faria
Keyword(s):  
Extracellular Matrix ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Matrix Accumulation ◽  
High Phosphate

scholarly journals CCN3 suppresses TGF-β1-induced extracellular matrix accumulation in human mesangial cells in vitro

2017 ◽  
Vol 39 (2) ◽  
pp. 222-229 ◽  
Author(s):  
Hai-fei Liu ◽  
Hong Liu ◽  
Lin-li Lv ◽  
Kun-ling Ma ◽  
Yi Wen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mesangial Cells ◽  
Human Mesangial Cells ◽  
Matrix Accumulation ◽  
Tgf Β1

Changes in extracellular matrix composition regulate cyclooxygenase-2 expression in human mesangial cells

2011 ◽  
Vol 300 (4) ◽  
pp. C907-C918 ◽  
Author(s):  
Matilde Alique ◽  
Laura Calleros ◽  
Alicia Luengo ◽  
Mercedes Griera ◽  
Miguel Ángel Iñiguez ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Collagen Type ◽  
Mesangial Cells ◽  
Collagen Type I ◽  
Collagen I ◽  
Type I ◽  
Camp Response Element ◽  
Response Element ◽  
Human Mesangial Cells ◽  
Cox 2

Glomerular diseases are characterized by a sustained synthesis and accumulation of abnormal extracellular matrix proteins, such as collagen type I. The extracellular matrix transmits information to cells through interactions with membrane components, which directly activate many intracellular signaling events. Moreover, accumulating evidence suggests that eicosanoids derived from cyclooxygenase (COX)-2 participate in a number of pathological processes in immune-mediated renal diseases, and it is known that protein kinase B (AKT) may act through different transcription factors in the regulation of the COX-2 promoter. The present results show that progressive accumulation of collagen I in the extracellular medium induces a significant increase of COX-2 expression in human mesangial cells, resulting in an enhancement in PGE2 production. COX-2 overexpression is due to increased COX-2 mRNA levels. The study of the mechanism implicated in COX-2 upregulation by collagen I showed focal adhesion kinase (FAK) activation. Furthermore, we observed that the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT pathway by collagen I and collagen I-induced COX-2 overexpression was abolished by PI3K and AKT inhibitors. Additionally, we showed that the cAMP response element (CRE) transcription factor is implicated. Finally, we studied COX-2 expression in an animal model, NG-nitro-l-arginine methyl ester hypertensive rats. In renal tissue and vascular walls, COX-2 and collagen type I content were upregulated. In summary, our results provide evidence that collagen type I increases COX-2 expression via the FAK/PI3K/AKT/cAMP response element binding protein signaling pathway.

scholarly journals Danggui buxue tang inhibited mesangial cell proliferation and extracellular matrix accumulation through GAS5/NF-κB pathway

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Rui Zhang ◽  
Xiao Han ◽  
Tao Huang ◽  
Xiuge Wang
Keyword(s):  
Extracellular Matrix ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Danggui Buxue Tang ◽  
Iκb Kinase ◽  
Non Coding Rna ◽  
The Common ◽  
Matrix Accumulation ◽  
Related Proteins ◽  
Long Non Coding Rna

Abstract Diabetic nephropathy (DN) is the common complications of diabetes mellitus, but the efficacy of available treatments for the prevention of DN is still unsatisfactory. In the present study, we aimed to explore the effect of Danggui buxue tang (DGT) on the proliferation of high glucose (HG)-induced mesangial cells and accumulation of extracellular matrix in mesangial cells. We found DGT up-regulated the expression of growth arrest specific transcript 5 (GAS5) and IκB kinase (IKK) dose-dependently in mouse mesangial cells (SV40 MES-13). We found DGT regulated the expression IKK and the activity of nuclear transcription factor-κB (NF-κB) via GAS5, and proved that long non-coding RNA (lncRNA) GAS5 was positively related with IKK. And we proved GAS5 regulated the expression of IKK and the activity of NF-κB. In addition, DGT inhibited the viability of MES-13 cells and extracellular matrix-related proteins (laminin (LN), fibronectin (FN) and collagen IV (Col IV)) via GAS5. Moreover, we proved GAS5 regulated the viability of SV40 MES-13 cells and extracellular matrix-related proteins through NF-κB pathway. DGT inhibited the proliferation of mesangial cells and accumulation of extracellular matrix via GAS5/NF-κB, therefore, DGT could be an effective treatment for the prevention of DN.

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