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.

Knock-Down of Long Non-Coding RNA ANRIL Suppresses Mouse Mesangial Cell Proliferation, Fibrosis, Inflammation via Regulating Wnt/β-Catenin and MEK/ERK Pathways in Diabetic Nephropathy

2020 ◽  
Author(s):  
Xun Fang ◽  
Jun Hu ◽  
Hongyan Zhou
Keyword(s):  
Cell Proliferation ◽  
Diabetic Nephropathy ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Knock Down ◽  
Non Coding Rna ◽  
Mesangial Cell Proliferation ◽  
Long Non Coding Rna

Abstract Aims Our study aimed to investigate the role of long non-coding RNA ANRIL (lnc-ANRIL) knock-down in regulating cell activities, inflammation and downstream signaling pathways in mouse mesangial cellular diabetic nephropathy (DN) model. Methods The mouse mesangial cells (SV40-MES13 cells) were treated with high-glucose (HG) to construct cellular DN model. Lnc-ANRIL knock-down plasmid and control knock-down plasmid were transfected into HG-treated SV40-MES13 cells as Sh-ANRIL group and Sh-NC group respectively. Results Lnc-ANRIL expression was significantly higher in HG-treated SV40-MES13 cells compared with normal glucose-treated SV40-MES13 cells and osmotic control-treated SV40-MES13 cells. Lnc-ANRIL knock-down suppressed cell proliferation and promoted cell apoptosis in HG-treated SV40-MES13 cells. As for fibrosis, lnc-ANRIL knock-down reduced fibronectin and collagen I expressions in HG-treated SV40-MES13 cells. Besides, the expressions of supernatant tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interleukin (IL)-1β, IL-6, IL-8 and IL-18 were reduced in Sh-ANRIL group compared with Sh-NC group. Furthermore, Wnt3, β-catenin, p-MEK1 and p-ERK1 expressions were suppressed in Sh-ANRIL group compared with Sh-NC group, which suggested that lnc-ANRIL knock-down inhibited Wnt/β-catenin and MEK/ERK pathways in HG-treated SV40-MES13 cells. Conclusions Lnc-ANRIL knock-down suppresses mouse mesangial cell proliferation, fibrosis, inflammation, Wnt/β-catenin and MEK/ERK pathways in DN.

scholarly journals Alterations of long non-coding RNA and mRNA profiles associated with extracellular matrix homeostasis and vascular aging in rats

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 832-843
Author(s):  
Qianqin Li ◽  
Zezhou Xiao ◽  
Yongsheng Wang ◽  
Ximao Liu ◽  
Hao Liu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Vascular Aging ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Reversible glomerular hypertrophy in adult patients with primary focal segmental glomerulosclerosis.

1997 ◽  
Vol 8 (11) ◽  
pp. 1668-1678
Author(s):  
K Nishimoto ◽  
H Shiiki ◽  
T Nishino ◽  
H Uyama ◽  
M Iwano ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Focal Segmental Glomerulosclerosis ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Cell Number ◽  
Glomerular Hypertrophy ◽  
Control Subjects ◽  
Segmental Glomerulosclerosis ◽  
The Mean ◽  
Glomerular Tuft

The present study was performed to assess the pathogenetic role of glomerular hypertrophy in patients with primary focal segmental glomerulosclerosis (FSGS). We studied 14 patients with FSGS by morphometry. In seven patients, minimal change nephrotic syndrome (MCNS) was diagnosed on the first renal biopsy, but FSGS was diagnosed on the second biopsy (MCNS-FSGS group). Seven other patients with FSGS on the first biopsy underwent second biopsies while in remission (FSGS-R group). Biopsy results were compared with biopsies from 10 patients with MCNS and seven control subjects. Nonsclerotic glomeruli were examined. The mean glomerular tuft area, whole glomerular area, and number of mesangial cells were significantly increased in both biopsies from the MCNS-FSGS group and in the first biopsies obtained during the nephrotic stage of the FSGS-R group, compared with control subjects and patients with MCNS. Biopsies from FSGS patients in remission showed that the mean glomerular tuft area and number of mesangial cells were significantly decreased. The fractional extracellular matrix area (extracellular matrix area/glomerular tuft area) and mesangial cell density (mesangial cell number/glomerular tuft area) in FSGS during both nephrotic and remission stages were the same as those in control subjects and patients with MCNS. The present study suggests that glomerular hypertrophy precedes the development of glomerulosclerosis in FSGS and is reversible when patients are in remission. These features support the pathogenetic importance of glomerular hypertrophy in patients with primary FSGS.

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