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Updated: Mar 25, 2026
Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells
Published on: March 7, 2025
KLF15 suppresses cell proliferation and extracellular matrix expression in mesangial cells under high glucose
Jun Zhang1, Hong-Bin Zhong1, Ying Lin1
1Department of Nephrology, The First Affiliated Hospital of Xiamen University, Tongmin Branch Court Xiamen 361000, China.
Abstract:
Excess mesangial extracellular matrix (ECM) and mesangial cell (MC) proliferation is the major pathologic feature of diabetic nephropathy. Kruppel-like factor 15 (KLF15) is a member of the KLF transcription factor family that plays a critical role in regulating renal fibrosis. However, the role of KLF15 in diabetic nephropathy remains poorly understood. This study was conducted to explore the role of KLF15 in the development and progress of diabetic nephropathy in high glucose (HG)-stimulated human MCs. Here, we found down-regulated expression of KLF15 in MCs induced by HG. Overexpression of KLF15 significantly inhibited MCs proliferation and ECM production induced by HG. Moreover, overexpression of KLF15 inhibited HG-induced ERK1/2 phosphorylation in MCs. In summary, our data demonstrate that KLF15 can suppress HG-induced cell proliferation and ECM protein fibronectin expression in human MCs via ERK1/2 MAPK signaling. The results provide evidence that KLF15 might be a potential molecular target for the treatment of diabetic nephropathy.
Insights
Kruppel-like factor 15 (KLF15) suppresses high glucose-induced cell growth and extracellular matrix production in diabetic nephropathy. This finding suggests KLF15 as a potential therapeutic target for kidney disease.
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Diabetic nephropathy is characterized by excess extracellular matrix (ECM) and mesangial cell (MC) proliferation.
- Kruppel-like factor 15 (KLF15), a transcription factor, is implicated in renal fibrosis.
- The specific role of KLF15 in diabetic nephropathy requires further elucidation.
Purpose of the Study:
- To investigate the role of KLF15 in high glucose (HG)-induced human MCs.
- To explore KLF15's function in the development and progression of diabetic nephropathy.
Main Methods:
- Human MCs were stimulated with high glucose (HG).
- KLF15 expression levels were analyzed.
- The effects of KLF15 overexpression on MC proliferation and ECM production were assessed.
- ERK1/2 phosphorylation was measured.
Main Results:
- HG stimulation led to down-regulated KLF15 expression in MCs.
- Overexpression of KLF15 significantly inhibited HG-induced MC proliferation and ECM production.
- KLF15 overexpression suppressed HG-induced ERK1/2 phosphorylation.
Conclusions:
- KLF15 suppresses HG-induced proliferation and fibronectin expression in human MCs through ERK1/2 MAPK signaling.
- KLF15 demonstrates potential as a molecular target for treating diabetic nephropathy.
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