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Cyclophosphamide ameliorates membranous nephropathy by upregulating miR-223 expression, promoting M2 macrophage
Chunying Yao1, Qiubo Ma1, Ying Shi1
1Department of Nephrology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, China.
Background:
Membranous nephropathy (MN), also known as membranous glomerulonephritis, is a leading cause of adult nephrotic syndrome. The main pathological features encompass the deposition of immune complexes within the glomerular basement membrane epithelial cells, thickening of the basement membrane, and fusion of the foot process.
Objective:
This study aims to investigate the role of the immune and inflammatory modulator miR-223 in the immunosuppressive and anti-inflammatory effects of cyclophosphamide (CTX) on membranous nephropathy (MN).
Methods:
miR-223 mimetics or inhibitors was used to regulate miR-223 levels. LPS induced inflammatory cell model and cell polarization. CTX was used to treat Lipopolysaccharides (LPS) induced inflammatory response and polarization. Cationic bovine serum albumin (c-BSA) induced BALB/c mouse MN model, while CTX was used to treat c-BSA induced MN.
Results:
The miR-223 level in LPS induced inflammatory model cells was lower than that in control cells. The levels of inflammatory factors in LPS+miR-223 mimetics and CTX+miR-223i cells were lower than those in LPS and miR-223i cells. The protein levels of LPS+miR-223 mimic, CTX+miR-223i macrophage M2 phenotype markers Arginase-1 (Arg1), transforming growth factor β1 (TGF-β1), anti-inflammatory factors interleukin-4 (IL4) and interleukin-13 (IL13) were significantly higher than those of LPS and miR-223i. The effect of CTX was confirmed in a BALB/c mouse MN model induced by cationic bovine serum albumin (c-BSA).
Conclusion:
CTX upregulates the expression of miR-223, promotes polarization of M2 macrophages, alleviates the inflammatory response and renal injury of MN.
Insights
Cyclophosphamide (CTX) treatment upregulates miR-223, promoting M2 macrophage polarization and reducing inflammation in membranous nephropathy (MN). This study reveals miR-223's role in CTX's therapeutic effects on MN.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Membranous nephropathy (MN) is a primary cause of adult nephrotic syndrome.
- Pathological hallmarks include immune complex deposition, basement membrane thickening, and foot process fusion.
Purpose of the Study:
- Investigate miR-223's role in cyclophosphamide (CTX)'s immunosuppressive and anti-inflammatory actions in MN.
- Elucidate the mechanism of CTX in modulating immune responses relevant to MN.
Main Methods:
- Utilized miR-223 mimetics/inhibitors to modulate miR-223 levels.
- Employed lipopolysaccharide (LPS)-induced inflammatory cell models and a cationic bovine serum albumin (c-BSA)-induced mouse MN model.
- Assessed the effects of CTX on inflammatory responses, cell polarization, and renal injury.
Main Results:
- miR-223 levels were lower in LPS-induced inflammatory cells.
- CTX and miR-223 mimetics reduced inflammatory factors.
- CTX treatment increased M2 macrophage markers (Arg1, TGF-β1, IL-4, IL-13) and alleviated renal injury in the MN model.
Conclusions:
- Cyclophosphamide (CTX) upregulates miR-223 expression.
- CTX promotes M2 macrophage polarization, mitigating inflammation and renal injury in membranous nephropathy.
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