Related Experiment Video
Updated: Aug 2, 2026
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206+ macrophages
Hualin Cao1,2, Xiaoye Chen2, Ruyue Jin3
1Department of Urology, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.
Insights
The peptide RP-182 targets CD206+ macrophages to reduce kidney fibrosis in obstructive nephropathy. This approach inhibits M2 polarization and macrophage-to-myofibroblast transition, offering a new therapeutic strategy for chronic kidney disease.
Area of Science:
- Nephrology
- Immunology
- Fibrosis Research
Background:
- Obstructive nephropathy causes chronic kidney disease (CKD) with progressive renal fibrosis.
- CD206+ macrophages are key drivers of fibrogenesis, but targeted therapies are lacking.
Purpose of the Study:
- To investigate the role of CD206+ macrophages in obstructive nephropathy.
- To evaluate the therapeutic potential of the peptide RP-182 targeting CD206+ macrophages.
Main Methods:
- Analysis of human UPJO tissues and a murine UUO model.
- Administration of RP-182 to UUO mice and subsequent histological, molecular, and flow cytometric analyses.
- In vitro studies on bone marrow-derived macrophages to elucidate RP-182's mechanism of action.
Main Results:
- CD206+ macrophages correlated with fibrosis severity in human and murine kidneys.
- RP-182 treatment reduced renal fibrosis, tubular damage, and inflammation in UUO mice.
- In vitro, RP-182 inhibited M2 polarization and MMT by downregulating beta-catenin signaling.
Conclusions:
- RP-182 effectively alleviates obstructive renal fibrosis by targeting CD206+ macrophages.
- RP-182 inhibits M2 polarization and MMT via beta-catenin suppression.
- RP-182 represents a promising therapeutic candidate for progressive kidney fibrosis.
Introduction:
Obstructive nephropathy is a major cause of chronic kidney disease (CKD), characterized by progressive renal fibrosis with limited treatment options. CD206+ macrophages have emerged as key drivers of fibrogenesis, yet targeted strategies against this subset remain undeveloped.
Methods:
Using human ureteropelvic junction obstruction (UPJO) tissues and a murine unilateral ureteral obstruction (UUO) model, we assessed the accumulation of CD206+ macrophages and the progression of fibrosis. The therapeutic peptide RP-182, which selectively targets CD206, was administered daily to UUO mice. Histological, molecular, and flow cytometric analyses were performed to evaluate renal injury, fibrosis, inflammation, and macrophage polarization. In vitro studies using bone marrow-derived macrophages elucidated the mechanisms underlying the action of RP-182.
Results:
CD206+ macrophages were significantly enriched in human UPJO kidneys and UUO mice, correlating with fibrosis severity. RP-182 treatment attenuated collagen deposition, α- SMA expression, tubular damage, and inflammatory cell infiltration in UUO kidneys. In vitro, RP-182 selectively inhibited IL-4/IL-13-induced M2 polarization and suppressed TGF- β-triggered macrophage-to-myofibroblast transition (MMT) in M2 macrophages, while sparing M1 responses. Mechanistically, RP-182 downregulated β-catenin signaling, a pathway crucial for M2 programming and MMT.
Discussion:
Our findings demonstrate that RP-182 alleviates obstructive renal fibrosis by specifically targeting CD206+ macrophages, inhibiting their M2 polarization and MMT via β-catenin suppression. This work highlights RP-182 as a novel macrophage- directed therapeutic candidate for progressive kidney fibrosis.
