Related Experiment Video
Updated: Apr 17, 2026
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Regulation of renal fibrosis by macrophage polarization
Bixia Pan1, Guohui Liu, Zongpei Jiang
1Department of Nephrology, Dongguan People's Hospital, Dongguan, China.
Background/Aims:
Since renal fibrosis always predisposes end-stage renal disease, elucidation of the molecular mechanisms that underlie the progression of renal fibrosis may substantially improve the understanding and treatment for renal failure. Previous studies have highlighted an important counteraction between transforming growth factor β 1 (TGFβ1) and bone morphogenic protein 7 (BMP7) in the epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells during chronic renal injury. Macrophages are also believed to play a critical role in renal fibrosis. However, the relationship between macrophages and EMT is unknown.
Methods:
Here, we used a mouse unilateral ureteral obstruction (UUO) model to address to these questions, and analyzed macrophage and its subpopulations purified by flow cytometry.
Results:
We found that the recruited macrophages are polarized to a M2 subtype after renal injury. M2 macrophages released high levels TGFβ1 to suppress BMP7 to enhance EMT-induced renal fibrosis. Depletion of M2 macrophages, but not of M1 macrophages, specifically inhibited EMT, and subsequently the renal fibrosis. Adoptive transplantation of M2 macrophages deteriorated renal fibrosis.
Conclusion:
Thus, our study highlights M2 macrophages as a critical target for treating renal fibrosis.
Insights
M2 macrophages drive renal fibrosis by releasing TGFβ1 and suppressing BMP7, promoting epithelial-to-mesenchymal transition (EMT). Targeting M2 macrophages offers a novel therapeutic strategy for renal fibrosis and failure.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Renal fibrosis progression to end-stage renal disease necessitates understanding underlying molecular mechanisms.
- Transforming growth factor β 1 (TGFβ1) and bone morphogenic protein 7 (BMP7) counteract each other in renal tubular epithelial cell (EMT) during injury.
- Macrophages are implicated in renal fibrosis, but their direct link to EMT remains unclear.
Purpose of the Study:
- To investigate the role of macrophages in renal fibrosis and their relationship with epithelial-to-mesenchymal transition (EMT).
- To elucidate the specific macrophage subtypes involved in promoting renal fibrosis.
Main Methods:
- Utilized a mouse unilateral ureteral obstruction (UUO) model.
- Analyzed macrophage populations and subpopulations using flow cytometry.
- Investigated the impact of M2 macrophage depletion and adoptive transplantation on renal fibrosis and EMT.
Main Results:
- Recruited macrophages in the injured kidney were predominantly M2 subtype.
- M2 macrophages secreted high levels of TGFβ1, suppressing BMP7 and enhancing EMT-driven renal fibrosis.
- Depletion of M2 macrophages, but not M1, significantly inhibited EMT and renal fibrosis.
- Adoptive transfer of M2 macrophages exacerbated renal fibrosis.
Conclusions:
- M2 macrophages play a critical role in promoting renal fibrosis through TGFβ1/BMP7 imbalance and EMT.
- M2 macrophages represent a key therapeutic target for mitigating renal fibrosis and preventing renal failure.
Related Concept Videos
01:12Chronic Inflammation: Introduction
01:28Inflammatory Response
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...