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Updated: May 16, 2026
09:43
Isolation, Culture, and Characterization of Prostate Cancer-Associated Fibroblasts
Published on: August 1, 2025
CXC-type chemokines promote myofibroblast phenoconversion and prostatic fibrosis
Mehrnaz Gharaee-Kermani1, Sathish Kasina, Bethany B Moore
1Department of Urology, The University of Michigan School of Medicine, Ann Arbor, Michigan, United States of America.
Plos One
|November 23, 2012
Summary
Inflammatory CXC-type chemokines can cause prostate tissue fibrosis by promoting myofibroblast phenoconversion. This process contributes to the development of Lower Urinary Tract Symptoms (LUTS) in men.
Area of Science:
- Urology
- Cell Biology
- Biochemistry
Background:
- Prostate fibrosis, characterized by extracellular matrix (ECM) deposition, is linked to Lower Urinary Tract Symptoms (LUTS).
- Aging prostate tissues exhibit chronic inflammation with elevated inflammatory proteins, including CXC-type chemokines.
- The role of these chemokines in mediating prostate fibrosis via myofibroblast activation remains unclear.
Purpose of the Study:
- To investigate if CXC-type chemokines can induce myofibroblast phenoconversion and extracellular matrix deposition in prostate stromal fibroblasts.
- To determine the role of specific CXC-type chemokines (CXCL5, CXCL8, CXCL12) in promoting prostate fibrosis.
- To explore the mechanism of CXCL12-induced myofibroblast activation, including the involvement of its receptor CXCR4.
Main Methods:
- Primary and immortalized prostate stromal fibroblasts were treated with TGF-β1, CXCL5, CXCL8, or CXCL12.
- Morphological changes, gene and protein expression (αSMA, collagen 1, vimentin, calponin, tenascin) were assessed using microscopy, immunofluorescence, and qRT-PCR.
- Functional myofibroblast phenoconversion was evaluated through gel contraction assays.
- The effect of CXCR4 inhibition on CXCL12-mediated responses was examined.
Main Results:
- Prostate stromal fibroblasts exhibited myofibroblast phenoconversion, expressing αSMA and collagen 1/3 transcripts and proteins in response to CXC-type chemokines.
- This phenoconversion occurred independently of exogenous TGF-β1.
- CXCL12-induced myofibroblast activation was significantly inhibited by blocking the CXCR4 receptor.
Conclusions:
- CXC-type chemokines, prevalent in aging prostate tissue, can directly induce myofibroblast phenoconversion.
- This chemokine-mediated process promotes ECM deposition and may drive prostate fibrosis.
- These findings implicate CXC-chemokines and subsequent fibrosis in the etiology and progression of male LUTS.
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