cxc-type chemokines promote myofibroblast phenoconversion and prostatic fibrosiscxc-type趋化因子促进myofibroblast phenoconversion和前列腺纤维化.pdfVIP
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cxc-type chemokines promote myofibroblast phenoconversion and prostatic fibrosiscxc-type趋化因子促进myofibroblast phenoconversion和前列腺纤维化
CXC-Type Chemokines Promote Myofibroblast
Phenoconversion and Prostatic Fibrosis
1 1 2,3 4 4
Mehrnaz Gharaee-Kermani , Sathish Kasina , Bethany B. Moore , Dafydd Thomas , Rohit Mehra ,
Jill A. Macoska1*
1 Department of Urology, The University of Michigan School of Medicine, Ann Arbor, Michigan, United States of America, 2 Department of Internal Medicine, The
University of Michigan School of Medicine, Ann Arbor, Michigan, United States of America, 3 Department of Microbiology and Immunology, The University of Michigan
School of Medicine, Ann Arbor, Michigan, United States of America, 4 Department of Pathology, The University of Michigan School of Medicine, Ann Arbor, Michigan,
United States of America
Abstract
Recent studies from our group suggest that extracellular matrix (ECM) deposition and fibrosis characterize the peri-urethral
prostate tissues of some men suffering from Lower Urinary Tract Symptoms (LUTS) and that fibrosis may be a contributing
factor to the etiology of LUTS. Fibrosis can generally be regarded as an errant wound-healing process in response to chronic
inflammation, and several studies have shown that the aging prostate tissue microenvironment is rich with inflammatory
cells and proteins. However, it is unclear whether these same inflammatory proteins, particularly CXC-type chemokines, can
mediate myofibroblast phenoconversion and the ECM deposition necessary for the development of prostatic tissue fibrosis.
To examine this, immortalized and primary prostate stromal fibroblasts treated with TGF- b1, CXCL5, CXCL8, or CXCL12 were
evaluated morphologically by microscopy, by immunofluorescence and qRT-PCR for aSMA, collagen 1, vimentin, calponin,
and tenascin protein and tra
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