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Transforming Growth Factor Beta Isoforms Production by Human Peritoneal Mesothelial Cells after Exposure to Hypoxia
Author(s) -
SAED GHASSAN M.,
ZHANG WENDY,
DIAMOND MICHAEL P.,
CHEGINI NASER,
HOLMDAHL LENA
Publication year - 2000
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.8755-8920.2000.430507.x
Subject(s) - hypoxia (environmental) , transforming growth factor , transforming growth factor beta , medicine , endocrinology , messenger rna , biology , mesothelial cell , gene isoform , microbiology and biotechnology , chemistry , andrology , gene , pathology , biochemistry , oxygen , organic chemistry
PROBLEM: Although human mesothelial cells (HMC) line nearly the entire abdominal cavity, little is known about their role in adhesion formation. This study determines the effect of hypoxia and transforming growth factor (TGF)‐β1 on the ability of HMC to produce TGF‐β1‐3, which have been implicated as mediators of the healing process.
METHOD OF STUDY: HMC were cultured under normal and hypoxic conditions, and treated with and without TGF‐β1 for 24 hr. RNA from each group was subjected to multiplex reverse transcription‐polymerase chain reaction to quantitate TGF‐β1‐3 mRNA levels.
RESULTS: Hypoxia resulted in 2‐ and 3.3‐fold increase, while TGF‐β1 treatment resulted in 1.4‐ and 1.2‐fold increase (normoxia) and 0‐ and 4.8‐fold increase (hypoxia) in TGF‐β1 and TGF‐β2 mRNA levels, respectively. There was no detectable TGF‐β3 mRNA in HMC before or after treatments.
CONCLUSION: TGF‐β1 treatment under hypoxia further extenuates endogenous TGF‐β2 but blocks TGF‐β1 production, thereby decreasing the TGF‐β1/TGF‐β2 ratio, which may result in the reduction of scarring and fibrosis.