Transforming Growth Factor Beta Isoforms Production by Human Peritoneal Mesothelial Cells after Exposure to Hypoxia

• Published in: American journal of reproductive immunology (1989) 2000-05, Vol.43 (5), p.285-291
• Main Authors: SAED, GHASSAN M., ZHANG, WENDY, DIAMOND, MICHAEL P., CHEGINI, NASER, HOLMDAHL, LENA
• Format: Article
• Language: English
• Subjects: Adhesion; Biological and medical sciences; Cell Adhesion; Cell Hypoxia; Cell physiology; Cells, Cultured; Effects of physical and chemical agents; Epithelial Cells - metabolism; Fundamental and applied biological sciences. Psychology; Humans; hypoxia; mesothelial cells; Molecular and cellular biology; peritoneum; Peritoneum - cytology; Peritoneum - metabolism; Protein Isoforms - metabolism; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; TGF-β; Transforming Growth Factor beta - biosynthesis; Transforming Growth Factor beta - genetics; Transforming Growth Factor beta - pharmacology; Transforming Growth Factor beta1; Transforming Growth Factor beta2
• ISSN: 1046-7408; 1600-0897
• DOI: 10.1111/j.8755-8920.2000.430507.x

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.