The effects of sulfur mustard on expression of TGF-βs variants in lung epithelial cell line.

Abstract

Sulfur mustard (SM) is a blister-forming agent and can cause damages in various momentous human organs. Previous studies have demonstrated that chemical and mechanical injuries of epithelial cells cause to give rise the secretion of TGF-β1 and TGF-β2. These cytokines play a key role in respiratory remodeling due to SM. In this study, we investigated the impact of SM on the expression level of TGF-β isoforms and their receptors in vitro using reverse transcriptase polymerase chain reaction and western blotting. Our finding revealed the significant increase at concentrations of 25 μl/ml SM for 30 min and 60 min and also 100 μl/ml for 60 min for TGF-β1, 25, 50 and 100 μl/ml SM for 30 min for TGF-βr1 and after exposing with 100 μl/ml SM for both 30 and 60 min for TGF-β2 (p < 0.05). Data from western blotting showed the increase of TGF-β1 expression at the level of protein as the same pattern as the mRNA level. In vitro short-time exposure of fibroblast to SM can induce the expression of TGF-β1, TGF-β2 and TGF-βR1 denoting that over-expression of TGF-β isoforms and their receptors leads to differentiation and collagen production, causing in airway remodeling and fibrosis.

• Authors: Faezeh Ghane Zadeh, Monireh Sadat Mirzamani, Raheleh Halabiyan, Hamideh Mahmoodzadeh Hosseini, Abbas Ali Imani Fooladi, Masoumeh Foroutan Koudehi, Mohammad Reza Nourani
• Journal: Journal of receptor and signal transduction research (J Recept Signal Transduct Res) Vol. 35 Issue 4 Pg. 284-8 ( 2015) ISSN: 1532-4281 [Electronic] England
• PMID: 25366589 (Publication Type: Journal Article)

Chemical References

• Chemical Warfare Agents
• RNA, Messenger
• Receptors, Transforming Growth Factor beta
• Transforming Growth Factor beta1
• Transforming Growth Factor beta2
• Protein Serine-Threonine Kinases
• Receptor, Transforming Growth Factor-beta Type I
• Mustard Gas

Topics

• Airway Remodeling (drug effects)
• Cell Line
• Chemical Warfare Agents (toxicity)
• Epithelial Cells (drug effects, metabolism)
• Gene Expression (drug effects)
• Humans
• Lung (drug effects, metabolism)
• Mustard Gas (toxicity)
• Protein Serine-Threonine Kinases (genetics, metabolism)
• RNA, Messenger (genetics, metabolism)
• Receptor, Transforming Growth Factor-beta Type I
• Receptors, Transforming Growth Factor beta (genetics, metabolism)
• Signal Transduction (drug effects)
• Transforming Growth Factor beta1 (genetics, metabolism)
• Transforming Growth Factor beta2 (genetics, metabolism)