Evaluation of the LTBP1 and Smad6 Genes Expression in Lung Tissue of Sulfur Mustard-exposed Individuals with Long-term Pulmonary Complications

Somayeh Mami | Sara Ghaffarpour | Soghrat Faghihzadeh | Tooba Ghazanfari

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URL :   http://research.shahed.ac.ir/WSR/WebPages/Report/PaperView.aspx?PaperID=137520
Date :  2019/10/02
Publish in :    Iranian Journal of Allergy Asthma and Immunology
DOI :  https://doi.org/10.18502/ijaai.v18i5.1895
Link :  http://dx.doi.org/10.18502/ijaai.v18i5.1895
Keywords :Latency TGF beta binding proteins 1 (LTBP1), Mothers against decapentaplegic homolog 6 (SMAD6), Sulfur mustard, Transforming growth factor ?

Abstract :

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Sulfur mustard (SM) exposure injures different organs such as the lungs and leads to short and long term complications Transforming growth factor beta (TGF-β) has the main role in altering fibroblast activities linked to airways remodeling. Latency TGF beta binding proteins 1 (LTBP1 facilitates localization of TGF-β in the extracellular matrix. Mothers against decapentaplegic homolog 6 (Smad6) negatively regulates TGF-β signaling, thus establishing a main negative feedback loop. In this study, we investigated the expression of LTBP1 and Smad6 in the lung tissues of SM-exposed and control individuals. Lung formalin-fixed paraffin-embedded (FFPE) blocks of SM-exposed (20 samples) and control groups (20 samples) were collected from archival pathology department of several general hospitals. The total mRNA of lung FFPE tissues was extracted. Quality of the extracted mRNA was evaluated by an Agilent Bio analyzer and RNA was quantified using a Nano Drop. LTBP1 and Smad6 expression levels were evaluated by real-time PCR. LTBP1 expression levels did not change between the two groups (p=0.626), howeverSmad6 expression levels were significantly higher (2.6 fold) in SM-exposed individuals compared to the control group (p=0.001). Our results revealed that Smad6 may be involved in lung tissue remodeling process in SM-exposed patients. Smad6 regulates fibrotic alterations in lung tissue and its function as negative feedback mechanisms in TGF-β.