The Role of miR-143 in Regulating Inflammation and Pulmonary Fibrosis Induced by Mustard Gas: Therapeutic Potential and Clinical Applications
Subject Areas : Journal of Animal Biology
atiyeh tavakoli
1
,
Mohadeseh Valizadeh
2
,
Mahya Rahmani
3
,
nasrin karimi
4
1 - Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
2 - Faculty Member, School of Medical Technologies, Shahid Beheshti University of Medical Sciences, Tehran, Iran
3 - Department of Biology, Research Sciences Branch, Islamic Azad University, Tehran, Iran
4 - Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
Keywords: miR-143, mustard gas, lung, gene expression, biomarker, chemical injury,
Abstract :
miR-143 is one of the important microRNAs involved in regulating cellular processes such as growth, differentiation, and cell death. Mustard gas (Sulfur Mustard, SM) is a chemical agent known for its destructive effects on the lungs. The damage caused by SM to lung cells can lead to changes in the expression of microRNAs, including miR-143. The aim of this study was to investigate the effects of mustard gas on the expression of miR-143 in the lung tissue of chemical warfare veterans. In this study, 30 lung biopsy samples were collected from chemical warfare veterans with varying degrees of damage (10 samples with moderate damage and 10 samples with severe damage), along with 10 healthy control samples. Total RNA was extracted, and after cDNA synthesis, miR-143 expression was measured using Real-time PCR. U6snRNA was used as an internal control, and GraphPad Prism version 6.07 software was used for statistical analysis. The results showed a significant decrease in miR-143 expression in the lungs of chemical warfare veterans compared to the control group. Specifically, in the severe damage group, this decrease was much more pronounced than in the other groups (P<0.0001). In the moderate damage group, a less significant decrease was observed (P value = 0.7602). ROC curve analysis also showed that miR-143 could be considered a potential biomarker for identifying lung damage caused by SM, though confirmation of these findings requires further studies.
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