Decreased expression of miR-20a and miR-92a in the serum from sulfur mustard-exposed patients during the chronic phase of resulting illness

Abstract

Our findings may provide a differential diagnostic method that is effective for diagnosing lung diseases caused by SM exposure. Additionally, these miRNAs may be regarded as probable targets for treatment of lung injuries.

Evaluating the Differential Effects of Valproic Acid on Wharton’s Jelly Mesenchymal Stem Cells

“…2^ -RΔΔCT formula was used to investigate the relative expression of the genes under study to GAPDH in WJMSCs with and without VPA treatments. 14 Melt curve analysis was performed to investigate the specificity of the primers and LinReg PCR software was employed for calculating primer efficiencies. Sequencing procedure was performed to validate PCR products (data not shown).…”

Deciphering the role of microRNAs in mustard gas–induced toxicity

“…The first study, conducted by Alvanegh et al, included 30 patients with documented SM exposure (admitted from March 1, 2013 to July 1, 2014) who had mild to severe mustard lung, as determined by the values of forced expiratory volume in 1 second. 69 The expression of miR-92a and miR-20a was analyzed in the sera (from venous blood) of patients with mustard lung and compared with the expression profile of the miRNAs in control individuals. Both these miRNAs have been implicated in hypoxia, 101 apoptosis, 102 and tumorigenesis, 103,104 all conditions associated with mustard lung.…”

“…109 Alvanegh et al thus proposed that decreased expression of these miRNAs could be responsible for dysregulation of bronchial repair and fibrosis in airways that is commonly observed in patients with mustard lung. 69 The second study was conducted in 2018 by Gharbi et al, in which they evaluated the expression levels of various miRNAs in the sera (from peripheral blood samples) of SM-exposed veterans of the Iran-Iraq war (SM exposure in February 1986) and matched controls. 76 SM exposure in patients enrolled in this study ranged from those with mild to severe symptoms of COPD, as assessed per GOLD standards.…”

“…A putative pathway that several of the miRNAs associated with long-term effects of SM-induced toxicity regulate is TGF-β signaling, which is involved in cell proliferation, cell differentiation, immunological response, and inflammation. 96 miR-20a, 69,71 miR-21, 71 miR-21-5p, 70 mi-92a, 69 miR-138, 75 miR-9, and miR-143 68 have been associated with SM-induced toxicity and regulation of the TGF-β pathway. One or more of these miRNAs could serve as therapeutic targets to alleviate inflammation, facilitate cell proliferation, promote wound healing, and delay fibrosis in SM-induced toxicity; however, further research into their detailed mechanisms of action is warranted.…”

“…[62][63][64][65][66] Thus, miRNAs could also be integrally involved in the toxicity caused by SM, and it is important to delve into these pathways. Recently, a plethora of research has been conducted into the role of miRNAs and SM toxicity, [67][68][69][70][71][72][73][74][75][76] specifically after it was detected that SM was used in the Iran-Iraq war in the 1980s [77][78][79] and most recently in the Syrian conflict. [79][80][81] Thus, this review will focus on the role of miRNAs in the toxicity mediated by SM and attempt to elucidate the underlying mechanisms.…”