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Wang, Qi, An, Lu, Li, Juan, Liu, Bing, Hui, Junpeng, Zhang, Qiang, Zhang, Xin. (1401). Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways. , 25(8), 947-953. doi: 10.22038/ijbms.2022.62113.13742
Qi Wang; Lu An; Juan Li; Bing Liu; Junpeng Hui; Qiang Zhang; Xin Zhang. "Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways". , 25, 8, 1401, 947-953. doi: 10.22038/ijbms.2022.62113.13742
Wang, Qi, An, Lu, Li, Juan, Liu, Bing, Hui, Junpeng, Zhang, Qiang, Zhang, Xin. (1401). 'Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways', , 25(8), pp. 947-953. doi: 10.22038/ijbms.2022.62113.13742
Wang, Qi, An, Lu, Li, Juan, Liu, Bing, Hui, Junpeng, Zhang, Qiang, Zhang, Xin. Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways. , 1401; 25(8): 947-953. doi: 10.22038/ijbms.2022.62113.13742

Knockdown of TRPM7 attenuates apoptosis and inflammation in neonatal necrotizing enterocolitis model cell IEC-6 via modulating TLR4/NF-κB and MEK/ERK pathways

Iranian Journal of Basic Medical Sciences
مقاله 3، دوره 25، شماره 8، آبان 2022، صفحه 947-953    اصل مقاله (1.11 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2022.62113.13742
نویسندگان
Qi Wang* 1؛ Lu An2؛ Juan Li3؛ Bing Liu4؛ Junpeng Hui3؛ Qiang Zhang3؛ Xin Zhang3
1The Affiliated Children Hospital of Xi’an Jiaotong University
2Department of Pathology,xi'an Chlidren's Hospital
3Department of Pathology,xi'an Chlidrend's Hospital
4Department of Patholoqy,xi'an Chlidrend's Hospital
چکیده
Objective(s): Neonatal necrotizing enterocolitis (NEC) is the most common gastrointestinal critical illness in neonatal infants. TRPM7 reportedly plays a role in human inflammatory bowel disease (IBD) and colorectal cancer, but the role of TRPM7 in the pathogenesis of NEC remains vague.
Materials and Methods: The expression of TRPM7 was determined in intestinal tissues of NEC patients and lipopolysaccharide (LPS)-induced IEC-6 cells. Subsequently, a loss-of-function assay was performed to assess the effects of TRPM7 on cell apoptosis and inflammatory response in IEC-6 cells after LPS induction. Furthermore, the modulation of TRPM7 on TLR4/NF-κB and MEK/ERK signaling pathways was validated.
Results: The expression of TRPM7 was higher in the intestinal tissues of NEC patients compared with the normal human intestinal tissues. Moreover, the expression level of TRPM7 was elevated in LPS stimulation IEC-6 cells. Knockdown of TRPM7 enhanced cell viability and suppressed apoptosis, accompanied by the decreased Bax/Bcl-1 ratio and cleaved-caspase3 expression in LPS-induced IEC-6 cells. Additionally, TRPM7 silencing attenuated LPS-induced expressions and secretions of proinflammatory cytokines. Mechanistically, TRPM7 knockdown inhibited the TLR4/NF-κB activation, while enhancing the MEK/ERK activation in LPS-treated IEC-6 cells. Overexpression of TLR4 or inhibition of MEK attenuated the inhibitory effects of TRPM7 knockdown on LPS-induced apoptosis and inflammation in IEC-6 cells.
Conclusion: Knockdown of TRPM7 attenuated LPS-induced IEC-6 cell apoptosis and inflammation by modulating TLR4/NF-κB and MEK/ERK pathways.
کلیدواژه‌ها
Apoptosis؛ Inflammation؛ Necrotizing enterocolitis؛ TRPM7؛ Viability
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