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Role of PIM2 in acute lung injury induced by sepsis

Pediatric sepsis can cause lung damage leading to death in children. In addition, its complicated pathogenesis currently presents a difficult problem in the medical field. Proviral integrations of Moloney virus 2 (PIM2) is a prognostic marker of pediatric sepsis; therefore, the aim of the present st...

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Autores principales: Ding, Juncai, Yang, Xiufang, Huang, Huijuan, Wang, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9366265/
https://www.ncbi.nlm.nih.gov/pubmed/35978927
http://dx.doi.org/10.3892/etm.2022.11480
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author Ding, Juncai
Yang, Xiufang
Huang, Huijuan
Wang, Bo
author_facet Ding, Juncai
Yang, Xiufang
Huang, Huijuan
Wang, Bo
author_sort Ding, Juncai
collection PubMed
description Pediatric sepsis can cause lung damage leading to death in children. In addition, its complicated pathogenesis currently presents a difficult problem in the medical field. Proviral integrations of Moloney virus 2 (PIM2) is a prognostic marker of pediatric sepsis; therefore, the aim of the present study was to investigate the role of PIM2 in lung injury caused by pediatric sepsis. To meet this aim, the expression of PIM2 in lipopolysaccharide (LPS)-induced BEAS-2B pulmonary epithelial cells was detected using reverse transcription-quantitative (RT-q)PCR and western blotting. Subsequently, the expression of PIM2 was inhibited using the cell transfection technique. Cell Counting Kit-8, TUNEL and western blotting, use of a fluorescence kit, ELISA detection kits were used to detect the expression of inflammatory- and cell injury-associated indicators following PIM2 inhibition. In addition, the expression of proteins known to be associated with the Toll-like receptor 2 (TLR2)/myeloid differentiation primary response 88 (MyD88) pathway were also assessed using western blotting. Finally, the simultaneous inhibition of PIM2 expression and overexpression of TLR2 were investigated in an attempt to elucidate the underlying mechanism. The expression level of PIM2 was revealed to be increased in LPS-induced BEAS-2B cells. Interference with PIM2 expression led to an increase in BEAS-2B cell viability, the inhibition of apoptosis and a reduction in oxidative stress and the inflammatory response. These processes were also revealed to be accomplished via downregulation of the TLR2/MyD88 signaling pathway. Overall, the present study demonstrated that knockdown of PIM2 alleviated LPS-induced bronchial epithelial cell injury by inhibiting the TLR2/MyD88 pathway.
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spelling pubmed-93662652022-08-16 Role of PIM2 in acute lung injury induced by sepsis Ding, Juncai Yang, Xiufang Huang, Huijuan Wang, Bo Exp Ther Med Articles Pediatric sepsis can cause lung damage leading to death in children. In addition, its complicated pathogenesis currently presents a difficult problem in the medical field. Proviral integrations of Moloney virus 2 (PIM2) is a prognostic marker of pediatric sepsis; therefore, the aim of the present study was to investigate the role of PIM2 in lung injury caused by pediatric sepsis. To meet this aim, the expression of PIM2 in lipopolysaccharide (LPS)-induced BEAS-2B pulmonary epithelial cells was detected using reverse transcription-quantitative (RT-q)PCR and western blotting. Subsequently, the expression of PIM2 was inhibited using the cell transfection technique. Cell Counting Kit-8, TUNEL and western blotting, use of a fluorescence kit, ELISA detection kits were used to detect the expression of inflammatory- and cell injury-associated indicators following PIM2 inhibition. In addition, the expression of proteins known to be associated with the Toll-like receptor 2 (TLR2)/myeloid differentiation primary response 88 (MyD88) pathway were also assessed using western blotting. Finally, the simultaneous inhibition of PIM2 expression and overexpression of TLR2 were investigated in an attempt to elucidate the underlying mechanism. The expression level of PIM2 was revealed to be increased in LPS-induced BEAS-2B cells. Interference with PIM2 expression led to an increase in BEAS-2B cell viability, the inhibition of apoptosis and a reduction in oxidative stress and the inflammatory response. These processes were also revealed to be accomplished via downregulation of the TLR2/MyD88 signaling pathway. Overall, the present study demonstrated that knockdown of PIM2 alleviated LPS-induced bronchial epithelial cell injury by inhibiting the TLR2/MyD88 pathway. D.A. Spandidos 2022-06-30 /pmc/articles/PMC9366265/ /pubmed/35978927 http://dx.doi.org/10.3892/etm.2022.11480 Text en Copyright: © Ding et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Ding, Juncai
Yang, Xiufang
Huang, Huijuan
Wang, Bo
Role of PIM2 in acute lung injury induced by sepsis
title Role of PIM2 in acute lung injury induced by sepsis
title_full Role of PIM2 in acute lung injury induced by sepsis
title_fullStr Role of PIM2 in acute lung injury induced by sepsis
title_full_unstemmed Role of PIM2 in acute lung injury induced by sepsis
title_short Role of PIM2 in acute lung injury induced by sepsis
title_sort role of pim2 in acute lung injury induced by sepsis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9366265/
https://www.ncbi.nlm.nih.gov/pubmed/35978927
http://dx.doi.org/10.3892/etm.2022.11480
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