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MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway

Alveolar macrophage phagocytosis is significantly reduced in Chronic obstructive pulmonary disease, and cigarette smoke extract is one of the chief reasons for this decrease. Nevertheless, the specific underlying mechanism remains elusive. In this study, the role and possible mechanism of miR-155-5p...

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Autores principales: Yang, Xinna, Zeng, Xiaoli, Shu, Juan, Bao, Hairong, Liu, Xiaoju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10476751/
https://www.ncbi.nlm.nih.gov/pubmed/37657048
http://dx.doi.org/10.1097/MD.0000000000034592
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author Yang, Xinna
Zeng, Xiaoli
Shu, Juan
Bao, Hairong
Liu, Xiaoju
author_facet Yang, Xinna
Zeng, Xiaoli
Shu, Juan
Bao, Hairong
Liu, Xiaoju
author_sort Yang, Xinna
collection PubMed
description Alveolar macrophage phagocytosis is significantly reduced in Chronic obstructive pulmonary disease, and cigarette smoke extract is one of the chief reasons for this decrease. Nevertheless, the specific underlying mechanism remains elusive. In this study, the role and possible mechanism of miR-155-5p/mTORC2/RhoA in the phagocytosis of mouse alveolar macrophages (MH-S) were explored. Our results revealed that cigarette smoke extract intervention reduced MH-S cell phagocytosis and miR-155-5p expression. Meanwhile, the dual-luciferase reporter assay validated that Rictor is a target of miR-155-5p. On the one hand, transfecting miR-155-5p mimic, mimic NC, miR-155-5p inhibitor, or inhibitor NC in MH-S cells overexpressing miR-155-5p increased the Alveolar macrophage phagocytotic rate, up-regulated the expression level of RhoA and p-RhoA, and down-regulated that of mTOR and Rictor mRNA and protein. On the other hand, inhibiting the expression of miR-155-5p lowered the phagocytotic rate, up-regulated the expression of mTOR, Rictor mRNA, and protein, and down-regulated the expression of RhoA and p-RhoA, which taken together, authenticated that miR-155-5p participates in macrophage phagocytosis via the mTORC2/RhoA pathway. Finally, confocal microscopy demonstrated that cells overexpressing miR-155-5p underwent cytoskeletal rearrangement during phagocytosis, and the phagocytic function of cells was enhanced, signaling that miR-155-5p participated in macrophage skeletal rearrangement and enhanced alveolar macrophage phagocytosis by targeting the expression of Rictor in the mTORC2/RhoA pathway.
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spelling pubmed-104767512023-09-05 MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway Yang, Xinna Zeng, Xiaoli Shu, Juan Bao, Hairong Liu, Xiaoju Medicine (Baltimore) 6700 Alveolar macrophage phagocytosis is significantly reduced in Chronic obstructive pulmonary disease, and cigarette smoke extract is one of the chief reasons for this decrease. Nevertheless, the specific underlying mechanism remains elusive. In this study, the role and possible mechanism of miR-155-5p/mTORC2/RhoA in the phagocytosis of mouse alveolar macrophages (MH-S) were explored. Our results revealed that cigarette smoke extract intervention reduced MH-S cell phagocytosis and miR-155-5p expression. Meanwhile, the dual-luciferase reporter assay validated that Rictor is a target of miR-155-5p. On the one hand, transfecting miR-155-5p mimic, mimic NC, miR-155-5p inhibitor, or inhibitor NC in MH-S cells overexpressing miR-155-5p increased the Alveolar macrophage phagocytotic rate, up-regulated the expression level of RhoA and p-RhoA, and down-regulated that of mTOR and Rictor mRNA and protein. On the other hand, inhibiting the expression of miR-155-5p lowered the phagocytotic rate, up-regulated the expression of mTOR, Rictor mRNA, and protein, and down-regulated the expression of RhoA and p-RhoA, which taken together, authenticated that miR-155-5p participates in macrophage phagocytosis via the mTORC2/RhoA pathway. Finally, confocal microscopy demonstrated that cells overexpressing miR-155-5p underwent cytoskeletal rearrangement during phagocytosis, and the phagocytic function of cells was enhanced, signaling that miR-155-5p participated in macrophage skeletal rearrangement and enhanced alveolar macrophage phagocytosis by targeting the expression of Rictor in the mTORC2/RhoA pathway. Lippincott Williams & Wilkins 2023-09-01 /pmc/articles/PMC10476751/ /pubmed/37657048 http://dx.doi.org/10.1097/MD.0000000000034592 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC) (https://creativecommons.org/licenses/by-nc/4.0/) , where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal.
spellingShingle 6700
Yang, Xinna
Zeng, Xiaoli
Shu, Juan
Bao, Hairong
Liu, Xiaoju
MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title_full MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title_fullStr MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title_full_unstemmed MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title_short MiR-155 enhances phagocytosis of alveolar macrophages through the mTORC2/RhoA pathway
title_sort mir-155 enhances phagocytosis of alveolar macrophages through the mtorc2/rhoa pathway
topic 6700
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10476751/
https://www.ncbi.nlm.nih.gov/pubmed/37657048
http://dx.doi.org/10.1097/MD.0000000000034592
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