MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice

Jingyi Pan,* Xinyu Li,* Xinyang Wang, Lili Yang, Houlin Chen, Nana Su, Chenghua Wu, Yu Hao, Shengwei Jin, Hui Li Department of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, People’s R...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Pan J, Li X, Wang X, Yang L, Chen H, Su N, Wu C, Hao Y, Jin S, Li H
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	pulmonary fibrosis mctr1 emt lung dysfunction Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/973ca06bcb83494bbcf20fd4d18e21f6
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:973ca06bcb83494bbcf20fd4d18e21f6
record_format	dspace
spelling	oai:doaj.org-article:973ca06bcb83494bbcf20fd4d18e21f62021-12-02T17:02:14ZMCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice1178-7031https://doaj.org/article/973ca06bcb83494bbcf20fd4d18e21f62021-05-01T00:00:00Zhttps://www.dovepress.com/mctr1-intervention-reverses-experimental-lung-fibrosis-in-mice-peer-reviewed-fulltext-article-JIRhttps://doaj.org/toc/1178-7031Jingyi Pan,* Xinyu Li,* Xinyang Wang, Lili Yang, Houlin Chen, Nana Su, Chenghua Wu, Yu Hao, Shengwei Jin, Hui Li Department of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Hui Li; Shengwei JinDepartment of Anaesthesia and Critical Care, Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, People’s Republic of ChinaEmail judy198406@sina.com; jinshengwei69@163.comPurpose: Pulmonary fibrosis (PF) is a progressing lethal disease, effective curative therapies remain elusive and mortality remains high. Maresin conjugates in tissue regeneration 1 (MCTR1) is a DHA-derived lipid mediator promoting inflammation resolution produced in macrophage. However, the effect of MCTR1 on PF remains unknown.Material and Methods: We established a lung fibrosis model in mice induced by intratracheal administration of bleomycin (BLM). On day 7 after lung fibrosis model establishment, treatment with MCTR1 up to day 21. The body weight of each mouse was recorded every day and survival curves were plotted. Histological staining was used to detect pulmonary inflammation and fibrosis. Lung sections were examined with transmission electron microscope to evaluate the ultrastructure of cells and deposit of collagen. Inflammatory cytokines in lung tissues were tested by ELISA. q-PCR and Western blot were used to evaluate the mRNA and the protein levels of EMT-related markers.Results: We found that MCTR1 intervention attenuated BLM-induced lung inflammatory and fibrotic response. Furthermore, MCTR1 protected BLM-induced epithelial cell destroy and reversed epithelial-to-mesenchymal transition phenotype into an epithelial one in lung fibrosis mice. Most importantly, post-treatment with MCTR1 restored BLM-induced lung dysfunction and enhanced survival rate significantly.Conclusion: Posttreatment with MCTR1 attenuated BLM-induced inflammation and fibrosis changes in mice, suggested MCTR1 may serve as a novel therapeutic strategy for fibrosis-related diseases.Keywords: pulmonary fibrosis, MCTR1, EMT, lung dysfunctionPan JLi XWang XYang LChen HSu NWu CHao YJin SLi HDove Medical Pressarticlepulmonary fibrosismctr1emtlung dysfunctionPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 1873-1881 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	pulmonary fibrosis mctr1 emt lung dysfunction Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	pulmonary fibrosis mctr1 emt lung dysfunction Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Pan J Li X Wang X Yang L Chen H Su N Wu C Hao Y Jin S Li H MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
description	Jingyi Pan,* Xinyu Li,* Xinyang Wang, Lili Yang, Houlin Chen, Nana Su, Chenghua Wu, Yu Hao, Shengwei Jin, Hui Li Department of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Hui Li; Shengwei JinDepartment of Anaesthesia and Critical Care, Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325027, People’s Republic of ChinaEmail judy198406@sina.com; jinshengwei69@163.comPurpose: Pulmonary fibrosis (PF) is a progressing lethal disease, effective curative therapies remain elusive and mortality remains high. Maresin conjugates in tissue regeneration 1 (MCTR1) is a DHA-derived lipid mediator promoting inflammation resolution produced in macrophage. However, the effect of MCTR1 on PF remains unknown.Material and Methods: We established a lung fibrosis model in mice induced by intratracheal administration of bleomycin (BLM). On day 7 after lung fibrosis model establishment, treatment with MCTR1 up to day 21. The body weight of each mouse was recorded every day and survival curves were plotted. Histological staining was used to detect pulmonary inflammation and fibrosis. Lung sections were examined with transmission electron microscope to evaluate the ultrastructure of cells and deposit of collagen. Inflammatory cytokines in lung tissues were tested by ELISA. q-PCR and Western blot were used to evaluate the mRNA and the protein levels of EMT-related markers.Results: We found that MCTR1 intervention attenuated BLM-induced lung inflammatory and fibrotic response. Furthermore, MCTR1 protected BLM-induced epithelial cell destroy and reversed epithelial-to-mesenchymal transition phenotype into an epithelial one in lung fibrosis mice. Most importantly, post-treatment with MCTR1 restored BLM-induced lung dysfunction and enhanced survival rate significantly.Conclusion: Posttreatment with MCTR1 attenuated BLM-induced inflammation and fibrosis changes in mice, suggested MCTR1 may serve as a novel therapeutic strategy for fibrosis-related diseases.Keywords: pulmonary fibrosis, MCTR1, EMT, lung dysfunction
format	article
author	Pan J Li X Wang X Yang L Chen H Su N Wu C Hao Y Jin S Li H
author_facet	Pan J Li X Wang X Yang L Chen H Su N Wu C Hao Y Jin S Li H
author_sort	Pan J
title	MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
title_short	MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
title_full	MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
title_fullStr	MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
title_full_unstemmed	MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice
title_sort	mctr1 intervention reverses experimental lung fibrosis in mice
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/973ca06bcb83494bbcf20fd4d18e21f6
work_keys_str_mv	AT panj mctr1interventionreversesexperimentallungfibrosisinmice AT lix mctr1interventionreversesexperimentallungfibrosisinmice AT wangx mctr1interventionreversesexperimentallungfibrosisinmice AT yangl mctr1interventionreversesexperimentallungfibrosisinmice AT chenh mctr1interventionreversesexperimentallungfibrosisinmice AT sun mctr1interventionreversesexperimentallungfibrosisinmice AT wuc mctr1interventionreversesexperimentallungfibrosisinmice AT haoy mctr1interventionreversesexperimentallungfibrosisinmice AT jins mctr1interventionreversesexperimentallungfibrosisinmice AT lih mctr1interventionreversesexperimentallungfibrosisinmice
_version_	1718381920778190848

MCTR1 Intervention Reverses Experimental Lung Fibrosis in Mice

Ejemplares similares