Resident Fibroblast MKL1 Is Sufficient to Drive Pro-fibrogenic Response in Mice

Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and contributes to the preservation of organ function. On the other hand, aberrant fibrogenic response may lead to tissue remodeling and precipitat...

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Published inFrontiers in cell and developmental biology Vol. 9; p. 812748
Main Authors Huang, Shan, Shao, Tinghui, Liu, Hong, Li, Tianfa, Gui, Xianhua, Zhao, Qianwen
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 01.02.2022
Subjects
Cell and Developmental Biology
fibroblast
fibrosis
MKL1 (MRTF-A)
transcription factor
wound healing
MKL1 (MRTF-A)
transcription factor
wound healing
fibrosis
fibroblast
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Abstract Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and contributes to the preservation of organ function. On the other hand, aberrant fibrogenic response may lead to tissue remodeling and precipitate organ failure. Recently lineage tracing studies have shown that resident fibroblasts are the primary mediator of fibrosis taking place in key organs such as the heart, the lungs, and the kidneys. Megakaryocytic leukemia 1 (MKL1) is transcriptional regulator involved in tissue fibrosis. Here we generated resident fibroblast conditional MKL1 knockout (CKO) mice by crossing the mice to the -Cre mice. Models of cardiac fibrosis, pulmonary fibrosis, and renal fibrosis were reproduced in the CKO mice and wild type (WT) littermates. Compared to the WT mice, the CKO mice displayed across-the-board attenuation of fibrosis in different models. Our data cement the pivotal role MKL1 plays in tissue fibrosis but point to the cellular origin from which MKL1 exerts its pro-fibrogenic effects.
AbstractList Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and contributes to the preservation of organ function. On the other hand, aberrant fibrogenic response may lead to tissue remodeling and precipitate organ failure. Recently lineage tracing studies have shown that resident fibroblasts are the primary mediator of fibrosis taking place in key organs such as the heart, the lungs, and the kidneys. Megakaryocytic leukemia 1 (MKL1) is transcriptional regulator involved in tissue fibrosis. Here we generated resident fibroblast conditional MKL1 knockout (CKO) mice by crossing the mice to the -Cre mice. Models of cardiac fibrosis, pulmonary fibrosis, and renal fibrosis were reproduced in the CKO mice and wild type (WT) littermates. Compared to the WT mice, the CKO mice displayed across-the-board attenuation of fibrosis in different models. Our data cement the pivotal role MKL1 plays in tissue fibrosis but point to the cellular origin from which MKL1 exerts its pro-fibrogenic effects.
Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and contributes to the preservation of organ function. On the other hand, aberrant fibrogenic response may lead to tissue remodeling and precipitate organ failure. Recently lineage tracing studies have shown that resident fibroblasts are the primary mediator of fibrosis taking place in key organs such as the heart, the lungs, and the kidneys. Megakaryocytic leukemia 1 (MKL1) is transcriptional regulator involved in tissue fibrosis. Here we generated resident fibroblast conditional MKL1 knockout (CKO) mice by crossing the Mkl1 f/f mice to the Col1a2 -Cre ERT2 mice. Models of cardiac fibrosis, pulmonary fibrosis, and renal fibrosis were reproduced in the CKO mice and wild type (WT) littermates. Compared to the WT mice, the CKO mice displayed across-the-board attenuation of fibrosis in different models. Our data cement the pivotal role MKL1 plays in tissue fibrosis but point to the cellular origin from which MKL1 exerts its pro-fibrogenic effects.
Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and contributes to the preservation of organ function. On the other hand, aberrant fibrogenic response may lead to tissue remodeling and precipitate organ failure. Recently lineage tracing studies have shown that resident fibroblasts are the primary mediator of fibrosis taking place in key organs such as the heart, the lungs, and the kidneys. Megakaryocytic leukemia 1 (MKL1) is transcriptional regulator involved in tissue fibrosis. Here we generated resident fibroblast conditional MKL1 knockout (CKO) mice by crossing the Mkl1f/f mice to the Col1a2-CreERT2 mice. Models of cardiac fibrosis, pulmonary fibrosis, and renal fibrosis were reproduced in the CKO mice and wild type (WT) littermates. Compared to the WT mice, the CKO mice displayed across-the-board attenuation of fibrosis in different models. Our data cement the pivotal role MKL1 plays in tissue fibrosis but point to the cellular origin from which MKL1 exerts its pro-fibrogenic effects.
Author Huang, Shan
Li, Tianfa
Gui, Xianhua
Shao, Tinghui
Liu, Hong
Zhao, Qianwen
AuthorAffiliation 2 Hainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research , Key Laboratory of Emergency and Trauma of Ministry of Education , Department of Cardiology , Research Unit of Island Emergency Medicine of Chinese Academy of Medical Sciences , The First Affiliated Hospital of Hainan Medical University , Haikou , China
1 Key Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Translational Medicine , Department of Pathophysiology , Nanjing Medical University , Nanjing , China
3 Department of Respiratory Medicine , Affiliated Nanjing Drum Tower Hospital , Nanjing University School of Medicine , Nanjing , China
AuthorAffiliation_xml – name: 1 Key Laboratory of Targeted Intervention of Cardiovascular Disease and Collaborative Innovation Center for Cardiovascular Translational Medicine , Department of Pathophysiology , Nanjing Medical University , Nanjing , China
– name: 3 Department of Respiratory Medicine , Affiliated Nanjing Drum Tower Hospital , Nanjing University School of Medicine , Nanjing , China
– name: 2 Hainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research , Key Laboratory of Emergency and Trauma of Ministry of Education , Department of Cardiology , Research Unit of Island Emergency Medicine of Chinese Academy of Medical Sciences , The First Affiliated Hospital of Hainan Medical University , Haikou , China
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Keywords MKL1 (MRTF-A)
transcription factor
wound healing
fibrosis
fibroblast
Language English
License Copyright © 2022 Huang, Shao, Liu, Li, Gui and Zhao.
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Edited by: Cheng Yang, Fudan University, China
Katalin Szaszi, St. Michael’s Hospital, Canada
Reviewed by: Fernando Rodriguez-Pascual, Spanish National Research Council (CSIC), Spain
This article was submitted to Molecular and Cellular Pathology, a section of the journal Frontiers in Cell and Developmental Biology
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Snippet Fibrosis is an evolutionarily conserved pathophysiological process serving bifurcated purposes. On the one hand, fibrosis is essential for wound healing and...
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SubjectTerms Cell and Developmental Biology
fibroblast
fibrosis
MKL1 (MRTF-A)
transcription factor
wound healing
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Title Resident Fibroblast MKL1 Is Sufficient to Drive Pro-fibrogenic Response in Mice
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