VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation

Myocardial fibrosis (MF) is an important cause of heart failure and cardiac arrest. Vasorin knockout (VASN−/−) leads to pathological cardiac hypertrophy (PCH); however, it is not yet clear whether this PCH transitions to MF in mice. VASN-knockout mice showed typical pathological, imaging, and molecu...

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Main Authors: Junming Sun, Siwei Yin, Qiurui Li, Jun Zhang, Xiaoping Guo, Na Yu, Bing Hu, Yiqiang Ouyang, Qiaojuan Huang, Min He
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-01-01
Series:Frontiers in Pharmacology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2024.1500617/full
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author Junming Sun
Siwei Yin
Qiurui Li
Jun Zhang
Xiaoping Guo
Na Yu
Bing Hu
Yiqiang Ouyang
Qiaojuan Huang
Min He
Min He
Min He
author_facet Junming Sun
Siwei Yin
Qiurui Li
Jun Zhang
Xiaoping Guo
Na Yu
Bing Hu
Yiqiang Ouyang
Qiaojuan Huang
Min He
Min He
Min He
author_sort Junming Sun
collection DOAJ
description Myocardial fibrosis (MF) is an important cause of heart failure and cardiac arrest. Vasorin knockout (VASN−/−) leads to pathological cardiac hypertrophy (PCH); however, it is not yet clear whether this PCH transitions to MF in mice. VASN-knockout mice showed typical pathological, imaging, and molecular features of MF upon hematoxylin and eosin staining, Masson staining, Sirius red staining, quantitative polymerase chain reaction (qPCR), immunohistochemistry-paraffin (IHC-P), and immunofluorescence analyses. RNA was extracted from mouse heart tissue, identified, and sequenced in vitro. Differential analysis of the genes showed that the extracellular matrix (ECM) genes (COL6A1, COL9A1, and FRAS1) had strong correlations while their expression levels were significantly reduced by qPCR, IHC-P, and Western blotting. The expression levels of the ECM genes were significantly reduced but those of the inflammatory factors (IL1β and IL6) were significantly upregulated in the heart tissues of VASN-knockout mice. These preliminary results reveal that VASN knockout induces MF by regulating the non-collagen fibers and inflammation.
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publishDate 2025-01-01
publisher Frontiers Media S.A.
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series Frontiers in Pharmacology
spelling doaj-art-b9987c0dcabb45549eb7a47e37e4228c2025-01-17T06:51:12ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-01-011510.3389/fphar.2024.15006171500617VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammationJunming Sun0Siwei Yin1Qiurui Li2Jun Zhang3Xiaoping Guo4Na Yu5Bing Hu6Yiqiang Ouyang7Qiaojuan Huang8Min He9Min He10Min He11Laboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaDepartment of Cardiology, The Second Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi, ChinaLaboratory Animal Center, Guangxi Medical University, Nanning, Guangxi, ChinaSchool of Public Health, Guangxi Medical University, Nanning, ChinaMinistry of Education, Key Laboratory of High-Incidence-Tumor Prevention and Treatment, Guangxi Medical University, Nanning, ChinaMyocardial fibrosis (MF) is an important cause of heart failure and cardiac arrest. Vasorin knockout (VASN−/−) leads to pathological cardiac hypertrophy (PCH); however, it is not yet clear whether this PCH transitions to MF in mice. VASN-knockout mice showed typical pathological, imaging, and molecular features of MF upon hematoxylin and eosin staining, Masson staining, Sirius red staining, quantitative polymerase chain reaction (qPCR), immunohistochemistry-paraffin (IHC-P), and immunofluorescence analyses. RNA was extracted from mouse heart tissue, identified, and sequenced in vitro. Differential analysis of the genes showed that the extracellular matrix (ECM) genes (COL6A1, COL9A1, and FRAS1) had strong correlations while their expression levels were significantly reduced by qPCR, IHC-P, and Western blotting. The expression levels of the ECM genes were significantly reduced but those of the inflammatory factors (IL1β and IL6) were significantly upregulated in the heart tissues of VASN-knockout mice. These preliminary results reveal that VASN knockout induces MF by regulating the non-collagen fibers and inflammation.https://www.frontiersin.org/articles/10.3389/fphar.2024.1500617/fullmyocardial fibrosisvasorinnon-collagen fibersinflammationmice
spellingShingle Junming Sun
Siwei Yin
Qiurui Li
Jun Zhang
Xiaoping Guo
Na Yu
Bing Hu
Yiqiang Ouyang
Qiaojuan Huang
Min He
Min He
Min He
VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
Frontiers in Pharmacology
myocardial fibrosis
vasorin
non-collagen fibers
inflammation
mice
title VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
title_full VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
title_fullStr VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
title_full_unstemmed VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
title_short VASN knockout induces myocardial fibrosis in mice by downregulating non-collagen fibers and promoting inflammation
title_sort vasn knockout induces myocardial fibrosis in mice by downregulating non collagen fibers and promoting inflammation
topic myocardial fibrosis
vasorin
non-collagen fibers
inflammation
mice
url https://www.frontiersin.org/articles/10.3389/fphar.2024.1500617/full
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