[Loss of Myeloid-Derived Growth Factor Leads to Increased Fibrosis in Mice After Myocardial Infarction].

Q3 Medicine 四川大学学报(医学版) Pub Date : 2024-07-20 DOI:10.12182/20240760206

Guoling Han, Yanyan Hao, Ruopu Li, Weijing Liu, Jun Liu, Yu Nie, Lina Bai, Yuyao Wang

{"title":"[Loss of Myeloid-Derived Growth Factor Leads to Increased Fibrosis in Mice After Myocardial Infarction].","authors":"Guoling Han, Yanyan Hao, Ruopu Li, Weijing Liu, Jun Liu, Yu Nie, Lina Bai, Yuyao Wang","doi":"10.12182/20240760206","DOIUrl":null,"url":null,"abstract":"Objective: To investigate the effect of the loss of myeloid-derived growth factor (Mydgf) on the transformation of cardiac fibroblasts into myofibroblasts after myocardial infarction (MI).Methods: Two adult mouse groups, including a wild-type (WT) group and another group with Mydgf knockout (Mydgf-KO), were examined in the study. The mice in these two groups were tested for their cardiac function by measuring left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) (n=10). Quantitative real-time PCR (qRT-PCR) (n=3) was performed to determine the mRNA expression levels of myofibroblast markers, including α-smooth muscle actin (α-SMA), periostin (postn), type Ⅷ collagen (col8al), and connective tissue growth factor (ctgf). Western blot (n=3) was performed to verify the protein expression levels of α-SMA. MI modeling was performed on the WT and the Mydgf-KO mice. Postoperative LVEF and LVFS (n=10) were then measured. The hearts were harvested and Masson staining was performed to determine the infarcted area (n=10). The heart samples of Mydgf-KO and WT mice were collected at d 7 and d 14 after MI, respectively, to verify the expression of myofibroblast markers (n=3).Results: Compared with WT mice, LVEF and LVFS in adult Mydgf-KO mice showed no significant changes (all P>0.05). However, the mRNA levels of α-SMA and postn were upregulated, and α-SMA protein expression was also increased (all P<0.05). After MI, compared with WT mice, LVEF and LVFS in Mydgf-KO mice decreased, and the infarcted area increased significantly (all P<0.05). Furthermore, mRNA levels of α-SMA, col8al, postn, and ctgf were increased in Mydgf-KO mice. In addition, the α-SMA protein expression level was upregulated and α-SMA-positive fibroblasts were increased (P<0.05).Conclusion: Mydgf deletion promotes the transformation of cardiac fibroblasts into myofibroblasts and aggravates myocardial fibrosis after MI.","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"55 4","pages":"886-892"},"PeriodicalIF":0.0000,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11334291/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"四川大学学报(医学版)","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.12182/20240760206","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: To investigate the effect of the loss of myeloid-derived growth factor (Mydgf) on the transformation of cardiac fibroblasts into myofibroblasts after myocardial infarction (MI).

Methods: Two adult mouse groups, including a wild-type (WT) group and another group with Mydgf knockout (Mydgf-KO), were examined in the study. The mice in these two groups were tested for their cardiac function by measuring left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) (n=10). Quantitative real-time PCR (qRT-PCR) (n=3) was performed to determine the mRNA expression levels of myofibroblast markers, including α-smooth muscle actin (α-SMA), periostin (postn), type Ⅷ collagen (col8al), and connective tissue growth factor (ctgf). Western blot (n=3) was performed to verify the protein expression levels of α-SMA. MI modeling was performed on the WT and the Mydgf-KO mice. Postoperative LVEF and LVFS (n=10) were then measured. The hearts were harvested and Masson staining was performed to determine the infarcted area (n=10). The heart samples of Mydgf-KO and WT mice were collected at d 7 and d 14 after MI, respectively, to verify the expression of myofibroblast markers (n=3).

Results: Compared with WT mice, LVEF and LVFS in adult Mydgf-KO mice showed no significant changes (all P>0.05). However, the mRNA levels of α-SMA and postn were upregulated, and α-SMA protein expression was also increased (all P<0.05). After MI, compared with WT mice, LVEF and LVFS in Mydgf-KO mice decreased, and the infarcted area increased significantly (all P<0.05). Furthermore, mRNA levels of α-SMA, col8al, postn, and ctgf were increased in Mydgf-KO mice. In addition, the α-SMA protein expression level was upregulated and α-SMA-positive fibroblasts were increased (P<0.05).

Conclusion: Mydgf deletion promotes the transformation of cardiac fibroblasts into myofibroblasts and aggravates myocardial fibrosis after MI.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

[髓系生长因子缺失导致小鼠心肌梗死后纤维化加重]。

研究目的研究髓源性生长因子（Mydgf）缺失对心肌梗死（MI）后心脏成纤维细胞向肌成纤维细胞转化的影响：方法：本研究考察了两组成年小鼠，包括野生型（WT）组和 Mydgf 基因敲除（Mydgf-KO）组。通过测量左心室射血分数（LVEF）和左心室折返缩短率（LVFS）来检测这两组小鼠的心脏功能（n=10）。进行定量实时 PCR（qRT-PCR）（n=3），以确定肌成纤维细胞标记物的 mRNA 表达水平，包括α-平滑肌肌动蛋白（α-SMA）、骨膜增生蛋白（postn）、Ⅷ型胶原（col8al）和结缔组织生长因子（ctgf）。进行 Western 印迹（n=3）以验证 α-SMA 蛋白表达水平。对WT和Mydgf-KO小鼠进行MI建模。然后测量术后 LVEF 和 LVFS（n=10）。收获心脏并进行马森染色以确定梗死面积（n=10）。分别在心肌梗死后第7天和第14天采集Mydgf-KO和WT小鼠的心脏样本，以验证肌成纤维细胞标记物的表达（n=3）：结果：与WT小鼠相比，成年Mydgf-KO小鼠的LVEF和LVFS无显著变化（均P>0.05）。然而，α-SMA和postn的mRNA水平上调，α-SMA蛋白表达也增加（所有PMydgf-KO小鼠均下降），梗死面积显著增加（所有Pα-SMA、col8al、postn和ctgf在Mydgf-KO小鼠中均增加）。此外，α-SMA 蛋白表达水平上调，α-SMA 阳性成纤维细胞增加（PConclusion：Mydgf缺失会促进心肌成纤维细胞向肌成纤维细胞转化，并加重心肌梗死后的心肌纤维化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

四川大学学报(医学版) Biochemistry, Genetics and Molecular Biology-Molecular Biology

CiteScore

0.70

自引率

0.00%

发文量

8695

期刊介绍： "Journal of Sichuan University (Medical Edition)" is a comprehensive medical academic journal sponsored by Sichuan University, a higher education institution directly under the Ministry of Education of the People's Republic of China. It was founded in 1959 and was originally named "Journal of Sichuan Medical College". In 1986, it was renamed "Journal of West China University of Medical Sciences". In 2003, it was renamed "Journal of Sichuan University (Medical Edition)" (bimonthly). "Journal of Sichuan University (Medical Edition)" is a Chinese core journal and a Chinese authoritative academic journal (RCCSE). It is included in the retrieval systems such as China Science and Technology Papers and Citation Database (CSTPCD), China Science Citation Database (CSCD) (core version), Peking University Library's "Overview of Chinese Core Journals", the U.S. "Index Medica" (IM/Medline), the U.S. "PubMed Central" (PMC), the U.S. "Biological Abstracts" (BA), the U.S. "Chemical Abstracts" (CA), the U.S. EBSCO, the Netherlands "Abstracts and Citation Database" (Scopus), the Japan Science and Technology Agency Database (JST), the Russian "Abstract Magazine", the Chinese Biomedical Literature CD-ROM Database (CBMdisc), the Chinese Biomedical Periodical Literature Database (CMCC), the China Academic Journal Network Full-text Database (CNKI), the Chinese Academic Journal (CD-ROM Edition), and the Wanfang Data-Digital Journal Group.