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Histamine Deficiency Promotes Myofibroblasts Transformation from HDC-Expressing CD11b+ Myeloid Cells in Injured Hearts Post Myocardial Infarction.
Zhu, Baoling; Zhu, Xiaowei; Wang, Xiangfei; Wu, Jian; Ding, Suling; Zhang, Weiwei; Zou, Yunzeng; Ge, Junbo; Yang, Xiangdong.
Affiliation
  • Zhu B; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Zhu X; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Wang X; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Wu J; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Ding S; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Zhang W; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China.
  • Zou Y; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China. wu.jian@zs-hospital.sh.cn.
  • Ge J; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai, China. wu.jian@zs-hospital.sh.cn.
  • Yang X; Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
J Cardiovasc Transl Res ; 15(3): 621-634, 2022 06.
Article in En | MEDLINE | ID: mdl-34734351
Myocardial infarction (MI) is a significant contributor to the development of heart failure. Histidine decarboxylase (HDC), the unique enzyme that converts L-histidine to histamine, is highly expressed in CD11b+ immature myeloid cells. However, the relationship between HDC-expressing macrophages and cardiac myofibroblasts remains to be explained. Here, we demonstrate that the GFP (green fluorescent protein)-labeled HDC+CD11b+ myeloid precursors and their descendants could differentiate into fibroblast-like cells in myocardial interstitium. Furthermore, we prove that CD11b+Ly6C+ monocytes/macrophages, but not CD11b+Ly6G+ granulocytes, are identified as the main cellular source for bone marrow-derived myofibroblast transformation, which could be regulated via histamine H1 and H2 receptor-dependent signaling pathways. Using HDC knockout mice, we find that histamine deficiency promotes myofibroblast transformation from Ly6C+ macrophages and cardiac fibrosis partly through upregulating the expression of Krüppel-like factor 5 (KLF5). Taken together, our data uncover a central role of HDC in regulating bone marrow-derived macrophage-to-myofibroblast transformation but also identify a histamine receptor (HR)-KLF5 related signaling pathway that mediates myocardial fibrosis post-MI. CD11b+Ly6C+ monocytes/macrophages are the main cellular source for bone marrow-derived myofibroblast transformation. Histamine inhibits myofibroblasts transformation via H1R and H2R-dependent signaling pathways, and ameliorates cardiac fibrosis partly through upregulating KLF5 expression.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Histamine / Myeloid Cells / Myofibroblasts / Histidine Decarboxylase / Myocardial Infarction Type of study: Prognostic_studies Limits: Animals Language: En Journal: J Cardiovasc Transl Res Journal subject: ANGIOLOGIA / CARDIOLOGIA Year: 2022 Document type: Article Affiliation country: Country of publication:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Histamine / Myeloid Cells / Myofibroblasts / Histidine Decarboxylase / Myocardial Infarction Type of study: Prognostic_studies Limits: Animals Language: En Journal: J Cardiovasc Transl Res Journal subject: ANGIOLOGIA / CARDIOLOGIA Year: 2022 Document type: Article Affiliation country: Country of publication: