Literature DB >> 22308302

Regulatory role of dendritic cells in postinfarction healing and left ventricular remodeling.

Atsushi Anzai1, Toshihisa Anzai, Shigenori Nagai, Yuichiro Maekawa, Kotaro Naito, Hidehiro Kaneko, Yasuo Sugano, Toshiyuki Takahashi, Hitoshi Abe, Satsuki Mochizuki, Motoaki Sano, Tsutomu Yoshikawa, Yasunori Okada, Shigeo Koyasu, Satoshi Ogawa, Keiichi Fukuda.   

Abstract

BACKGROUND: Inflammation and immune responses are integral components in the healing process after myocardial infarction. We previously reported dendritic cell (DC) infiltration in the infarcted heart; however, the precise contribution of DC in postinfarction healing is unclear. METHODS AND
RESULTS: Bone marrow cells from CD11c-diphtheria toxin receptor/green fluorescent protein transgenic mice were transplanted into lethally irradiated wild-type recipient mice. After reconstitution of bone marrow-derived cells, the recipient mice were treated with either diphtheria toxin (DC ablation) or vehicle (control), and myocardial infarction was created by left coronary ligation. CD11c(+) green fluorescent protein-positive DCs expressing CD11b and major histocompatibility complex class II were recruited into the heart, peaking on day 7 after myocardial infarction in the control group. Mice with DC ablation for 7 days showed deteriorated left ventricular function and remodeling. The DC-ablated group demonstrated enhanced and sustained expression of inflammatory cytokines such as interleukin-1β, interleukin-18, and tumor necrosis factor-α, prolonged extracellular matrix degradation associated with a high level of matrix metalloproteinase-9 activity, and diminished expression level of interleukin-10 and endothelial cell proliferation after myocardial infarction compared with the control group. In vivo analyses revealed that DC-ablated infarcts had enhanced monocyte/macrophage recruitment. Among these cells, marked infiltration of proinflammatory Ly6C(high) monocytes and F4/80(+) CD206(-) M1 macrophages and, conversely, impaired recruitment of anti-inflammatory Ly6C(low) monocytes and F4/80(+) CD206(+) M2 macrophages in the infarcted myocardium were identified in the DC-ablated group compared with the control group.
CONCLUSIONS: These results suggest that the DC is a potent immunoprotective regulator during the postinfarction healing process via its control of monocyte/macrophage homeostasis.

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Year:  2012        PMID: 22308302     DOI: 10.1161/CIRCULATIONAHA.111.052126

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  118 in total

1.  Enhanced efferocytosis of apoptotic cardiomyocytes through myeloid-epithelial-reproductive tyrosine kinase links acute inflammation resolution to cardiac repair after infarction.

Authors:  Elaine Wan; Xin Yi Yeap; Shirley Dehn; Rachael Terry; Margaret Novak; Shuang Zhang; Shinichi Iwata; Xiaoqiang Han; Shunichi Homma; Konstantinos Drosatos; Jon Lomasney; David M Engman; Stephen D Miller; Douglas E Vaughan; John P Morrow; Raj Kishore; Edward B Thorp
Journal:  Circ Res       Date:  2013-07-08       Impact factor: 17.367

Review 2.  Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction.

Authors:  Mingyuan Huang; Du Yang; Meixiang Xiang; Jianan Wang
Journal:  Heart Fail Rev       Date:  2015-01       Impact factor: 4.214

Review 3.  Immunosenescence in monocytes, macrophages, and dendritic cells: lessons learned from the lung and heart.

Authors:  Phyllis-Jean Linton; Marilyn L Thoman
Journal:  Immunol Lett       Date:  2014-09-22       Impact factor: 3.685

4.  Caveolin-1 deletion exacerbates cardiac interstitial fibrosis by promoting M2 macrophage activation in mice after myocardial infarction.

Authors:  Pooja Shivshankar; Ganesh V Halade; Cheresa Calhoun; Gladys P Escobar; Ali J Mehr; Fabio Jimenez; Cindy Martinez; Harshita Bhatnagar; Corey H Mjaatvedt; Merry L Lindsey; Claude Jourdan Le Saux
Journal:  J Mol Cell Cardiol       Date:  2014-08-12       Impact factor: 5.000

5.  Targeted injection of a biocomposite material alters macrophage and fibroblast phenotype and function following myocardial infarction: relation to left ventricular remodeling.

Authors:  Jeremy R McGarvey; Sara Pettaway; James A Shuman; Craig P Novack; Kia N Zellars; Parker D Freels; Randall L Echols; Jason A Burdick; Joseph H Gorman; Robert C Gorman; Francis G Spinale
Journal:  J Pharmacol Exp Ther       Date:  2014-07-14       Impact factor: 4.030

Review 6.  Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges.

Authors:  Shuaibo Huang; Nikolaos G Frangogiannis
Journal:  Br J Pharmacol       Date:  2018-03-04       Impact factor: 8.739

7.  Cell biological mechanisms in regulation of the post-infarction inflammatory response.

Authors:  Nikolaos G Frangogiannis
Journal:  Curr Opin Physiol       Date:  2017-12-13

8.  It takes two to tango: monocyte and macrophage duality in the infarcted heart.

Authors:  Sumanth D Prabhu
Journal:  Circ Res       Date:  2014-05-09       Impact factor: 17.367

9.  Regeneration-associated cells improve recovery from myocardial infarction through enhanced vasculogenesis, anti-inflammation, and cardiomyogenesis.

Authors:  Amankeldi A Salybekov; Akira T Kawaguchi; Haruchika Masuda; Kosit Vorateera; Chisa Okada; Takayuki Asahara
Journal:  PLoS One       Date:  2018-11-28       Impact factor: 3.240

10.  Gr1+ Macrophages and Dendritic Cells Dominate the Inflammatory Infiltrate 12 Hours After Experimental Intracerebral Hemorrhage.

Authors:  Matthew D Hammond; Youxi Ai; Lauren H Sansing
Journal:  Transl Stroke Res       Date:  2012-07       Impact factor: 6.829

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