Hydrogen Sulfide Reduces Recruitment of CD11b+DG Gr-1+DG Cells in Mice with Myocardial Infarction
Author(s) -
Ting Wu,
Hua Li,
Bing Wu,
Lei Zhang,
San-Wu Wu,
JiaNing Wang,
Youen Zhang
Publication year - 2017
Publication title -
cell transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.043
H-Index - 100
eISSN - 1555-3892
pISSN - 0963-6897
DOI - 10.3727/096368917x695029
Subject(s) - sodium hydrosulfide , medicine , ligation , myocardial infarction , cardiology , ventricular remodeling , saline , heart failure , cystathionine gamma lyase , left coronary artery , cardiac fibrosis , edema , ligature , infarction , cystathionine beta synthase , hydrogen sulfide , chemistry , sulfur , biochemistry , organic chemistry , cysteine , enzyme
The present study aimed to elucidate the mechanisms by which hydrogen sulfide (H 2 S) attenuates left ventricular remodeling after myocardial infarction (MI). MI was created in mice by left coronary artery ligation. One group of mice received injections of the H 2 S donor sodium hydrosulfide (NaHS) immediately before and 1 h after ligation, while the control group received saline alone. During both the subacute and chronic stages (1 and 4 weeks postinfarction, respectively), NaHS-treated mice demonstrated attenuation of cardiac dilation in the infarcted myocardium. Furthermore, fewer CD11b + Gr-1 + myeloid cells were detected in the infarct myocardium and peripheral blood from NaHS-treated mice, while more CD11b + Gr-1 + cells remained in the spleen and bone marrow in these animals. NaHS-treated mice also exhibited reduction in cardiomyocyte apoptosis, interstitial fibrosis, cardiac hypertrophy, and pulmonary edema, as well as overall better survival rates, when compared to controls. Thus, exogenous H 2 S has favorable effects on cardiac remodeling after MI. These observations further support the emerging concept that H 2 S treatment might have therapeutic benefits in the setting of ischemia-induced heart failure.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom