Premium
Protective role of Ac‐SDKP and thymosin β4 on cardiac rupture after myocardial infarction
Author(s) -
Peng Hongmei,
Carretero Oscar A.,
Yang Xiao-Ping,
Xu Jiang,
Peterson Edward,
Rhaleb Nour-Eddine
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.864.10
Subject(s) - myocardial infarction , medicine , cardiology , thymosin , ejection fraction , cardiac rupture , infarction , angiogenesis , heart failure
N‐acetyl‐seryl‐aspartyl‐lysyl‐proline (Ac‐SDKP), released from its precursor thymosin β4 (Tβ4), has anti‐inflammatory, pro‐angiogenic and anti‐fibrotic effects. We hypothesized that Tβ4 and Ac‐SDKP reduce cardiac rupture after myocardial infarction (MI). C57BL/6J mice were subjected to MI and divided into groups: 1) sham MI, 2) MI + vehicle (VEH), 3) MI + Ac‐SDKP or 4) MI + Tβ4. Ac‐SDKP and Tβ4 (1.6 mg/kg/day) were given i.p. via osmotic pump for 7 days before MI and 7 more days after MI. Ejection fraction (EF) was assessed by echocardiography. Infarct size was similar in all MI groups. Interstitial collagen fraction (ICF) and capillary density were measured and ICAM‐1 was detected by Western blot. Ac‐SDKP and Tβ4 decreased cardiac rupture rate, both tended to increase EF but the difference did not reach statistical significance (Table). Decline in cardiac rupture by Ac‐SDKP or Tβ4 may be due to angiogenesis, and decreased inflammation and metalloproteinase activity. The use of Ac‐SDKP and Tβ4 may reduce cardiac rupture after MI. The NIH (R01HL071806).