[Dynamic changes of peripheral blood monocyte subsets after myocardial ischemia/reperfusion in rats]

Ruiyi Lu1, Xin Zhou2, Wenjie Ji3

  • 1School of Graduates, Tianjin Medical University, Tianjin 300070; Institute of Cardiovascular Diseases and Heart Center, Pingjin Hospital, Logistics University of Chinese People's Armed Police Forces, Tianjin 300162, China.

Abstract

Insights

Myocardial ischemia/reperfusion (I/R) injury in rats involves dynamic changes in monocyte subsets. Proinflammatory CD172a(+)CD43(low) monocytes increase after I/R and correlate with cardiac repair, suggesting a therapeutic target.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Regenerative Medicine

Background:

  • Myocardial ischemia/reperfusion (I/R) injury triggers complex inflammatory responses.
  • Monocyte subsets play a critical role in post-injury inflammation and repair.
  • Understanding monocyte dynamics is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the dynamic changes of circulating monocyte subsets following myocardial I/R injury in rats.
  • To explore the correlation between these monocyte subsets and myocardial repair processes.
  • To identify potential therapeutic targets for mitigating I/R injury.

Main Methods:

  • Myocardial I/R was induced in male Wistar rats.
  • Peripheral blood monocyte subsets (CD172a(+)CD43(low) and CD172a(+)CD43(high)) were analyzed by flow cytometry at multiple time points post-I/R.
  • Cardiac fibrosis and hypertrophy were assessed using Masson's trichrome and wheat-germ agglutinin staining, respectively.

Main Results:

  • A significant increase in CD172a(+)CD43(low) monocytes was observed on day 1 post-I/R, peaking on day 3 and returning to baseline by day 7.
  • The proportion of CD172a(+)CD43(low) monocytes was significantly higher in the I/R group compared to the sham group on day 3.
  • CD172a(+)CD43(low) monocyte levels on day 3 positively correlated with infarct area collagen deposition, indicating reparative fibrosis.

Conclusions:

  • Circulating monocyte subset dynamics are altered following myocardial I/R injury in rats.
  • The proinflammatory CD172a(+)CD43(low) monocyte subset emerges as a key player in the early stages of myocardial repair.
  • Targeting CD172a(+)CD43(low) monocytes may offer a novel therapeutic strategy to attenuate myocardial I/R injury.

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