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[Dynamic changes of peripheral blood monocyte subsets after myocardial ischemia/reperfusion in rats]
Objective:
To investigate the dynamic changes of monocyte subsets after myocardial ischemia/reperfusion (I/R) in rats and their correlations with myocardial repair after I/R injury.
Methods:
Sixteen male Wistar rats were randomly divided into two groups: I/R group and sham group. Myocardial I/R was induced by left anterior descending coronary artery ligation for 45 min followed by permanent reperfusion. Peripheral blood was harvested from the tail vein to evaluate the dynamics of CD172a(+);CD43(low); and CD172a(+);CD43(high); monocyte subsets by flow cytometry at baseline and on day 1, 3, 5, 7 and 14 after I/R injury. Survival rats were sacrificed on day 30, and the hearts were prepared for the evaluation of collagen deposition (Masson's trichrome staining) and myocardial hypertrophy (wheat-germ agglutinin staining).
Results:
In I/R group, there was a significant increase of CD172a(+);CD43(low); monocytes on day 1 compared with the baseline (P<0.05), followed by an increasing trend, which peaked on day 3 (P<0.01), and then underwent a gradual decreasing trend to the baseline on day 7. In sham group, a similar increasing trend of CD172a(+);CD43(low); monocytes was observed on day 1 (P<0.05) compared with the baseline, whereas this trend declined rapidly to the baseline level on day 3. The proportion of CD172a(+);CD43(low); in I/R group on day 3 was much higher than that in the sham group (P<0.01). There were no significant differences between the two groups at any other time points. A reciprocal change of CD172a(+);CD43(high); monocytes was observed during investigation. Cardiac pathological evaluation revealed that there was a significant reparative fibrosis in the infarct area (P<0.05) along with a significant myocardial hypertrophy in non-infarct area (P<0.01) in I/R group. Correlation analysis showed that the proportion of CD172a(+);CD43(low); monocytes on day 3, but not CD172a(+);CD43(high); monocytes, was positively correlated with the level of collagen deposition in the infarct area (r=0.86, P<0.05).
Conclusion:
The study demonstrates the dynamic profile of circulating monocyte subsets following myocardial I/R injury in rats, which indicates that the proinflammatory CD172a(+);CD43(low); monocytes might be a therapeutic target to attenuate myocardial I/R injury.
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.

