In diabetic rats there was however an ongoing exacerbation of post-infarct remodeling, such as increased cardiomyocyte hypertrophy, a sustained increase in cardiomyocyte apoptosis both at the remote and border zone of the infarct, and a slight increase in collagen deposition, evident 12 weeks postligation.
Interestingly, the Conjugates could effectively improve phosphor-Stat3 expression in both remote and border zones, to investigate whether Stat-3 was essential in the Conjugates' anti-fibrosis effect, Stat3 inhibitor and siRNA were used.
These differences were evident in the remote and border zones.
Our results, showing a preservation of contractile function in remote and border zones, but no effect on the infarct area, suggest that adenosine may target other signalling pathways than ACE inhibitors and beta-blockers.
We have shown that, when administrated long-term after MI, adenosine exerts beneficial effects on the myocardial contractility of remote and border zones, but with limited impact on global LV remodelling.
Using FDG-PET in a rat infarct model, the present study shows that adenosine provides beneficial effects within the remote and border zones, but not within the MI area.
Active Wnt signaling increased significantly in both the remote area and the border zone (Fig. 3d, e).
Representative pictures of annexin-5 immunostaining in the remote, border and infarct (MI) zones are shown.
HE, CD31 (endothelial cells), CD61 (β3 integrin) and F4/80 (macrophages) staining in infarct, border zone and remote areas.
Myocardial thickening, assessed through the percentage of systolic increase in myocardial counts, exhibited a continuous decline between remote (40% ± 9%), border zone (23% ± 13%) and MI (12% ± 4%) segments (p < 0.001).
