T3 enhances Ang2 in rat aorta in myocardial I/R: comparison with left ventricle

Abstract

Angiogenesis is important for recovery after tissue damage in myocardial ischemia/reperfusion, and tri-iodothyronine (T3) has documented effects on angiogenesis. The angiopoietins 1/2 and tyrosine kinase receptor represent an essential system in angiogenesis controlling endothelial cell survival and vascular maturation. Recently, in a 3-day ischemia/reperfusion rat model, the infusion of a low dose of T3improved the post-ischemic recovery of cardiac function.Adopting this model, our study aimed to investigate the effects of T3on the capillary index and the expression of angiogenic genes as the angiopoietins 1/2 and tyrosine kinase receptor system, in the thoracic aorta and in the left ventricle. In the thoracic aorta, T3infusion significantly improved the angiogenic sprouting and angiopoietin 2 expression. Instead, Sham-T3group did not show any significant increment of capillary density and angiopoietin 2 expression. In the area at risk (AAR) of the left ventricle, T3infusion did not increase capillary density but restored levels of angiopoietin 1, which were reduced in I/R group. Angiopoietin 2 levels were similar to Sham group and unchanged by T3administration. In the remote zone, T3induced a significant increment of both angiopoietin 1/2. In conclusion, T3infusion induced a different response of angiopoietin 1/2 between the ventricle (the AAR and the remote zone) and the thoracic aorta, probably reflecting the different action of angiopoietin 1/2 in cardiomyocytes and endothelial cells. Overall, these data suggest a new aspect of T3-mediated cardioprotection through angiogenesis.

Vitamin D, Thyroid Hormones and Cardiovascular Risk: Exploring the Components of This Novel Disease Triangle

“…More specifically, nitric oxide (NO) production by VSMC, other than by endothelium, has been considered the driving factor in local regulation of vascular response ( Lee et al, 2008 ) mainly via PI3K/Akt signaling pathway activation ( Carrillo-Sepúlveda et al, 2010 ). Furthermore, it has been observed that both T4 and T3 administration induce new blood vessel formation via surface receptor ανβ3-mediated pathway in human microvascular endothelial cells ( Balzan et al, 2013 ; Liu et al, 2014 ) and in rat heart and aorta tissues during ischemic reperfusion procedure ( Sabatino et al, 2016 ).…”

Dynorphins in Development and Disease: Implications for Cardiovascular Disease

“…Evidence indicates that Dyn-A 1-17 administration causes an increase in total free fatty acids and nor-BNI reduces Dyn-A 1-17 -induced motor dysfunction [63]. Importantly, recent studies suggest that IGF-1 is cardioprotective by inhibiting Na + /H + exchanger activity via phosphorylation at Ser648 of the exchanger [64] and T3 aids in early-phase CV angiogenic sprouting after ischemia/reperfusion (I/R) through angiopoietin-1 and VEGF upregulation [65]; (Fig. 2A).…”