Deletion of Transient Receptor Channel Vanilloid 4 Aggravates CaCl2-Induced Abdominal Aortic Aneurysm and Vascular Calcification: A Histological Study

Abstract

Vascular calcification is calcium deposition occurring in the wall of blood vessels, leading to mechanical stress and rupture due to a loss of elasticity and the hardening of the vessel wall. The role of the Transient Receptor Channel Vanilloid 4 (TRPV4), a Ca2+-permeable cation channel, in the progression of vascular calcification is poorly explored. In this study, we investigated the role of TRPV4 in vascular calcification and the development of abdominal aortic aneurysm (AAA). Experimental mice were randomly divided into four groups: wild-type (WT) sham operated group, WT CaCl2-induced aortic injury, TRPV4-KO sham operated group, and TRPV4-KO CaCl2-induced aortic injury. The TRPV4-knockout (TRPV4-KO) mice and wild-type (WT) mice were subjected to the CaCl2-induced abdominal aortic injury. In histopathological analysis, the aorta of the TRPV4-KO mice showed extensive calcification in the tunica media with a significant increase in the outer diameter (p < 0.0001), luminal area (p < 0.05), and internal circumference (p < 0.05) after CaCl2 injury when compared to WT mice. Additionally, the tunica media of the TRPV4-KO mice aorta showed extensive damage with apparent elongation and disruption of the elastic lamella. These results indicate a protective function of TRPV4 against vascular calcification and the progression of AAA after CaCl2 injury.