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

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 prog...

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Published inApplied sciences Vol. 14; no. 6; p. 2566
Main Authors Al-Huseini, Isehaq, Al-Ismaili, Maryam, Boudaka, Ammar, Sirasanagandla, Srinivasa Rao
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.03.2024
Subjects
Abdomen
aneurysm
aorta
Aortic aneurysms
Blood vessels
Calcification
Coronary vessels
Endothelium
Inflammation
Investigations
Ketamine
Laboratory animals
Proteins
Smooth muscle
Surgery
TRPV4 channel
vascular calcification
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Summary: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.
ISSN:2076-3417
2076-3417
DOI:10.3390/app14062566