{Reference Type}: Journal Article
{Title}: T-Cadherin Deficiency Is Associated with Increased Blood Pressure after Physical Activity.
{Author}: Popov VS;Brodsky IB;Balatskaya MN;Balatskiy AV;Ozhimalov ID;Kulebyakina MA;Semina EV;Arbatskiy MS;Isakova VS;Klimovich PS;Sysoeva VY;Kalinina NI;Tkachuk VA;Rubina KA;
{Journal}: Int J Mol Sci
{Volume}: 24
{Issue}: 18
{Year}: 2023 Sep 17
{Factor}: 6.208
{DOI}: 10.3390/ijms241814204
{Abstract}: T-cadherin is a regulator of blood vessel remodeling and angiogenesis, involved in adiponectin-mediated protective effects in the cardiovascular system and in skeletal muscles. GWAS study has previously demonstrated a SNP in the Cdh13 gene to be associated with hypertension. However, the role of T-cadherin in regulating blood pressure has not been experimentally elucidated. Herein, we generated Cdh13∆Exon3 mice lacking exon 3 in the Cdh13 gene and described their phenotype. Cdh13∆Exon3 mice exhibited normal gross morphology, life expectancy, and breeding capacity. Meanwhile, their body weight was considerably lower than of WT mice. When running on a treadmill, the time spent running and the distance covered by Cdh13∆Exon3 mice was similar to that of WT. The resting blood pressure in Cdh13∆Exon3 mice was slightly higher than in WT, however, upon intensive physical training their systolic blood pressure was significantly elevated. While adiponectin content in the myocardium of Cdh13∆Exon3 and WT mice was within the same range, adiponectin plasma level was 4.37-fold higher in Cdh13∆Exon3 mice. Moreover, intensive physical training augmented the AMPK phosphorylation in the skeletal muscles and myocardium of Cdh13∆Exon3 mice as compared to WT. Our data highlight a critically important role of T-cadherin in regulation of blood pressure and stamina in mice, and may shed light on the pathogenesis of hypertension.