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Article Abstract

Aim & Objective: We have reported that T-cadherin (T-cad), a glycosylphosphatidylinositol-anchored protein that specifically binds to adiponectin, exists in the human serum as a soluble form (sT-cad). sT-cad promotes pancreatic β-cell proliferations, indicating a potential organ-protective role. This study aimed to the cardioprotective effect of sT-cad.

Methods & Results: The sT-cad-expressing plasmid was administered to 7-week-old wild-type mice. One week after administration, transverse aortic constriction (TAC) surgery was performed to induce pressure-overload heart failure. Then, the mice were sacrificed at 2 weeks after the surgery. In the mice that received sT-cad, the TAC-induced increase in heart weight and decline in cardiac function were significantly attenuated. Based on the cardiac histological analysis, sT-cad suppressed both cardiomyocyte hypertrophy and cardiac fibrosis. Cardiac RNA sequencing analysis showed that sT-cad inhibited the TAC-induced upregulation of fibrosis-related genes. In addition, in NIH-3T3 fibroblasts, sT-cad supplementation suppressed the TGF-β-induced mRNA expression of Acta2, a myofibroblast marker.

Conclusion: sT-cad ameliorated the pressure overload-induced heart failure in mice.

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http://dx.doi.org/10.1016/j.bbrc.2025.152459DOI Listing

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