T-cadherin is critical for adiponectin-mediated cardioprotection in mice

Martin S Denzel ¹, Maria-Cecilia Scimia , Philine M Zumstein

⁰Sanford-Burnham Medical Research Institute, La Jolla, California, USA.

The Journal of Clinical Investigation +

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November 3, 2010

View abstract on PubMed

Summary

T-cadherin binds adiponectin (APN) to protect the heart from stress. Lacking T-cadherin prevents APN

Area Of Science

Cardiovascular Biology
Endocrinology
Molecular Cardiology

Background

Adiponectin (APN), an adipocyte-secreted hormone, offers cardiac protection during stress.
The specific cardiac receptors for APN have not been identified, limiting understanding of its mechanism.

Purpose Of The Study

To identify the cardiac receptors for adiponectin (APN).
To elucidate the role of T-cadherin in mediating APN's cardioprotective effects.

Main Methods

Investigated T-cadherin (Cdh13) and APN colocalization in mouse cardiomyocytes.
Utilized T-cadherin-deficient and APN-null mouse models under pressure overload and ischemia-reperfusion stress.
Assessed cardiac hypertrophy, infarct size, and myocardial AMPK phosphorylation.

Main Results

T-cadherin and APN extensively colocalized on cardiomyocytes in vivo.
T-cadherin deficiency disrupted APN binding to cardiac tissue, increasing circulating APN levels.
T-cadherin-null mice exhibited exacerbated cardiac hypertrophy and increased infarct size, mirroring APN-null mice.
T-cadherin was essential for APN-mediated AMPK phosphorylation in cardiac stress models.

Conclusions

T-cadherin acts as a cardiac receptor for adiponectin (APN).
T-cadherin mediates APN's protective functions against stress-induced cardiac remodeling.
T-cadherin binding of APN is crucial for activating downstream cardioprotective signaling pathways like AMPK phosphorylation.

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