A cardioprotective hormone, adiponectin, prevents damage induced by stress to the heart, claim scientists at Sanford-Burnham Medical Research Institute.
"Whereas healthy people usually have high adiponectin levels circulating in their bodies, obese fat is different from healthy fat. Obese fat produces less adiponectin, reflected in lower levels of adiponectin found in serum," explained Dr. Ranscht.
Ranscht and colleagues engineered mice that lacked T-cadherin and looked at their hearts.
They found that adiponectin was no longer able to bind to heart tissue, leaving more hormone flowing in the bloodstream. They also found that without the ability to bind adiponectin to the heart, mice with mutant T-cadherin suffered from increased cardiac damage and experienced the same symptoms as mice lacking adiponectin under those conditions.
If T-cadherin were necessary for mediating adiponectin-induced cardioprotection, then a rescue by administering adiponectin to adiponectin-deficient mice should not work in T-cadherin-deficient mice.
Indeed, adding adiponectin to the double mutant mice did not rescue the stress-damaged hearts, underscoring the importance of T-cadherin for adiponectin functions in the heart.
"Our work shows that T-cadherin is necessary for adiponectin functions, but we still don't know how T-cadherin transmits the adiponectin-binding signal into the cell. We are now searching for proteins that might functionally associate with T-cadherin and thus form the molecular link between T-cadherin and AMPK."
This new study is published November 1 in The Journal of Clinical Investigation.