T-cadherin, a major adiponectin binding partner, suppresses ERK signaling in metabolic tissues

Area of Science:

• Cellular biology
• Molecular signaling
• Metabolic research

Background:

• T-cadherin is an adiponectin binding partner with organ-protective effects.
• Intracellular signaling changes induced by T-cadherin in metabolic tissues are not well understood.

Purpose of the Study:

• To investigate the role of T-cadherin in modulating intracellular signaling pathways.
• To elucidate the effects of T-cadherin on cardiac and skeletal muscle homeostasis.

Main Methods:

• Cell culture experiments (C2C12 myocytes, F2 endothelial cells) with T-cadherin knockdown and overexpression.
• Proteomic analysis to identify downstream targets of ERK signaling.
• Murine models with T-cadherin knockout in cardiac and skeletal muscles.

Main Results:

• T-cadherin suppresses ERK (extracellular signal-regulated kinase) signaling in cultured cells and murine tissues.
• T-cadherin knockdown increased ERK phosphorylation and upregulated downstream targets.
• T-cadherin ablation in mice led to increased ERK signaling, cardiac hypertrophy, and altered muscle atrophy during starvation.

Conclusions:

• T-cadherin modulates intracellular signaling, specifically suppressing ERK pathways.
• T-cadherin plays a role in maintaining cardiac and skeletal muscle homeostasis.
• Adiponectin-maintained T-cadherin influences exosome production and cellular signaling.