Dr. Liang Zhang received his Bachelor of Medicine (MD equivalent) degree from Peking University. He obtained his PhD degree from the University of Iowa and performed his postdoctoral training at the Lunenfeld-Tanenbaum Research Institute in Toronto, Canada. He is currently an Associate Professor in the Department of Biomedical Sciences at City University of Hong Kong.
His research is centred on understanding how interactions and modifications of biomolecules regulate health and diseases. His laboratory applies integrative approaches that combine mass spectrometry-based proteomics and systems biology tools to dissect the wiring of signaling networks. Special interests are focused on exosomes and Wnt signaling in cancer and aging.
Adipocytes have the potential to dedifferentiate into multipotent mesenchymal cells. Recent studies demonstrated that elevated osmolarity and compressive force could induce adipocyte dedifferentiation, representing an appealing procedure for regenerative toolsets. However, it remains elusive about the molecular mechanism that underlies the compression-induced reprogramming of adipocytes. Here we report that osmotic force prompted the adipocytes to eject mitochondrial components in extracellular vesicles, reflecting stresses in energetic metabolism. The ejected mitochondria in turn stimulated the secretion of TNF- α as a pro-inflammatory cytokine, which was necessary for adipocyte dedifferentiation. Ameliorating the metabolic stress of mitochondria inhibited TNF- α signaling and adipocyte dedifferentiation. Mechanistically, we showed that TNF- α activated the β -catenin signaling that drives adipocyte dedifferentiation. Our results defined a novel mitochondria-TNF- α / β -catenin signaling that drives adipocyte reprogramming in response to osmotic stress.