Prof. LIU and his collaborator found that depleting neuronal lipin1, a key enzyme controlling the balanced synthesis of glycerolipids through the glycerol phosphate pathway, enhanced axon regeneration after optic nerve injury. Axotomy elevated lipin1 in retinal ganglion cells, which contributed to regeneration failure in the CNS by favorably producing triglyceride (TG) storage lipids rather than phospholipid (PL) membrane lipids in neurons. Regrowth induced by lipin1 depletion required TG hydrolysis and PL synthesis. Decreasing TG synthesis by deleting neuronal diglyceride acyltransferases (DGATs) and enhancing PL synthesis through the Kennedy pathway promoted axon regeneration.
In addition, peripheral neurons adopted this mechanism for their spontaneous axon regeneration. The study reveals a critical role of lipin1 and DGATs as intrinsic regulators of glycerolipid metabolism in neurons and indicates that directing neuronal lipid synthesis away from TG synthesis and toward PL synthesis may promote axon regeneration.
- Cheng Associate Professor of Science
- Associate Professor, Division of Life Science
- Associate Director of HKUST-Nan Fung Life Sciences Joint Laboratory
An international research team co-led by HKUST, Beijing Neurosurgical Institute, and the Spanish National Cancer Research Center (CNIO) has discovered a mechanism that...
Researchers from HKUST discovered a novel molecular mechanism that controls the delivery of a key protein in planar cell polarity (PCP)...