Survival effect of PDGF-CC rescues neurons from apoptosis in both brain and retina by regulating GSK3β phosphorylation
- Zhongshu Tang,
- Pachiappan Arjunan,
- Chunsik Lee,
- Yang Li,
- Anil Kumar,
- Xu Hou
- National Institutes of Health,
- Weifang Medical University,
- Uppsala University,
- University of Manitoba,
- Kindai University,
- Karolinska Institutet
Open access
Abstract
Platelet-derived growth factor CC (PDGF-CC) is the third member of the PDGF family discovered after more than two decades of studies on the original members of the family, PDGF-AA and PDGF-BB. The biological function of PDGF-CC remains largely to be explored. We report a novel finding that PDGF-CC is a potent neuroprotective factor that acts by modulating glycogen synthase kinase 3β (GSK3β) activity. In several different animal models of neuronal injury, such as axotomy-induced neuronal death, neurotoxin-induced neuronal injury, 6-hydroxydopamine-induced Parkinson's dopaminergic neuronal death, and ischemia-induced stroke, PDGF-CC protein or gene delivery protected different types of neurons from apoptosis in both the retina and brain. On the other hand, loss-of-function assays using PDGF-C null mice, neutralizing antibody, or short hairpin RNA showed that PDGF-CC deficiency/inhibition exacerbated neuronal death in different neuronal tissues in vivo. Mechanistically, we revealed that the neuroprotective effect of PDGF-CC was achieved by regulating GSK3β phosphorylation and expression. Our data demonstrate that PDGF-CC is critically required for neuronal survival and may potentially be used to treat neurodegenerative diseases. Inhibition of the PDGF-CC-PDGF receptor pathway for different clinical purposes should be conducted with caution to preserve normal neuronal functions.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 867-880 (14 pages)Journal (Volume, Issue Number)
Journal of Experimental Medicine (Volume 207, Issue 4)Publication milestones
- Published - 04/12/2010
Publication status
ISSN
0022-1007Publication IDs
- Scopus: 77951074818
- PubMed: 20231377
