TRPM2 mediates the lysophosphatidic acid-induced neurite retraction in the developing brain
- Title
- TRPM2 mediates the lysophosphatidic acid-induced neurite retraction in the developing brain
- Author
- 손현
- Keywords
- TRP channels; TRPM2; Neurite outgrowth; Neuritogenesis; Lysophosphatidic acid; RECEPTOR-DEFICIENT MICE; NEURONAL GROWTH CONES; ADP-RIBOSE; CHEMOTROPIC GUIDANCE; NEUROTROPHIC FACTOR; OXIDATIVE STRESS; CATION CHANNELS; PC12 CELLS; OUTGROWTH; ACTIVATION
- Issue Date
- 2014-01
- Publisher
- SPRINGER, 233 SPRING ST, NEW YORK, NY 10013 USA
- Citation
- PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY; OCT 2014, Vol.466, No.10, p1987-p1998, 12p.
- Abstract
- Intracellular Ca2+ signal is a key regulator of axonal growth during brain development. As transient receptor potential (TRP) channels are permeable to Ca2+ and mediate numerous brain functions, it is conceivable that many TRP channels would regulate neuronal differentiation. We therefore screened TRP channels that are involved in the regulation of neurite growth. Among the TRP channels, the Trpm2 level was inversely associated with neurite growth. TRPM2 was highly expressed in embryonic brain. Pharmacological perturbation or knockdown of TRPM2 markedly increased the axonal growth, whereas its overexpression inhibited the axonal growth. Addition of ADP ribose, an endogenous activator of TRPM2, to PC12 cells significantly repressed the axonal growth. TRPM2 was actively involved in the neuronal retraction induced by cerebrospinal fluid-rich lysophosphatidic acid (LPA). More importantly, neurons isolated from the brain of Trpm2-deficient mice have significantly longer neurites with a greater number of spines than those obtained from the brain of wild-type mice. Therefore, we conclude that TRPM2 mediates the LPA-induced suppression of axonal growth, which provides a long-sought mechanism underlying the effect of LPA on neuronal development.
- URI
- http://link.springer.com/content/pdf/10.1007%2Fs00424-013-1436-4.pdfhttp://hdl.handle.net/20.500.11754/47517
- ISSN
- 0031-6768
- DOI
- 10.1007/s00424-013-1436-4
- Appears in Collections:
- COLLEGE OF MEDICINE[S](의과대학) > MEDICINE(의학과) > Articles
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