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Glia and Glia-Neuron Interaction

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

RhoGDI2 controls for migration of astrocytes following an excitotoxic lesion in the mouse hippocampus

  • P3-021
  • Hyunjung Baek:1 Min-Hee YI:● Nara Shin:● Dong Woon Kim:● 
  • 1:Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, South Korea 

Numerous studies over the past years have revealed that Rho GTPases are crucial for the signaling pathways underlying the establishment of polarity, including polarized outgrowth of protrusions that precedes cell migration.
RhoGDI (Rho GDP-dissociation inhibitor) was identified as a down-regulator of Rho family GTPases typified by its ability to prevent nucleotide exchange and membrane association.Although RhoGDI2 was shown to function as a metastasis regulator, little is known about PDK1 changes in glial cells under neuropathological conditions. Three RhoGDI isoforms exist: RhoGDI1, RhoGDI2 and RhoGDI3. Both RhoGDI1 and RhoGDI2 are cytosolic whereas RhoGDI3 is a non-cytosolic isoform which contains a unique amino-terminal extension that targets it to the Golgi complex and other cellular membranes. In current report, RhoGDI2 was monitored specially on astrocyte migration, following the induction of an excitotoxic lesion in mouse brain by using kainic acid administration. In injured hippocampal CA3 region, RhoGDI2 was increased from 1 day until 3 day2 post-injection. Double immunohistochemistry further evaluated that these RhoGDI2 were localized in astrocytes not other cells. RhoGDI2 overexpression leads to inhibit phosphorylation of Protein kinase B (PKB/Akt). In conclusion, our results suggested for the first time that RhoGDI2 is required for control of astrocyte migration via PKB signaling in KA-mediated excitotoxic lesion in mouse brain

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