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2011 | 71 | S |
Tytuł artykułu

The potential role of FAK- and PYK2 coupled pathway in the neurogenesis in gerbil hippocampus after global ischemia

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Recently published data indicate that in physiological conditions proteolytic remodeling of extracellular matrix (ECM) by matrix metalloproteinases (MMPs) participates in the stem cells development. Signal derived from ECM may activate specific intracellular signaling pathways which involve non-receptor tyrosine kinases such focal adhesion kinase (FAK) and proline-rich tyrosine kinase 2 (Pyk2), key components responsible for the flow of information to the cell. FAK and Pyk2 might act through a diverse array of downstream molecules such a phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK). Activation (PI3K)/ Akt and ERK pathways in neural precursors plays a central role in induction of adult neurogenesis. These prompted us to evaluate the possible involvement of FAK/PYK2-coupled pathway in the regulation of neurogenesis-associated processes stimulated by transient global ischemia in gerbil hippocampus. For this purpose we checked if there is temporal relationship between activation/phosphorylation of these kinases and proliferation and/or determination of neural progenitor cells. We found that short-term (5 min) ischemia increased Pyk-2 phosphorylation level in dentate gyrus ( neurogenic part of hippocampus) after 2 and 4 weeks of recovery, the time when we observed the intensive proliferation rate and differentiation of progenitors toward neuronal phenotypes. In contrast, in the CA1 region of the hippocampus the level of phosphorylated Pyk-2 was slightly reduced after 2, 4 and 6 weeks of reperfusion. At the same time the level of phosphorylated FAK was significantly increased in both investigated hippocampal regions. In contrast activation of ERK and Akt kinases was significantly reduced in all investigated time points with more pronounced effect in CA1. The elevation of PYK-2 activity in dentate gyrus might suggest the involvement of this kinase in the post-ischemic stimulation of neurogenesis after global ischemia.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
71
Numer
S
Opis fizyczny
p.36-37
Twórcy
  • NeuroRepair Department, Mossakowski Medical Research Centre PAS, Warsaw, Poland
  • NeuroRepair Department, Mossakowski Medical Research Centre PAS, Warsaw, Poland
autor
  • NeuroRepair Department, Mossakowski Medical Research Centre PAS, Warsaw, Poland
autor
  • NeuroRepair Department, Mossakowski Medical Research Centre PAS, Warsaw, Poland
Bibliografia
Uwagi
Rekord w opracowaniu
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.agro-6694f808-4f1e-4197-ad82-e52c82c87d3a
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