FAK-and Pyk2-coupled pathway may contribute to the neurogenesis in gerbil hippocampus after ischemia

• Autorzy: Ziemka-Nalecz M. , Wojcik-Stanaszek L. , Zajac H. , Zalewska T.
• 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 their flow of information to the cell. The function of these enzymes is believed to be tightly linked to its autophosphorylation and association with Src kinase necessary for reciprocal activation/phosphorylation of both enzymes in response to adhesion-dependent signals. FAK and Pyk2 might act through a diverse array of downstream molecules and may regulate biological functions of the cell. 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 both 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. 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. Supported by MSHE grant no 0154/B/P01/2009/38.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: 1
• Opis fizyczny: p.173-174

Twórcy

autor

Ziemka-Nalecz M.

• Medical Research Centre, NeuroRepair Department, Polish Academy of Sciences, Warsaw, Poland

autor

Wojcik-Stanaszek L.

• Medical Research Centre, NeuroRepair Department, Polish Academy of Sciences, Warsaw, Poland

autor

Zajac H.

• Medical Research Centre, NeuroRepair Department, Polish Academy of Sciences, Warsaw, Poland

autor

Zalewska T.

• Medical Research Centre, NeuroRepair Department, Polish Academy of Sciences, Warsaw, Poland