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1 Integrin-Focal Adhesion Kinase Survival

Santos, Andrea Rachelle C ; Corredor, Raul G ; Obeso, Betty Albo ; Trakhtenberg, Ephraim F ; Wang, Ying ; Ponmattam, Jamie ; Dvoriantchikova, Galina ; Ivanov, Dmitry ; Shestopalov, Valery I ; Goldberg, Jeffrey L ; Fini, Mary Elizabeth ; Bajenaru, Michaela Livia

PloS one, 2012-10, Vol.7 (10), p.e48332 [Periódico revisado por pares]

Public Library of Science

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  • Título:
    1 Integrin-Focal Adhesion Kinase Survival
  • Autor: Santos, Andrea Rachelle C ; Corredor, Raul G ; Obeso, Betty Albo ; Trakhtenberg, Ephraim F ; Wang, Ying ; Ponmattam, Jamie ; Dvoriantchikova, Galina ; Ivanov, Dmitry ; Shestopalov, Valery I ; Goldberg, Jeffrey L ; Fini, Mary Elizabeth ; Bajenaru, Michaela Livia
  • Assuntos: Antibodies ; Cell death ; Ganglion cysts ; Integrins ; Ischemia ; Laminin ; Proteolysis
  • É parte de: PloS one, 2012-10, Vol.7 (10), p.e48332
  • Descrição: Extracellular matrix (ECM) integrity in the central nervous system (CNS) is essential for neuronal homeostasis. Signals from the ECM are transmitted to neurons through integrins, a family of cell surface receptors that mediate cell attachment to ECM. We have previously established a causal link between the activation of the matrix metalloproteinase-9 (MMP-9), degradation of laminin in the ECM of retinal ganglion cells (RGCs), and RGC death in a mouse model of retinal ischemia-reperfusion injury (RIRI). Here we investigated the role of laminin-integrin signaling in RGC survival in vitro, and after ischemia in vivo. In purified primary rat RGCs, stimulation of the [beta]1 integrin receptor with laminin, or agonist antibodies enhanced RGC survival in correlation with activation of [beta]1 integrin's major downstream regulator, focal adhesion kinase (FAK). Furthermore, [beta]1 integrin binding and FAK activation were required for RGCs' survival response to laminin. Finally, in vivo after RIRI, we observed an up-regulation of MMP-9, proteolytic degradation of laminin, decreased RGC expression of [beta]1 integrin, FAK and Akt dephosphorylation, and reduced expression of the pro-survival molecule bcl-xL in the period preceding RGC apoptosis. RGC death was prevented, in the context of laminin degradation, by maintaining [beta]1 integrin activation with agonist antibodies. Thus, disruption of homeostatic RGC-laminin interaction and signaling leads to cell death after retinal ischemia, and maintaining integrin activation may be a therapeutic approach to neuroprotection.
  • Editor: Public Library of Science
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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