Protein kinase C mediates caspase 3 activation: A role for erythrocyte morphology changes.

Cristiana Carelli Alinovi, Francesco Misiti

Risultato della ricerca: Contributo in rivistaArticolo in rivista

6 Citazioni (Scopus)

Abstract

We have previously showed that morphological alterations in Red Blood Cells (RBCs) are correlated to an impaired eNOS enzymatic activity and a concomitant reduced NO derived metabolites formation. Here we extend our previous observations, reporting that RBC morphology is regulated by a series of specific cell signaling events linked to Protein Kinase C (PKC)-mediated activation of caspase 3. Pretreatment of RBCs with the PKC inhibitor chelerythrine, prior to the addition of phorbol-12-myristate-13-acetate (PMA), an activator of PKC, blocks the appearance of the morphology alterations and the sustained decrease in nitrates and nitrites levels induced by PMA. Inhibition of PKC also completely inhibits PMA mediated caspase-3 activation. On the other hand, caspase 3 inhibition, lessens the PMA induced-effects on the appearance of RBC morphology alterations, although it enhances PMA-mediated effects on nitric oxide (NO) derived metabolites levels. These data demonstrate that PKC-mediated activation of caspase 3 is an integral and essential part of signaling pathway in RBCs, that may be a regulatory factor of RBC mechanical properties, through regulation of NO metabolism.
Lingua originaleEnglish
pagine (da-a)345-354
Numero di pagine10
RivistaClinical Hemorheology and Microcirculation
DOI
Stato di pubblicazionePubblicato - 2015

Keywords

  • Protein kinase C
  • Red Blood Cells
  • nitric oxide
  • phorbol-12-myristate-13-acetate (PMA)

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