α-Tocopherol (vitamin E) regulates vascular smooth muscle cell proliferation and protein kinase C activity

d‐α‐Tocopherol inhibits low density lipoprotein induced proliferation and protein kinase C activity in vascular smooth muscle cells

“…The fact that both normal and modified LDL were able to stimulate cell proliferation under the experimental conditions employed in this study suggests that the lipoprotein receptor as well as the scavenger receptor can initiate a proliferative event. d-a-Tocopherol appears to act at some point in the cascade of events further leading to activation of cell proliferation, Inhibition of protein kinase C activity has been indicated to be a central event in the mechanism of cell growth inhibition by d-a-tocopherol [14,15]. Fig.…”

Early vitamin E supplementation attenuates diabetes-associated vascular dysfunction and the rise in protein kinase C-β in mesenteric artery and ameliorates wall stiffness in femoral artery of Wistar rats

“…Important physiological effects of VitE involve its incorporation into vascular tissue [23], including inhibition of leucocyte adhesion to endothelial cells [24], reduced smooth muscle proliferation [25] and protection against oxidant-mediated cytotoxicity [26]. It is possible that the benefit derived from VitE on endothelial function may be concentration-dependent and occur regardless of its effect on oxidant stress as measured by isoprostane levels.…”

“…The fact that other antioxidants, even β-tocopherol, do not inhibit PKC suggests that these mechanisms are not related to the anti-oxidant effect of vitamin E [32]. The inhibitory effect of α-tocopherol (VitE) on PKC activation is concordant with its effect on phosphorylation of the myristolated, alaninerich C kinase substrate protein, a substrate of PKC [25], and with the fact that it also increased protein phosphatase type 2A activity, which results in PKCdephosphorylation [32]. These observations suggest that a ligand/receptor type of mechanism is the basis of the action of VitE on PKC.…”

“…These observations suggest that a ligand/receptor type of mechanism is the basis of the action of VitE on PKC. There is also evidence that VitE may inhibit PKC translocation to the cell membrane [25].…”

INTERRELATION OF VITAMIN E ISOFORMS AND ATHEROGENESIS MARKERS IN PATIENTS WITH TYPE 2 DIABETES MELLITUS (literature review and own results)

“…Так, у 1991 роцi групою пiд керiвництвом Анджело Аццi (Angelo Azzi) вперше були комплексно описанi не пов'язанi з антиокси-дантними функцiї α-токоферола у клiтинно-му сигналiнгу, що знаходили свою реалiза-цiю в iнгiбуваннi активностi протеїнкiнази С в гладеньком'язових клiтинах [11]. У подаль-шому було визначено, що α-токоферол моду-лює два головних шляхи сигнальної транс-дукцiї, сфокусованих на протеїнкiназi С та фосфатидилiнозитол-3-кiназi [12].…”