Interleukin 6 reduces vascular smooth muscle cell apoptosis via Prep1 and is associated with aging

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Omi/HtrA2 promotes cell death by binding and degrading the anti-apoptotic protein ped/pea-15

ped/pea-15 is a ubiquitously expressed 15-kDa protein featuring a broad anti-apoptotic function. In a yeast two-hybrid screen, the pro-apoptotic Omi/HtrA2 mitochondrial serine protease was identified as a specific interactor of the ped/pea-15 death effector domain. Omi/HtrA2 also bound recombinant ped/pea-15 in vitro and co-precipitated with ped/pea-15 in 293 and HeLa cell extracts. In these cells, the binding of Omi/HtrA2 to ped/pea-15 was induced by UVC exposure and followed the mitochondrial release of Omi/HtrA2 into the cytoplasm. Upon UVC exposure, cellular ped/pea-15 protein expression levels decreased. This effect was prevented by the ucf-101 specific inhibitor of the Omi/HtrA2 proteolytic activity, in a dose-dependent fashion. In vitro incubation of ped/pea-15 with Omi/HtrA2 resulted in ped/pea-15 degradation. In intact cells, the inhibitory action of ped/pea-15 on UVC-induced apoptosis progressively declined at increasing Omi/HtrA2 expression. This further effect of Omi/HtrA2 was also inhibited by ucf-101. In addition, ped/pea-15 expression blocked Omi/HtrA2 co-precipitation with the caspase inhibitor protein XIAP and caspase 3 activation. Thus, in part, apoptosis following Omi/HtrA2 mitochondrial release is mediated by reduction in ped/pea-15 cellular levels. The ability of Omi/HtrA2 to relieve XIAP inhibition on caspases is modulated by the relative levels of Omi/HtrA2 and ped/pea-15

Omi/HtrA2 promotes cell death by binding and degrading the anti-apoptotic protein ped/pea-15

ped/pea-15 is a ubiquitously expressed 15-kDa protein featuring a broad anti-apoptotic function. In a yeast two-hybrid screen, the pro-apoptotic Omi/HtrA2 mitochondrial serine protease was identified as a specific interactor of the ped/pea-15 death effector domain. Omi/HtrA2 also bound recombinant ped/pea-15 in vitro and co-precipitated with ped/pea-15 in 293 and HeLa cell extracts. In these cells, the binding of Omi/HtrA2 to ped/pea-15 was induced by UVC exposure and followed the mitochondrial release of Omi/HtrA2 into the cytoplasm. Upon UVC exposure, cellular ped/pea-15 protein expression levels decreased. This effect was prevented by the ucf-101 specific inhibitor of the Omi/HtrA2 proteolytic activity, in a dose-dependent fashion. In vitro incubation of ped/pea-15 with Omi/HtrA2 resulted in ped/pea-15 degradation. In intact cells, the inhibitory action of ped/pea-15 on UVC-induced apoptosis progressively declined at increasing Omi/HtrA2 expression. This further effect of Omi/HtrA2 was also inhibited by ucf-101. In addition, ped/pea-15 expression blocked Omi/HtrA2 co-precipitation with the caspase inhibitor protein XIAP and caspase 3 activation. Thus, in part, apoptosis following Omi/HtrA2 mitochondrial release is mediated by reduction in ped/pea-15 cellular levels. The ability of Omi/HtrA2 to relieve XIAP inhibition on caspases is modulated by the relative levels of Omi/HtrA2 and ped/pea-15

LA PSORIASI ARTROPATICA: UN MODELLO DI PROTOCOLLO CLINICO

We propose a new protocol for a diagnosis of arthropathic psoriasis, different from Wright and Moll proposed criteria. This protocol is intentionally more detailed and complete. It consists of eight distinct sections. The first four ones are traditional anamnestical. The fifth section includes cutis and joints physical examination; the sixth section concerns general physical examination; the seventh section is dedicated to laboratory investigation, both biochemical (particularly for detection of acute phase reactants: ESR, CRP, blood copper, iron, ceruplasmin) and immunological (Ig, antibodies, complement). The eighth section includes joint scintiscan evaluation, followed by traditional Rx study

VARIABILITA GEOGRAFICA E FATTORI PREDITTIVI DELL'ARTRITE REUMATOIDE. LO STUDIO SUI PIMA INDIANS

Pima Indians of Arizona, a native American population, are subjects of a longitudinal study that has shown the unusually high prevalence and incidence of Rheumatoid Arthritis (RA) in the population. Incidence data form the basis for analysis of risk factors. The present paper reviews the available results. Data suggest that several factors have a predictive role for the development of RA. Among them, Rheumatoid Factor is discussed and data reported concerning the effect of its titer, idiotype and level of galactosylation. Variations in serum cholesterol concentration before the onset of RA and characteristics of the genotype are additional factors analysed. Data provide evidence on the presence of several factors that can be considered markers of the earliest phases of the pathogenetic process of RA