Articolele autorului Adrian Lupescu
Link la profilul stiintific al lui Adrian Lupescu

Hexavalent chromium-induced erythrocyte membrane phospholipid asymmetry.
Apigenin-induced suicidal erythrocyte death.

Apigenin, a flavone in fruits and vegetables, stimulates apoptosis and thus counteracts cancerogenesis. Erythrocytes may similarly undergo suicidal cell death or eryptosis, characterized by cell shrinkage and phosphatidylserine exposure at the cell surface. Triggers of eryptosis include increase of cytosolic Ca(2+) activity ([Ca(2+)](i)), ceramide formation and ATP depletion. The present study explored the effect of apigenin on eryptosis. [Ca(2+)](i)

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Tabebuia avellanedae extracts inhibit IL-2-independent T-lymphocyte activation and proliferation

In order to identify new, immune modulating compounds, aqueous extracts of plants pre-selected on ethno-pharmacological knowledge were screened for inhibitory effects in an anti-CD3 driven lymphocyte proliferation assay (MTT-assay). We found for the extract of the inner bark of Tabebuia avellanedae (Tabebuia) dose dependent and reproducible inhibitory effects on lymphocyte proliferation. We further analyzed Tabebuia in flow cytometry based whole

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Association of SGK1 Gene Polymorphisms with Type 2 Diabetes

The serum and glucocorticoid inducible kinase SGK1 is genomically upregulated by glucocorticoids and in turn stimulates a variety of carriers and channels including the renal epithelial Na(+) channel ENaC and the intestinal Na(+) glucose transporter SGLT1. Twin studies disclosed an association of a specific SGK1 haplotype with moderately enhanced blood pressure in individuals who are carrying simultaneously a homozygous genotype for a variant in

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Liver cell death and anemia in Wilson disease involve acid sphingomyelinase and ceramide

Wilson disease is caused by accumulation of Cu(2+) in cells, which results in liver cirrhosis and, occasionally, anemia. Here, we show that Cu(2+) triggers hepatocyte apoptosis through activation of acid sphingomyelinase (Asm) and release of ceramide. Genetic deficiency or pharmacological inhibition of Asm prevented Cu(2+)-induced hepatocyte apoptosis and protected rats, genetically prone to develop Wilson disease, from acute hepatocyte death, liver

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Mitochondria are not required for death receptor-mediated cytosolic acidification during apoptosis.

In addition to cell shrinkage, membrane blebbing, DNA fragmentation and phosphatidylserine exposure, intracellular acidification represents a hallmark of apoptosis. Although the mechanisms underlying cytosolic acidification during apoptosis remained largely elusive, a pivotal role of mitochondria has been proposed. In order to investigate the involvement of mitochondria in cytosolic acidification during apoptosis, we blocked the mitochondrial death

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Phospholipase A2-Activity Dependent Stimulation of Ca2+ Entry by Human Parvovirus B19 Capsid Protein VP1

Recent reports demonstrated an association of human parvovirus B19 (B19) with inflammatory cardiomyopathy (iCMP) which is accompanied by endothelial dysfunction. As intracellular Ca2+-activity is a key regulator of cell function and participates in mechanisms leading to endothelial dysfunction, the present experiments explored the effects of the B19 capsid proteins VP1 and VP2 on the regulation of cytosolic Ca2+-activity. A secreted phospholipase

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Human parvovirus B19: A new emerging pathogen of inflammatory

The human parvovirus B19 (PVB19), an erythrovirus causing diverse clinical manifestations ranging from asymptomatic or mild to more severe outcomes such as hydrops fetalis, is the only known human pathogenic parvovirus so far. Although enteroviruses have long been considered the most common cause of in.ammatory cardiomyopathy, PVB19 is emerging as a important candidate. Recent studies have indicated an association of PVB19 with paediatric and adult

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Glycogen metabolism in rat ependymal primary cultures: Regulation by serotonin.

Ependymal primary cultures are a model for studying ependymal energy metabolism. Intracellular glycogen is built up in the cultures dependent on culture age and the presence of glucose and glutamate. This energy store is mobilized upon glucose withdrawal, stimulation with isoproterenol, forskolin or serotonin and after uncoupling of oxidative phosphorylation from ATP production. Serotonin regulates ependymal glycogen metabolism predominantly via

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SGK1 mediated glucocorticoid induced inhibition of insulin secretion

Glucocorticoid excess predisposes to the development of diabetes, at least in part through impairment of insulin secretion. The underlying mechanism has remained elusive. We show here that dexamethasone upregulates transcription and expression of the serum- and glucocorticoid-inducible kinase 1 (SGK1) in insulin-secreting cells, an effect reversed by mifepristone (RU486), an antagonist of the nuclear glucocorticoid receptor. When coexpressed in Xenopus

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