staurosporine/hypoxia

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Chronic hypoxia increases staurosporine sensitivity of pulmonary artery smooth muscle to endothelin-1.

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Endothelins (ET) have been implicated in the pathogenesis of hypoxia-induced pulmonary hypertension. We evaluated the contribution of protein kinase C (PKC) to the ET-1 response of isolated endothelium-denuded extralobar pulmonary artery (PA) from rats exposed to chronic hypoxia (10% O2-90% N2, 1

Probing hypoxia-induced staurosporine resistance in prostate cancer cells with a microfluidic culture system.

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A microfluidic system for cell culture and drug response studies was developed to elucidate the effects of hypoxia on drug susceptibility. Drug response studies were performed in prostate cancer cells and Ramos B cells under normoxic and hypoxic conditions. A vacuum actuated microfluidic culture

SIRT3 protects from hypoxia and staurosporine-mediated cell death by maintaining mitochondrial membrane potential and intracellular pH.

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Mitochondrial sirtuin 3 (SIRT3) mediates cellular resistance toward various forms of stress. Here, we show that in mammalian cells subjected to hypoxia and staurosporine treatment SIRT3 prevents loss of mitochondrial membrane potential (ΔΨ(mt)), intracellular acidification and reactive oxygen

Hypoxia induces myocyte-dependent COX-2 regulation in endothelial cells: role of VEGF.

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There is increasing evidence that cyclooxygenase (COX)-2 possess both angiogenic and cardioprotective properties. We examined the effects of hypoxic cardiac myocytes (H9c2 cells) on COX-2 expression in human umbilical vein endothelial cells (HUVECs) to determine the pathway involved in COX-2

Phorbol ester-induced ventricular fibrillation in the Langendorff-perfused rabbit heart: antagonism by staurosporine and glibenclamide.

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Using a paced Lagendorff-perfused rabbit heart paradigm, we investigated the role of protein kinase C (PKC) in the development of ventricular fibrillation (VF) in hearts subjected to hypoxia (12 min) and re-oxygenation (40 min). We studied the effect of putative activators and inhibitors of PKC on

NUPR1 acts as a pro-survival factor in human bone marrow-derived mesenchymal stem cells and is induced by the hypoxia mimetic reagent deferoxamine.

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Differences in the culturing conditions of mesenchymal stem cells used in regenerative medicine may affect their differentiation ability, genome instability, and therapeutic effects. In particular, bone marrow-derived mesenchymal stem cells cultured under hypoxia are known to proliferate while

[Influence of Erigeron breviscapus on the expression of collagen type I , MMP1 and TIMP1 of MRC-5 cells under hypoxia].

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OBJECTIVE Study the influence of Erigeron breviscapus on collagen type I, matrix metalloproteinase1 (MMP1) and tissue inhibitor of metalloproteinase1(TIMP1) in human embryo lung fibroblast MRC-5 under hypoxia. METHODS MRC-5 cultured in vitro were individed into 4 groups, including normoxia control,

Bcl-x pre-mRNA splicing regulates brain injury after neonatal hypoxia-ischemia.

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The bcl-x gene appears to play a critical role in regulating apoptosis in the developing and mature CNS and following CNS injury. Two isoforms of Bcl-x are produced as a result of alternative pre-mRNA splicing: Bcl-x(L) (the long form) is anti-apoptotic, while Bcl-x(S) (short form) is pro-apoptotic.

Release of dopamine and norepinephrine by hypoxia from PC-12 cells.

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We examined the effects of hypoxia on the release of dopamine (DA) and norepinephrine (NE) from rat pheochromocytoma 12 (PC-12) cells and assessed the involvement of Ca2+ and protein kinases in stimulus-secretion coupling. Catecholamine release was monitored by microvoltammetry using a carbon fiber

Chronic hypoxia impairs the differentiation of 3T3-L1 fibroblast in culture: role of sustained protein kinase C activation.

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The effect of hypoxia on 3T3-L1 cell differentiation was examined in confluent cultures incubated with differentiation medium (DM) followed by incubation in growth medium (GM). Control cultures remained in GM throughout the incubation period. Eight days after the incubation, cells were assessed

Characterization of cell clones isolated from hypoxia-selected renal proximal tubular cells.

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Under hypoxia, some cells survive and others are irreversibly injured and die. The factors that determine cell fate under stress remain largely unknown. We recently selected death-resistant cells via repeated episodes of hypoxia. In the present study, 80 clones were isolated from the selected cells

Protection of myocytes from hypoxia-reoxygenation injury by nitric oxide is mediated by modulation of transforming growth factor-beta1.

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BACKGROUND Reoxygenation injury is a result of several complex events, including release of reactive oxygen species, protein kinase C (PKC) activation, and altered expression of transforming growth factor-beta1 (TGF-beta(1)). Nitric oxide (NO) generally protects tissues from reperfusion

Augmentation of calcium current by hypoxia in carotid body glomus cells.

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Several lines of evidence indicate that transduction of the hypoxic stimulus at the carotid body involves an increase in cytosolic Ca2+ ([Ca2+]i) via activation of voltage-gated Ca2+ channels in the glomus cells. However, reported responses to hypoxia include either no effect on or inhibition of

The Nrf1 CNC-bZIP protein is regulated by the proteasome and activated by hypoxia.

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BACKGROUND Nrf1 (nuclear factor-erythroid 2 p45 subunit-related factor 1) is a transcription factor mediating cellular responses to xenobiotic and pro-oxidant stress. Nrf1 regulates the transcription of many stress-related genes through the electrophile response elements (EpREs) located in their

CGP 41251, a new potential anticancer drug, improves contractility of rat isolated cardiac muscle subjected to hypoxia.

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The aim of the present work was to examine the effects of 4'-N-benzoyl staurosporine (CGP 41251), a protein kinase C inhibitor with broad antiproliferative activity in many cell lines, on the rat isolated heart contractility under normoxic and hypoxic conditions. Additionally, we examined the

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