cholera/hypoxia

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Hypoxia-induced localization of chemotaxis-related signaling proteins in Vibrio cholerae.

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Vibrio cholerae has three sets of chemotaxis-related signaling proteins, of which only System II has been shown to be involved in chemotaxis. Here, we examined localization of green fluorescent protein (GFP)-fused components of System I. The histidine kinase (CheA1) and the adaptor (CheW0) of System

Prolonged hypoxia induces lipid raft formation and increases Pseudomonas internalization in vivo after contact lens wear and lid closure.

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OBJECTIVE To investigate the effects of hypoxia on lipid raft formation and Pseudomonas aeruginosa internalization by the corneal epithelium with and without the physical effects of contact lens wear. METHODS One eye of each rabbit was randomly fitted with a low-Dk rigid gas-permeable contact lens

Hypoxia and the hypoxic response pathway protect against pore-forming toxins in C. elegans.

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Pore-forming toxins (PFTs) are by far the most abundant bacterial protein toxins and are important for the virulence of many important pathogens. As such, cellular responses to PFTs critically modulate host-pathogen interactions. Although many cellular responses to PFTs have been recorded, little is

Cholera and pertussis toxins reveal multiple regulation of cAMP levels in the rabbit carotid body.

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It is known that hypoxia (PO2 approximately equal to 66-18 mm Hg), acting via unknown receptors, increases carotid body cAMP levels in Ca(2+)-free solutions, indicating that low PO2 activates adenylate cyclases independently of the action of the released neurotransmitters. The aim of the present

Differential alterations in cardiac adrenergic signaling in chronic hypoxia or norepinephrine infusion.

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Norepinephrine (NE)-induced desensitization of the adrenergic receptor pathway may mimic the effects of hypoxia on cardiac adrenoceptors. The mechanisms involved in this desensitization were evaluated in male Wistar rats kept in a hypobaric chamber (380 Torr) and in rats infused with NE (0.3 mg.

Prostaglandin E1, E2, and cholera toxin increase transcription of the brain creatine kinase gene in human U87 glioblastoma cells.

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The creatine kinase isoenzymes play an important role in maintaining ATP levels in some cell types during times of high energy demand. We have previously shown in primary cell cultures from rat brain that glial cells express much higher levels of brain creatine kinase (CKB) mRNA than neurons. In a

High-salt diet impairs hypoxia-induced cAMP production and hyperpolarization in rat skeletal muscle arteries.

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This study determined the effects of hypoxia on diameter, vascular smooth muscle (VSM) transmembrane potential (E(m)), and vascular cAMP levels for in vitro cannulated skeletal muscle resistance arteries (gracilis arteries) from Sprague-Dawley rats fed a low-salt (LS) or a high-salt (HS) diet.

Hypoxia-stimulated membrane trafficking requires T-plastin.

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OBJECTIVE Traffic between the plasma membrane and the endomembrane compartments is an essential feature of eukaryotic cells. The secretory pathway sends cargoes from biosynthetic compartments to the plasma membrane. This is counterbalanced by a retrograde endocytic route and is essential for cell

Ablation of vagal preganglionic neurons innervating the extra-thoracic trachea affects ventilatory responses to hypercapnia and hypoxia.

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This study tested the hypothesis that during hypercapnia or hypoxia, airway-related vagal preganglionic neurons (AVPNs) of the nucleus ambiguus (NA) release acetylcholine (ACh), which in a paracrine fashion, activates ACh receptors expressed by inspiratory rhythm generating cells. AVPNs in the NA

Chronic intermittent hypoxia-induced augmented cardiorespiratory outflow mediated by vasopressin-V₁A receptor signaling in the medulla.

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A co-morbidity of sleep-disordered breathing is hypertension associated with elevated sympathetic nerve activity, which may result from chronic intermittent hypoxia (CIH). CIH evokes plasticity in cardiorespiratory regulating sites, including the paraventricular nucleus (PVN), which acts to sustain

Enhanced erythropoietin secretion in hepatoblastoma cells in response to hypoxia.

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Erythropoietin (Ep) levels in spent culture media of a Hep G2 human hepatoblastoma cell line were measured by radioimmunoassay (RIA), fetal mouse liver erythroid colony formation (FMLC), and the exhypoxic polycythemic mouse assay (EHPCMA). The Hep G2 cells at high density produced approximately 700

Effects of fluoride and cholera and pertussis toxins on sensory transduction in the carotid body.

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The regulation of the chemoreceptor cell function by G proteins has been studied by measuring the release of 3H-labeled catecholamines ([3H]CA) in carotid bodies (CBs) treated with fluoride, cholera toxin (CTX), and pertussis toxin (PTX). Fluoride augmented the basal release of [3H]CA in a dose-

Acute hypoxia activates hypothalamic paraventricular nucleus-projecting catecholaminergic neurons in the C1 region.

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Catecholaminergic C1 cells reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM) and can be activated by hypoxia. These neurons regulate the hypothalamic pituitary axis via direct projections to the hypothalamic paraventricular nucleus (PVH) and regulate the autonomic

Genetic dissection of the fermentative and respiratory contributions supporting Vibrio cholerae hypoxic growth

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Both fermentative and respiratory processes contribute to bacterial metabolic adaptations to low oxygen tension (hypoxia). In the absence of O₂ as a respiratory electron sink, many bacteria utilize alternative electron acceptors such as nitrate (NO₃ ^-). During

In vitro hypoxia impairs beta2-adrenergic receptor signaling in primary rat alveolar epithelial cells.

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Hypoxia inhibits beta(2)-adrenergic receptor (beta(2)-AR) signaling in a variety of tissues, but effects in alveolar epithelium are unclear. We therefore examined the effect of 24 h of hypoxia on beta(2)-AR function in primary rat alveolar epithelial [alveolar type II (ATII)] cells. ATII cells were

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