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hydrogen sulfide/hypoxia
L'enllaç es desa al porta-retalls
Pàgina 1 des de 314 resultats
Hydrogen sulfide promotes proliferation and neuronal differentiation of neural stem cells and protects hypoxia-induced decrease in hippocampal neurogenesis.
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Accumulating evidence has suggested that hydrogen sulfide (H2S) acts as a novel neuro-modulator and neuroprotective agent; however, it remains to be investigated whether H2S has a direct effect on neural stem cells (NSCs). In the present study, we examined the effects of H2S donor, sodium
Hydrogen sulfide protects cardiomyocytes from hypoxia/reoxygenation-induced apoptosis by preventing GSK-3beta-dependent opening of mPTP.
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Hydrogen sulfide (H(2)S) is an endogenously generated gaseous transmitter, which has recently been suggested to regulate cardiovascular functions. The present study aims to clarify the mechanisms underlying the cardioprotective effects of H(2)S. Signaling elements were examined in cardiomyocytes
Ontogenetic and temperature-dependent changes in tolerance to hypoxia and hydrogen sulfide during the early life stages of the Manila clam Ruditapes philippinarum.
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Wind-induced upwelling of hypoxic waters containing hydrogen sulfide (H2S) sometimes causes mass mortalities of aquatic organisms inhabiting coastal areas, including the hypoxia-tolerant Manila clam Ruditapes philippinarum. We examined the tolerance of Manila clam to H2S under controlled laboratory
Hypoxia-induced arterial chemoreceptor stimulation and hydrogen sulfide: too much or too little?
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This brief review presents and discusses some of the important issues surrounding the theory which asserts that endogenous hydrogen sulfide (H(2)S) is the mediator of, or at least an important contributor to, hypoxia-induced arterial chemorereceptor stimulation. The view presented here is that
Modulation of hydrogen sulfide by vascular hypoxia.
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Hydrogen sulfide (H2S) has emerged as a key regulator of cardiovascular function. This gasotransmitter is produced in the vasculature and is involved in numerous processes that promote vascular homeostasis, including vasodilation and endothelial cell proliferation. Although H2S plays a role under
[Effect of a new gasotransmitter, hydrogen sulfide, on collagen remodeling of pulmonary artery under hypoxia].
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OBJECTIVE
To study the modulatory effect of hydrogen sulfide (H(2)S) on the accumulation of collagen type I and type III in the wall of pulmonary small artery during hypoxic pulmonary vascular remodeling.
METHODS
Nineteen male Wistar rats were randomly divided into a control group (n = 6), a hypoxic
Involvement of hydrogen sulfide in perivascular and hypoxia-induced inhibition of endothelin contraction in porcine retinal arterioles.
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Perivascular retina has been shown to regulate retinal vascular tone. In the present study, we evaluated an ex vivo retina preparation, and investigated whether hydrogen sulfide (H2S) mediates an inhibitory effect of retina and/or hypoxia on arteriolar tone. In retina, immunolabeling showed an
Development of dansyl based copper(ii) complex to detect hydrogen sulfide in hypoxia.
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Hydrogen sulfide (H2S) has been reported as a gaseous signaling molecule in cells. H2S modulation is dependent on the partial pressure of oxygen in cells, which means hypoxia can induce H2S production under various pathophysiological conditions. Hypoxia is a common condition in solid tumors and can
Hydrogen sulfide (H(2)S): a physiologic mediator of carotid body response to hypoxia.
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Carotid bodies are sensory organs for monitoring arterial blood O(2) levels. Nitric oxide and carbon monoxide function as inhibitory gasotransmitters in the carotid body. Hydrogen sulfide (H2S) is another emerging gasotransmitter. The purpose of this article is to review recent studies addressing
Involvement of endogenous central hydrogen sulfide (H2S) in hypoxia-induced hypothermia in spontaneously hypertensive rats.
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Spontaneously hypertensive rats (SHR) display autonomic imbalance and abnormal body temperature (Tb) adjustments. Hydrogen sulfide (H2S) modulates hypoxia-induced hypothermia, but its role in SHR thermoregulation is unknown. We tested the hypothesis that SHR display peculiar thermoregulatory
Role of central hydrogen sulfide on ventilatory and cardiovascular responses to hypoxia in spontaneous hypertensive rats.
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Central hydrogen sulfide (H2S) has been reported to act as a gaseous neuromodulator involved in the ventilatory and cardiovascular control of normotensive rats, whereas no information is available in spontaneously hypertensive rats (SHR). We recorded minute ventilation (VE), mean arterial pressure
Involvement of endogenous hydrogen sulfide (H2S) in the rostral ventrolateral medulla (RVLM) in hypoxia-induced hypothermia.
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Hypoxia evokes a regulated decrease in deep body temperature (Tb). Hydrogen sulfide (H2S), a signaling molecule that belongs to the gasotransmitter family, has been demonstrated to participate in several brain-mediated responses. Rostral ventrolateral medulla (RVLM) is a brainstem region involved in
Endogenous hydrogen sulfide in the rostral ventrolateral medulla/Bötzinger complex downregulates ventilatory responses to hypoxia.
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Hydrogen sulfide (H2S) is now recognized as a new gaseous transmitter involved in several brain-mediated responses. The rostral ventrolateral medulla (RVLM)/Bötzinger complex is a region in the brainstem that is involved in cardiovascular and respiratory functions. Recently, it has been shown that
Plant pathogenic bacteria utilize biofilm growth-associated repressor (BigR), a novel winged-helix redox switch, to control hydrogen sulfide detoxification under hypoxia.
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Winged-helix transcriptional factors play important roles in the control of gene expression in many organisms. In the plant pathogens Xylella fastidiosa and Agrobacterium tumefaciens, the winged-helix protein BigR, a member of the ArsR/SmtB family of metal sensors, regulates transcription of the
Hydrogen sulfide and hypoxia-induced changes in TASK (K2P3/9) activity and intracellular Ca(2+) concentration in rat carotid body glomus cells.
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Acute hypoxia depolarizes carotid body chemoreceptor (glomus) cells and elevates intracellular Ca(2+) concentration ([Ca(2+)]i). Recent studies suggest that hydrogen sulfide (H2S) may serve as an oxygen sensor/signal in the carotid body during acute hypoxia. To further test such a role for H2S, we
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