Hypoxia-Inducible Factor-1.ALPHA. Is Involved in the Pro-angiogenic Effect of Hydrogen Sulfide under Hypoxic Stress

Liu, Xinhua; Pan, Li-Long; Yang, Zhuo; Gong, Qihai; Rose, Peter; Zhu, Yizhun

doi:10.1248/bpb.33.1550

Cited by 73 publications

(61 citation statements)

References 19 publications

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“…Previously, VEGF-A expression has been shown to correlate with mobilization of BM-EPCs in patients with coronary artery disease (33,34,62) and during neovascularization (4,5,9). HIF-1␣-induced VEGF-A increase under hypoxic stress has also been shown to increase EC and BM-EPC migration (40,67). These data, along with the previous literature, suggest that VEGF-A stimulation of BM-EPCs may be an important factor in migration to sites of neovascularization where other factors may contribute to endothelium incorporation.…”

Section: Discussionmentioning

confidence: 96%

“…During physiological angiogenesis, an increase in VEGF expression stimulates endothelial cell (EC) tube formation and increased microvessel density (3,16,39). Hypoxia is known to produce an angiogenic response, and heightened levels of VEGF-A have been seen in oxygendeprived epithelial, endothelial, and bone marrow cells (13,16,40,51,57). Hypoxic conditions increase levels of hypoxiainducible factor 1␣ (HIF-1␣), which in turn upregulates VEGF-A expression by binding to a hypoxia response element (51,57,61).…”

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confidence: 99%

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Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress

Wagner

Prisco

Janiak

et al. 2013

Physiological Genomics

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 99%

Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress

Wagner

Prisco

Janiak

et al. 2013

Physiological Genomics

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“…The beneficial effects of H 2 S in treating ischemia/reperfusion injury and in pre-and postconditioning have been well documented, and it has been suggested that the beneficial effects of exogenous H 2 S are due to mimicking transient hypoxia, which is also used in conditioning (128). It is also evident that H 2 S is involved in long-term O 2 sensing through its inhibitory effects on hypoxia inducible factor (HIF)-1a expression (70,148,149,188), although opposite effects have also been reported (17,91,93). In an elegant study, Ma et al (93) identified a novel genetic pathway where an increase in H 2 S produced by prolonged (24 h) hypoxia increases HIF-1 expression in C. elegans.…”

Section: General Metabolismmentioning

confidence: 99%

Hydrogen sulfide as an oxygen sensor

Olson

2013

Clinical Chemistry and Laboratory Medicine

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Significance: Although oxygen (O 2 )-sensing cells and tissues have been known for decades, the identity of the O 2 -sensing mechanism has remained elusive. Evidence is accumulating that O 2 -dependent metabolism of hydrogen sulfide (H 2 S) is this enigmatic O 2 sensor. Recent Advances: The elucidation of biochemical pathways involved in H 2 S synthesis and metabolism have shown that reciprocal H 2 S/O 2 interactions have been inexorably linked throughout eukaryotic evolution; there are multiple foci by which O 2 controls H 2 S inactivation, and the effects of H 2 S on downstream signaling events are consistent with those activated by hypoxia. H 2 S-mediated O 2 sensing has been demonstrated in a variety of O 2 -sensing tissues in vertebrate cardiovascular and respiratory systems, including smooth muscle in systemic and respiratory blood vessels and airways, carotid body, adrenal medulla, and other peripheral as well as central chemoreceptors. Critical Issues: Information is now needed on the intracellular location and stoichometry of these signaling processes and how and which downstream effectors are activated by H 2 S and its metabolites. Future Directions: Development of specific inhibitors of H 2 S metabolism and effector activation as well as cellular organelle-targeted compounds that release H 2 S in a timeor environmentally controlled way will not only enhance our understanding of this signaling process but also provide direction for future therapeutic applications. Antioxid. Redox Signal. 22, 377-397.

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“…Further, it was recently proposed that the metabolism of H 2 S may serve as an O 2 sensor in vertebrate vascular smooth muscle (36,38). Moreover, there is a report indicating that H 2 S activates HIF-1 independent of von Hippel-Lindau in Caenorhabditis elegans (C. elegans) under 20% O 2 conditions (2) and also enhances HIF-1-dependent gene expression induced by CoCl 2 in cells from vascular origin (27). However, the influence of H 2 S on HIF-1 activity and hypoxia-induced HIF-1 activation in mammalian cells is largely unknown at the moment.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Inhibits Hypoxia- But Not Anoxia-Induced Hypoxia-Inducible Factor 1 Activation in a von Hippel-Lindau- and Mitochondria-Dependent Manner

Kai

Tanaka²,

Daijo³

et al. 2012

Antioxidants & Redox Signaling

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Aims: In addition to nitric oxide and carbon monoxide, hydrogen sulfide (H 2 S) is an endogenously synthesized gaseous molecule that acts as an important signaling molecule in the living body. Transcription factor hypoxiainducible factor 1 (HIF-1) is known to respond to intracellular reduced oxygen (O 2 ) availability, which is regulated by an elaborate balance between O 2 supply and demand. However, the effect of H 2 S on HIF-1 activity under hypoxic conditions is largely unknown in mammalian cells. In this study, we tried to elucidate the effect of H 2 S on hypoxia-induced HIF-1 activation adopting cultured cells and mice. Results: The H 2 S donors sodium hydrosulfide and sodium sulfide in pharmacological concentrations reversibly reduced cellular O 2 consumption and inhibited hypoxia-but not anoxia-induced HIF-1a protein accumulation and expression of genes downstream of HIF-1 in established cell lines. H 2 S did not affect HIF-1 activation induced by the HIF-a hydroxylases inhibitors desferrioxamine or CoCl 2 . Experimental evidence adopting von Hippel-Lindau (VHL)-or mitochondria-deficient cells indicated that H 2 S did not affect neosynthesis of HIF-1a protein but destabilized HIF-1a in a VHL-and mitochondria-dependent manner. We also demonstrate that exogenously administered H 2 S inhibited HIF-1-dependent gene expression in mice. Innovation: For the first time, we show that H 2 S modulates intracellular O 2 homeostasis and regulates activation of HIF-1 and the subsequent gene expression induced by hypoxia by using an in vitro system with established cell lines and an in vivo system in mice. Conclusions: We demonstrate that H 2 S inhibits hypoxia-induced HIF-1 activation in a VHL-and mitochondriadependent manner. Antioxid. Redox Signal. 16,[203][204][205][206][207][208][209][210][211][212][213][214][215][216]

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Hypoxia-Inducible Factor-1.ALPHA. Is Involved in the Pro-angiogenic Effect of Hydrogen Sulfide under Hypoxic Stress

Cited by 73 publications

References 19 publications

Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress

Vascular endothelial growth factor-A signaling in bone marrow-derived endothelial progenitor cells exposed to hypoxic stress

Hydrogen sulfide as an oxygen sensor

Hydrogen Sulfide Inhibits Hypoxia- But Not Anoxia-Induced Hypoxia-Inducible Factor 1 Activation in a von Hippel-Lindau- and Mitochondria-Dependent Manner

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