Similarities between the oxygen-sensing mechanisms regulating the expression of vascular endothelial growth factor and erythropoietin.

Goldberg, Mark A.; Schneider, Thomas J.

doi:10.1016/s0021-9258(17)41787-x

Cited by 523 publications

(27 citation statements)

References 47 publications

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“…In the hypoxic microenvironment, HIF-1/2 α , two transcriptional factors, can be massively induced to regulate certain gene expressions in response to oxygen deficiency-induced stress [ 16 ]. CoCl 2 can chelate Fe 2+ ions in hemoglobin to decrease the oxygen supply to cells [ 38 ]. Additionally, administration of CoCl 2 raises levels of cellular HIF-1 α by inhibiting the activity of prolyl-4-hydroxylase, a HIF-1 α -specific proteinase [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug‐Resistant Glioblastoma Cells through Targeting the PI3K‐AKT‐mTOR Signaling Pathway

Lee

Cherng

Yang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Glioblastoma multiforme (GBM) is the most aggressive brain tumor. Drug resistance mainly drives GBM patients to poor prognoses because drug-resistant glioblastoma cells highly defend against apoptotic insults. This study was designed to evaluate the effects of cobalt chloride (CoCl2) on hypoxic stress, autophagy, and resulting apoptosis of human and mouse drug-resistant glioblastoma cells. Treatment of drug-resistant glioblastoma cells with CoCl2 increased levels of hypoxia-inducible factor- (HIF-) 1α and triggered hypoxic stress. In parallel, the CoCl2-induced hypoxia decreased mitochondrial ATP synthesis, cell proliferation, and survival in chemoresistant glioblastoma cells. Interestingly, CoCl2 elevated the ratio of light chain (LC)3-II over LC3-I in TMZ-resistant glioblastoma cells and subsequently induced cell autophagy. Analyses by loss- and gain-of-function strategies further confirmed the effects of the CoCl2-induced hypoxia on autophagy of drug-resistant glioblastoma cells. Furthermore, knocking down HIF-1α concurrently lessened CoCl2-induced cell autophagy. As to the mechanisms, the CoCl2-induced hypoxia decreased levels of phosphoinositide 3-kinase (PI3K) and successive phosphorylations of AKT and mammalian target of rapamycin (mTOR) in TMZ-resistant glioblastoma cells. Interestingly, long-term exposure of human chemoresistant glioblastoma cells to CoCl2 sequentially triggered activation of caspases-3 and -6, DNA fragmentation, and cell apoptosis. However, pretreatment with 3-methyladenine, an inhibitor of autophagy, significantly attenuated the CoCl2-induced autophagy and subsequent apoptotic insults. Taken together, this study showed that long-term treatment with CoCl2 can induce hypoxia and subsequent autophagic apoptosis of drug-resistant glioblastoma cells via targeting the PI3K-AKT-mTOR pathway. Thus, combined with traditional prescriptions, CoCl2-induced autophagic apoptosis can be clinically applied as a de novo strategy for therapy of drug-resistant GBM patients.

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Section: Discussionmentioning

confidence: 99%

Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug‐Resistant Glioblastoma Cells through Targeting the PI3K‐AKT‐mTOR Signaling Pathway

Lee

Cherng

Yang

et al. 2021

Oxidative Medicine and Cellular Longevity

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show abstract

“…VEGF plays a protective role in early PAH. The increase in VEGF in hypoxia tissue promotes angiogenesis, which is beneficial for the body to adapt to a hypoxia environment and ensures that oxygen and nutrients are delivered to hypoxia cells [51][52][53]. Under a hypoxia environment, the hypoxia response element in the VEGF gene promoter directly participates in pulmonary vascular remodeling by stimulating HIF-1α and a complex signal transduction pathway, which leads to an increase in pulmonary arterial pressure.…”

Section: Discussionmentioning

confidence: 99%

Mean Pulmonary Arterial Pressure Decreases with Exposure Time in the Tibet Plateau

Wang

2021

AJBSR

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“… 48 HIF, in turn, stimulates the production of vascular endothelial growth factors that causes neovascularization and aberrant angiogenesis. 49 CoCl 2 ‐mediated hypoxic injury involves intravitreal administration and has been used to target different retinal layers such as the photoreceptors 11 and ganglionic layers. 50 …”

Section: Mechanisms Of Retinal Injurymentioning

confidence: 99%

An insight on established retinal injury mechanisms and prevalent retinal stem cell activation pathways in vertebrate models

Sherpa

Hui

2021

Anim Models and Exp Med

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The brain processes visual information when light energy transduces into neural activity in the retina. The close-knit components of the central nervous system (CNS), the brain, and its extension retina are thus the critical players in visual perception, thereby aiding in daily activities. While the brain remains well protected inside the skull, the eyes are quite susceptible to physical injuries and chemical accidents. 1 Furthermore, one's genetic makeup and increasing age also invite multiple numbers of eye diseases such as retinitis pigmentosa (RP), age-related macular degeneration (AMD), glaucoma, etc All this has contributed to the recent "World Reports on vision (2019)," which shows that a whopping 2.2 billion people globally fell victim to visual impairment in the past year. 2 The discovery of the existence of adult retinal stem/progenitor cells among different vertebrate species 3 and its high reparative activity in the case of lower vertebrates has presented us with a possibility to "self-heal" the retina one day. 4 Consequently, high regeneration competent animals, which include the amphibian newts and Xenopus, teleost zebrafish (Danio rerio), and chick are thus being explored 5 to investigate different genetic and epigenetic features, signaling pathways, and factors 6,7 that regulate stem cell activation, thus gradually filling in the gaps of our knowledge of mammals, which appear to be the least competent among the group. 8 With the hope of updating and giving researchers an idea about how these animal models have significantly shaped our understanding of the retinal regeneration process, in this review,

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Similarities between the oxygen-sensing mechanisms regulating the expression of vascular endothelial growth factor and erythropoietin.

Cited by 523 publications

References 47 publications

Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug‐Resistant Glioblastoma Cells through Targeting the PI3K‐AKT‐mTOR Signaling Pathway

Hypoxia Induced by Cobalt Chloride Triggers Autophagic Apoptosis of Human and Mouse Drug‐Resistant Glioblastoma Cells through Targeting the PI3K‐AKT‐mTOR Signaling Pathway

Mean Pulmonary Arterial Pressure Decreases with Exposure Time in the Tibet Plateau

An insight on established retinal injury mechanisms and prevalent retinal stem cell activation pathways in vertebrate models

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