Hypoxia inducible factor-1α and expression of vascular endothelial growth factor and its receptors in cerebral arteriovenous malformations

Ng, Ivan; Tan, Wan-Loo; Ng, Puay-Yong; Lim, Jeanette

doi:10.1016/j.jocn.2005.02.005

Cited by 30 publications

(24 citation statements)

References 58 publications

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“…17 In and around the vessel walls of AVMs, various growth factors, including vascular endothelial growth factor, basic fibroblast growth factor, and transforming growth factor-b 1 , are observed. [18][19][20] Proliferation-related transcription factors, such as hypoxia-inducing factor and extracellular signal-regulated protein kinase, are expressed, 21,22 and endothelial proliferation takes place in vascular walls. 21 Cell death (via apoptotic pathways) is also detected in the vessel walls of cerebral AVMs.…”

Section: Discussionmentioning

confidence: 99%

“…[18][19][20] Proliferation-related transcription factors, such as hypoxia-inducing factor and extracellular signal-regulated protein kinase, are expressed, 21,22 and endothelial proliferation takes place in vascular walls. 21 Cell death (via apoptotic pathways) is also detected in the vessel walls of cerebral AVMs. 23 Chen et al 24 proposed that inflammation is involved in the clinical course of the disease state, if not in the pathogenesis of the lesion.…”

Section: Discussionmentioning

confidence: 99%

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Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

et al. 2010

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

et al. 2010

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“…For this reason, nuclear expression of HIF-1α reflects the hypoxic state of local tissue (6). Recently, HIF-1α has been associated with various hemorrhagic events such as hemorrhagic infarction (7,8), trauma hemorrhage (9), and hemorrhage in cerebral arteriovenous malformations (10). Mechanistic study revealed that HIF-1α may promote hemorrhagic transformation via activating its downstream genes, including vascular endothelial growth factor (VEGF) and the proapoptotic gene BNIP3.…”

Section: Introductionmentioning

confidence: 99%

Hypoxia induces hemorrhagic transformation in pituitary adenomas via the HIF-1α signaling pathway

Zhang

Liu²,

Zhao³

et al. 2011

Oncol Rep

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Abstract. The hypoxia inducible factor 1 α (HIF-1α) activity has been associated with various hemorrhagic events. The biological role of HIF-1α in the hemorrhagic transformation of pituitary adenomas remains unknown. We hypothesized that fast growing tumor cells tend to predispose themselves to sublethal hypoxia and activate the HIF-1α signaling pathway, leading to hemorrhagic transformation in pituitary adenomas. Here, we used apoplectic and non-apoplectic pituitary adenomas to determine the involvement of HIF-1α signaling in intratumoral hemorrhage. We employed HIF-1α overexpression/knockdown strategies to examine the association between HIF-1α signaling and hemorrhagic presentation in vitro and in vivo. In support of our hypothesis, compared with nonhemorrhagic pituitary adenomas, higher cellular proliferation was observed in hemorrhagic ones and it correlated with increased HIF-1α signaling. HIF-1α overexpression activated its downstream genes, vascular endothelial growth factor and the proapoptotic BNIP3, in MMQ pituitary adenoma cells and this up-regulation was attenuated by HIF-1 siRNA. In vivo studies using MMQ cell xenografts in nude mice showed that HIF-1α overexpression significantly promoted hemorrhagic transformation. Our study indicates that tumor hypoxia, following rapid tumor growth, may promote hemorrhagic transformation in pituitary adenomas via the HIF-1α signaling pathway.

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“…Familial CCM is known to be associated with loss of function mutations in three genes that each plays a pivotal role in controlling signaling pathways responsible for cellular responses to oxidative stress [18,32,37], including KRIT1 [9], CCM2 [22], and PDCD10 [3]. It has been well documented that hypoxia plays a critical role in the formation of both sporadic and familial CCMs [27,35,39].…”

Section: Discussionmentioning

confidence: 99%

PHACE syndrome is associated with intracranial cavernous malformations

et al. 2016

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At present, CCMs are not listed among the diagnostic criteria for PHACE syndrome, and they have not previously been reported in association with PHACE syndrome. Hypoxic injury in utero may be the common denominator in the pathogenesis of many of the abnormalities already accepted in the criteria for PHACE syndrome and the formation of CCMs. In the setting of PHACE syndrome, we encourage clinicians to evaluate children for CCMs, which are readily apparent on the already-recommended screening MRIs.

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Hypoxia inducible factor-1α and expression of vascular endothelial growth factor and its receptors in cerebral arteriovenous malformations

Cited by 30 publications

References 58 publications

Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

Activation of Nuclear Factor κB in Cerebral Arteriovenous Malformations

Hypoxia induces hemorrhagic transformation in pituitary adenomas via the HIF-1α signaling pathway

PHACE syndrome is associated with intracranial cavernous malformations

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