Evidence that hypoxia-inducible factor-1 (HIF-1) mediates transcriptional activation of interleukin-1β (IL-1β) in astrocyte cultures

Zhang, Wandong; Petrović, Jelena; Callaghan, Debbie; Jones, Aimee; Cui, Hong; Howlett, Clare; Stanimirovic, Danica

doi:10.1016/j.jneuroim.2006.01.014

Cited by 112 publications

(120 citation statements)

References 43 publications

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“…Inhibiting one specific PHD in cartilage could thus lead, through the specific HIF-2a increase, to a better control of the chondrocyte phenotype without HIF-1a overexpression [which promotes angiogenic phenotype, favouring tumourigenesis (Fang et al 2001), or induces catabolic cytokines such as Interleukin-1 (Zhang et al 2006)]. In vivo approaches targeting HIFs proteins have already been performed: inhibition of HIF-1a expression has been obtained in mouse knee after intra-articular injection of the anti-angiogenic compound 2-methoxyestradiol (through inhibition of HIFs) (Gelse et al 2008).…”

Section: Role Of Phds In Cartilagementioning

confidence: 99%

Lack of oxygen in articular cartilage: consequences for chondrocyte biology

Lafont

2010

Int J Experimental Path

105

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Summary Controlling the chondrocytes phenotype remains a major issue for cartilage repair strategies. These cells are crucial for the biomechanical properties and cartilage integrity because they are responsible of the secretion of a specific matrix. But chondrocyte dedifferentiation is frequently observed in cartilage pathology as well as in tissue culture, making their study more difficult. Given that normal articular cartilage is hypoxic, chondrocytes have a specific and adapted response to low oxygen environment. While huge progress has been performed on deciphering intracellular hypoxia signalling the last few years, nothing was known about the particular case of the chondrocyte biology in response to hypoxia. Recent findings in this growing field showed crucial influence of the hypoxia signalling on chondrocytes physiology and raised new potential targets to repair cartilage and maintain tissue integrity. This review will thus focus on describing hypoxia‐mediated chondrocyte function in the native articular cartilage.

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Section: Role Of Phds In Cartilagementioning

confidence: 99%

Lack of oxygen in articular cartilage: consequences for chondrocyte biology

Lafont

2010

Int J Experimental Path

105

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“…Further interpretation of the data suggested that HIF-1α and VEGF in the vascular endothelium of the intraparenchymal vessels may be critical in the BBB disruption after neonatal brain injury. Whether, HIF-1α and VEGF from astrocytes (Ishikawa et al, 2007;Zhang et al, 2006) and neurons (Halterman et al, 1999) contribute to BBB permeability and brain edema formation needs to be clarified in future studies.…”

Section: Discussionmentioning

confidence: 99%

HIF-1α inhibition ameliorates neonatal brain injury in a rat pup hypoxic–ischemic model

Chen

Jadhav

Tang

et al. 2008

Neurobiology of Disease

112

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Hypoxia-inducible factor-1alpha (HIF-1α) has been considered as a regulator of both prosurvival and prodeath pathways in the nervous system. The present study was designed to elucidate the role of HIF-1α in neonatal hypoxic-ischemic (HI) brain injury. Rice-Vannucci model of neonatal hypoxicischemic brain injury was used in seven-day-old rats, by subjecting unilateral carotid artery ligation followed by 2h of hypoxia (8% O 2 at 37°C). HIF-1α activity was inhibited by 2-methoxyestradiol (2ME2) and enhanced by dimethyloxalylglycine (DMOG). Results showed that 2ME2 exhibited dose-dependent neuroprotection by decreasing infarct volume and reducing brain edema at 48 h post HI. The neuroprotection was lost when 2ME2 was administered 3 h post HI. HIF-1α upregulation by DMOG increased the permeability of the BBB and brain edema compared with HI group. 2ME2 attenuated the increase in HIF-1α and VEGF 24 h after HI. 2ME2 also had a long-term effect of protecting against the loss of brain tissue. The study showed that the early inhibition of HIF-1α acutely after injury provided neuroprotection after neonatal hypoxia-ischemia which was associated with preservation of BBB integrity, attenuation of brain edema, and neuronal death.

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“…Inhibitors of oxidative phosphorylation have no effect following LPS treatment, indicating that this process is already downregulated by LPS (46). IL-1β production in response to LPS treatment has been shown to be inhibited by 2-DG, and HIF1α has been implicated in this process (17,47).…”

Section: Hif1α and Immune-related Genesmentioning

confidence: 99%