Hypoxia-inducible factor-1 (HIF-1) is involved in the regulation of hypoxia-stimulated expression of monocyte chemoattractant protein-1 (MCP-1/CCL2) and MCP-5 (Ccl12) in astrocytes

Mojsilovic-Petrovic, Jelena; Callaghan, Debbie; Cui, Hong; Dean, Clare; Stanimirovic, Danica; Zhang, Wandong

doi:10.1186/1742-2094-4-12

Cited by 168 publications

(138 citation statements)

References 44 publications

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“…We also found increased protein concentration of CCL12, a proinflammatory chemokine, after hyperoxic reoxygenation, consistent with our recent reports of increased Ccl12 expression in the eye and brain of neonatal mice after hyperoxic reoxygenation (17,26). Mojsilovic-Petrovic et al (27) found increased expression of Ccl12 in astrocyte cultures from P7 mice after hypoxia alone. Hmox1 expression is responsive to both hypoxia and hyperoxia (28), and we found that hyperoxic reoxygenation gave a stronger induction of Hmox1 gene expression than reoxygenation with air.…”

Section: Igf1rsupporting

confidence: 92%

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

et al. 2014

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Background: Hyperoxic reoxygenation following hypoxia increases the expression of inflammatory genes in the neonatal mouse brain. We have therefore compared the temporal profile of 44 a priori selected genes after hypoxia and hyperoxic or normoxic reoxygenation. Methods: Postnatal day 7 mice were subjected to 2 h of hypoxia (8% O 2 ) and 30 min reoxygenation with 60% or 21% O 2 . After 0 to 72 h observation, mRNA and protein were examined in the hippocampus and striatum. results: There were significantly higher gene expression changes in six genes after hyperoxic compared to normoxic reoxygenation. Three genes had a generally higher expression throughout the observation period: the inflammatory genes Hmox1 (mean difference: 0.52, 95% confidence interval (CI): 0.15-1.01) and Tgfb1 (mean difference: 0.099, CI: 0.003-0.194), and the transcription factor Nfkb1 (mean difference: 0.049, CI: 0.011-0.087). The inflammatory genes Cxcl10 and Il1b, and the DNA repair gene Neil3, had a higher gene expression change after hyperoxic reoxygenation at one time point only. Nineteen genes involved in inflammation, transcription regulation, apoptosis, angiogenesis, and glucose transport had significantly different gene expression changes with time in all intervention animals. conclusion: We confirm that hyperoxic reoxygenation induces a stronger inflammatory gene response than reoxygenation with air.

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Section: Igf1rsupporting

confidence: 92%

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

et al. 2014

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“…[33][34][35] Regulation of chemokine expression at the posttranscriptional level involves alterations in mRNA stability. For example, the CXCL1 and CXCL8 mRNA levels increase upon IL-1b stimulation, and the levels remain high up to 8 h in the continued presence of IL-1b, even when coincubated with actinomycin D, an inhibitor of transcription.…”

Section: -24mentioning

confidence: 99%

Chemokines and Their Receptors Are Key Players in the Orchestra That Regulates Wound Healing

Martins‐Green

Petreaca

Wang

2013

Advances in Wound Care

129

118

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“…HIF1␣ heterodimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT, also known as HIF1␤) forming the functional transcription factor HIF1. HIF1 regulates the expression of more than 100 genes, including genes for glycolytic enzymes, sugar transporters, and proangiogenic and inflammatory factors (8,13,18,25). Moreover, HIF1␣ has also been shown to modulate inflammation indirectly by influencing the NF-B signaling pathway (13,20).…”

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confidence: 99%

Role of hypoxia-inducible factor 1α in modulating cobalt-induced lung inflammation

Saini¹,

Kim

Lewandowski

et al. 2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Hypoxia plays an important role in development, cellular homeostasis, and pathological conditions, such as cancer and stroke. There is also growing evidence that hypoxia is an important modulator of the inflammatory process. Hypoxia-inducible factors (HIFs) are a family of proteins that regulate the cellular response to oxygen deficit, and loss of HIFs impairs inflammatory cell function. There is little known, however, about the role of epithelial-derived HIF signaling in modulating inflammation. Cobalt is capable of eliciting an allergic response and promoting HIF signaling. To characterize the inflammatory function of epithelialderived HIF in response to inhaled cobalt, a conditional lung-specific HIF1␣, the most ubiquitously expressed HIF, deletion mouse, was created. Control mice showed classic signs of metal-induced injury following cobalt exposure, including fibrosis and neutrophil infiltration. In contrast, HIF1␣-deficient mice displayed a Th2 response that resembled asthma, including increased eosinophilic infiltration, mucus cell metaplasia, and chitinase-like protein expression. The results suggest that epithelial-derived HIF signaling has a critical role in establishing a tissue's inflammatory response, and compromised HIF1␣ signaling biases the tissue towards a Th2-mediated reaction. deletion mouse LUNG DISEASES, including chronic obstructive pulmonary disease and asthma, involve a large inflammatory component. The lung's response to allergens involves a complex interplay between resident inflammatory and epithelial cells, cytokine signaling, and the environmental conditions within the tissue. One of the critical environmental features that can impact the inflammatory process is hypoxia.Hypoxia, a decrease in available oxygen reaching the tissues of the body, has profound cellular and metabolic consequences. The cellular response to hypoxia is regulated by a family of transcription factors called the hypoxia-inducible factors (HIFs) (3). HIFs are primarily regulated at the level of protein stability by a family of prolyl hydroxylases. These prolyl hydroxylase domain (PHD) proteins are members of a broader family of non-heme, iron-, and 2-oxoglutarate-dependent dioxygenases (7). Cobalt has been shown to inhibit PHDs, and this inhibition causes very similar transcriptional outputs to that of hypoxia (24,28). Recent research using human peripheral blood mononuclear cells has shown that this transcriptional overlap applies to tungsten carbide-cobalt particles, linking hard metal lung disease to hypoxia signaling (17).HIF1␣ is the most ubiquitously expressed and widely studied HIF isoform. HIF1␣ heterodimerizes with the aryl hydrocarbon receptor nuclear translocator (ARNT, also known as HIF1␤) forming the functional transcription factor HIF1. HIF1 regulates the expression of more than 100 genes, including genes for glycolytic enzymes, sugar transporters, and proangiogenic and inflammatory factors (8,13,18,25). Moreover, HIF1␣ has also been shown to modulate inflammation indirectly by influencing the NF-B ...

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Hypoxia-inducible factor-1 (HIF-1) is involved in the regulation of hypoxia-stimulated expression of monocyte chemoattractant protein-1 (MCP-1/CCL2) and MCP-5 (Ccl12) in astrocytes

Cited by 168 publications

References 44 publications

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

Increased expression of inflammatory genes in the neonatal mouse brain after hyperoxic reoxygenation

Chemokines and Their Receptors Are Key Players in the Orchestra That Regulates Wound Healing

Role of hypoxia-inducible factor 1α in modulating cobalt-induced lung inflammation

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