ArticleMolecules and cells2011
Oxidative stress mediates chemical hypoxia-induced injury and inflammation by activating NF-κb-COX-2 pathway in HaCaT cells.
Article in Molecules and cells, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 64 citations in OpenAlex.
- Development of endothelial injury under chemical hypoxia: early migration impairment precedes cytotoxicity in CoClMolecular biology reports · 2026Article
- Benfotiamine promotes diabetic wound healing by modulating Trisk95 and reducing oxidative stress.Diabetology & metabolic syndrome · 2026Article
- The Mitochondrial-Astrocyte-Neuron Triad Hypothesis in Parkinson's Disease: A Toxic Feedback Loop of Metabolism, Aggregation, and Oxidative Stress.Neurochemical research · 2025Review
- Advancements in incorporating metal ions onto the surface of biomedical titanium and its alloys via micro-arc oxidation: a research review.Frontiers in chemistry · 2024Review
- Priming with caffeic acid enhances the potential and survival ability of human adipose-derived stem cells to counteract hypoxia.Regenerative therapy · 2023Article
- The role of cellular crosstalk in the progression of diabetic nephropathy.Frontiers in endocrinology · 2023Review
- High-altitude Hypoxia Influences the Activities of the Drug-Metabolizing Enzyme CYP3A1 and the Pharmacokinetics of Four Cardiovascular System Drugs.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cobalt (II) Chloride Regulates the Invasion and Survival ofPathogens (Basel, Switzerland) · 2022Article
- Ameliorative effects of epigallocatechin-3-gallate nanoparticles on 2,4-dinitrochlorobenzene induced atopic dermatitis: A potential mechanism of inflammation-related necroptosis.Frontiers in nutrition · 2022Article
- Woodsmoke Extracts Cross-Link Proteins and Induce Cornified Envelope Formation without Stimulating Keratinocyte Terminal Differentiation.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Haplopine Ameliorates 2,4-Dinitrochlorobenzene-Induced Atopic Dermatitis-Like Skin Lesions in Mice and TNF-α/IFN-γ-Induced Inflammation in Human Keratinocyte.Antioxidants (Basel, Switzerland) · 2021Article
- Article
- Role of microRNAs in Pressure Ulcer Immune Response, Pathogenesis, and Treatment.International journal of molecular sciences · 2020Review
- Is Hydrogen Sulfide a Concern During Treatment of Lung Adenocarcinoma With Ammonium Tetrathiomolybdate?Frontiers in oncology · 2020Article
- Article
- Antiphotoaging and Antimelanogenic Effects ofOxidative medicine and cellular longevity · 2019Article
- Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma.Journal of neuroinflammation · 2018Article
- Suppression of LRRC19 promotes cutaneous wound healing in pressure ulcers in mice.Organogenesis · 2018Article
- Fish Scale Collagen Peptides Protect against CoClOxidative medicine and cellular longevity · 2017Article
- Controls of Nuclear Factor-Kappa B Signaling Activity by 5'-AMP-Activated Protein Kinase Activation With Examples in Human Bladder Cancer Cells.International neurourology journal · 2016Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia of skin is an important physiopathological process in many diseases, such as pressure ulcer, diabetic ulcer, and varicose ulcer. Although cellular injury and inflammation have been involved in hypoxia-induced dermatic injury, the underlying mechanisms remain largely unknown. This study was conducted to investigate the effects of cobalt chloride (CoCl(2)), a hypoxia-mimicking agent, on human skin keratinocytes (HaCaT cells) and to explore the possible molecular mechanisms. Exposure of HaCaT cells to CoCl(2) reduced cell viability and caused overproduction of reactive oxygen species (ROS) and oversecretion of interleukin-6 (IL-6) and interleukin-8 (IL-8). Importantly, CoCl(2) exposure elicited overexpression of cyclooxygenase-2 (COX-2) and phosphorylation of nuclear factor-kappa B (NF-κB) p65 subunit. Inhibition of COX-2 by NS-398, a selective inhibitor of COX-2, significantly repressed the cytotoxicity, as well as secretion of IL-6 and IL-8 induced by CoCl(2). Inhibition of NF-κB by PDTC (a selective inhibitor of NF-κB) or genetic silencing of p65 by RNAi (Si-p65), attenuated not only the cytotoxicity and secretion of IL-6 and IL-8, but also overexpression of COX-2 in CoCl(2)-treated HaCaT cells. Neutralizing anti-IL-6 or anti-IL-8 antibody statistically alleviated CoCl(2)-induced cytotoxicity in HaCaT cells. N-acetyl-L-cysteine (NAC), a well characterized ROS scavenger, obviously suppressed CoCl(2)-induced cytotoxicity in HaCaT cells, as well as secretion of IL-6 and IL-8. Additionally, NAC also repressed overexpression of COX-2 and phosphorylation of NF- B κ p65 subunit induced by CoCl(2) in HaCaT cells. In conclusion, our results demonstrated that oxidative stress mediates chemical hypoxia-induced injury and inflammatory response through activation of NF-κB-COX-2 pathway in HaCaT cells.
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