Hypochlorous acid-induced heme oxygenase-1 gene expression promotes human endothelial cell survival

Abstract

Durante W. Hypochlorous acid-induced heme oxygenase-1 gene expression promotes human endothelial cell survival.

Activation of AMP-Activated Protein Kinase Inhibits the Proliferation of Human Endothelial Cells

“…Antibodies against cyclin D1, cyclin E, cyclin A, p21, p27, p53, and ␤-actin were from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA Cell Culture. Human umbilical vein endothelial cells (HUVECs) and human aortic endothelial cells (HAECs) were purchased from Lonza Incorporated (Allendale, NJ) and subcultured on gelatincoated dishes as described previously (Wei et al, 2009). Cells were grown in M199 medium supplemented with 20% bovine calf serum, 2 mM L-glutamine, 50 g/ml endothelial cell growth factor, 90 g/ml heparin, and 100 U/ml of penicillin and streptomycin at 37°C in a humidified 95% air-5% CO 2 atmosphere.…”

“…Cells were treated with trypsin (0.25%), collected, diluted (1:4) with trypan blue, and examined by microscopy. Viability was determined by the percentage of cells that excluded the dye (Wei et al, 2009).…”

Topical hypochlorite ameliorates NF-κB–mediated skin diseases in mice

“…Taken together, our findings indicate that oxidation of Cys 114-115 to cysteic acid is responsible for HOCl-mediated IKKβ inactivation. NRF2 (nuclear factor [erythroid-derived 2]-like 2 or NFE2L2) regulates cellular responses to oxidative stress and induces HMOX1, a major effector protein (29). Thus, it is possible that HOCl pretreatment induced a strong antioxidant response driven by the NRF2 pathway to inhibit TNF-α-induced NF-κB activation.…”

Actions of “antioxidants” in the protection against atherosclerosis

“…HO-1 degrades heme to CO, Fe 2 þ , and biliverdin, biliverdin to the antioxidant bilirubin [93]. HO-1 is the inducible of two forms of heme oxygenases, and its expression is mediated by a variety of oxidants, including H 2 O 2 , hypochlorous acid [94], oxidized phospholipids. and ''oxidized LDL'' [95].…”

“…In endothelial cells, for example, expression of HO-1 has been suggested to protect against HOClmediated mitochondrial dysfunction, caspase-3 activation, and cell death via its enzymatic activity and the generation of biliverdin and CO [94]. In addition, HO-1 induction is thought to contribute to the efficacy of a variety of pharmacological agents used in the treatment of CVD, including statins, rapamycin, aspirin, and probucol (reviewed in Refs.…”