Heme oxygenase overexpression attenuates glucose-mediated oxidative stress in quiescent cell phase: linking heme to hyperglycemia complications
| Autor: | David Sacerdoti, Nader G. Abraham, Giovanni Li Volti, C Colombrita, Giovanni Scapagnini, Rafał Olszanecki |
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| Rok vydání: | 2005 |
| Předmět: |
medicine.medical_specialty
Bilirubin Heme Dinoprost medicine.disease_cause Resting Phase Cell Cycle Culture Media Serum-Free Cellular and Molecular Neuroscience Transduction (genetics) chemistry.chemical_compound Developmental Neuroscience Computer Systems Superoxides Internal medicine Gene expression medicine Humans RNA Messenger Cells Cultured Messenger RNA Reverse Transcriptase Polymerase Chain Reaction Superoxide Cell Cycle G1 Phase Endothelial Cells Heme oxygenase Oxidative Stress Glucose Endocrinology Neurology chemistry Biochemistry Hyperglycemia Heme Oxygenase (Decyclizing) Oxidative stress |
| Zdroj: | Current neurovascular research 2(2) (2005): 103–111. info:cnr-pdr/source/autori:Sacerdoti D, Olszanecki R, Li Volti G, Colombrita C, Scapagnini G, Abraham NG./titolo:Heme oxygenase overexpression attenuates glucose-mediated oxidative stress in quiescent cell phase: linking heme to hyperglycemia complications./doi:/rivista:Current neurovascular research/anno:2005/pagina_da:103/pagina_a:111/intervallo_pagine:103–111/volume:2(2) 15 (2005): 509–521. info:cnr-pdr/source/autori:Sacerdoti D, Olszanecki R, Li Volti G, Colombrita C, Scapagnini G, Abraham NG./titolo:Heme oxygenase overexpression attenuates glucose-mediated oxidative stress in quiescent cell phase: linking heme to hyperglycemia complications./doi:/rivista:/anno:2005/pagina_da:509/pagina_a:521/intervallo_pagine:509–521/volume:15 |
| Popis: | Heme oxygenase (HO-1) is a stress protein, which has been suggested to participate in defense mechanisms against glucose induced oxidative injury. The purpose of this study was to examine the role of human HO-1 in attenuating glucose-mediated oxidative stress. We investigated the effect of high ambient glucose (15, 33 and 66 mM) on HO-1 gene expression in endothelial cells grown in a serum deprived media compared to the effect of glucose on exponentially grown cells (10% FBS). High glucose at 15 and 33 mM caused significant inhibition of HO-1 protein and activity in G0/G1 and in cells exponentially grown. Glucose concentration at 66 mM caused a significant increase in HO-1. Addition of heme (10 microM) increased HO-1 protein and bilirubin formation in G0/G1, in a time dependent manner peaking at 16 h. Glucose attenuated heme mediated increase in HO-1 proteins. RT-PCR demonstrated that glucose decreased the levels of HO-1 mRNA in both G0/G1 or cells grown in 10% FBS. The rate of HO-1 induction in response to heme was several fold higher in serum-starved cells compared to cells cultured in 10% FBS. Cells exposed to high glucose for up to 24 h had a significant increase in cellular heme and potentiated heme-mediated increase in generation of superoxide anion and 8-epi-isoprostane PGF(2alpha). HO-1 gene transduction prevented glucose-mediated elevation of 8-epi-isoprostane PGF(2alpha). These results imply that expression of HO-1 in G0/G1 cells may be a key player in decreasing cellular heme, associated with increased generation of bilirubin, and in attenuating glucose mediated oxidative stress. |
| Databáze: | OpenAIRE |
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