Nrf2 activation and down-regulation of HMGB1 and MyD88 expression by amnion membrane extracts in response to the hypoxia-induced injury in cardiac H9c2 cells - 09/12/18
, Mohammad Nouri a, f, g, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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| pages | 9 |
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Highlights |
• | AMPs elicits potent cardioprotective effects in H9c2 cells by the apoptotic changes of H9c2 during hypoxia. |
• | AMPs protection mediated by inhibition of Ca2+ overload and mitochondrial membrane potential dysfunction during hypoxia. |
• | AMPs mitigated HMGB1expression and its intracellular adaptor gene, Myd88, in response to the hypoxia in H9c2 cells. |
• | AMPs increased Nrf2/heme oxygenase-1 (HO-1) content and attenuated hypoxia-induced injuries in H9c2 cells. |
Abstract |
Background |
human Amniotic Membrane (hAM) extracts contain bioactive molecules such as growth factors and cytokines. Studies have confirmed the ability of hAM in reduction of post-operative dysfunction in patients with cardiac surgery. However, the function of Amniotic Membrane Proteins (AMPs), extracted from hAM, against hypoxia-induced H9c2 cells injury have never been investigated. In this study, we aimed to appraise the protective impact of AMPs on H9c2 cells under hypoxia condition.
Methods |
Cardiomyocyte cells were pre-incubated with AMPs and subjected to 24 h hypoxia to elucidate its effects on expression of Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1(HO-1). Furthermore, the high mobility group box-1 (HMGB1) and Myeloid differentiation primary response 88 (MyD88) expressions were detected by qPCR and western-blotting. The mitochondrial membrane potential (ΔΨm) was estimated by JC-1 using fluorescent microscopy and fluorimetry. Moreover, the cell apoptosis and intracellular calcium levels were measured by flow cytometry.
Results |
Pre-treatment of AMPs resulted in significant induction in cell viability and decreased the LDH release under hypoxic condition in H9c2 cells. Accordingly, these protective effects of AMPs were associated with a reduction in apoptosis rates and intracellular Ca2+, meanwhile, ΔΨm was increased. Pre-treatment with AMPs resulted in degradation of HMGB1 and MyD88 levels and depicted pro-survival efficacy of AMPs against hypoxia-induced cell damage through induction of HO-1 and Nrf2.
Conclusion |
The data indicated that AMPs mediated HO-1 regulation by Nrf2 activation and plays critical protective effects in hypoxia-induced H9c2 injury in vitro by the inhibition of myocardial HMGB1 and MyD88 inflammatory cascade.
Le texte complet de cet article est disponible en PDF.Keywords : Amniotic membrane proteins, Hypoxia, Nrf2, HO-1, HMGB1, H9c2 cardiomyocytes
Plan
Vol 109
P. 360-368 - janvier 2019 Retour au numéro
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