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المؤلفSobh, Ahmed
المؤلفAbdulrahman, Nabeel
المؤلفBouchoucha, Soumaya
المؤلفMraiche, Fatima
تاريخ الإتاحة2022-04-13T06:55:11Z
تاريخ النشر2014
اسم المنشورQatar Foundation Annual Research Conference Proceedings
المصدرqscience
الاقتباسSobh, Ahmed. Abdulrahman, Nabeel. Bouchoucha, Soumaya. Mraiche, Fatima.(2014). Heme Oxygenase Isoform 1 Regresses Cardiomyocyte Hypertrophy Through Regressing Sodium Proton Exchanger Isoform 1 Activity. Qatar Foundation Annual Research Conference Proceedings 2014: HBSP1112 https://doi.org/10.5339/qfarc.2014.HBSP1112
الرقم المعياري الدولي للكتاب2226-9649
معرّف المصادر الموحدhttps://doi.org/10.5339/qfarc.2014.HBSP1112
معرّف المصادر الموحدhttp://hdl.handle.net/10576/29642
الملخصBackground: Pathological cardiac hypertrophy is a worldwide problem and an independent risk factor that predisposes the heart to failure. Enhanced activity or expression of the sodium proton exchanger isoform 1 (NHE1) has been implicated in conditions of cardiac hypertrophy. Induction of cGMP has previously been demonstrated to reduce NHE1 activity and expression, which could be through the expression of heme oxygenase isoform 1 (HO-1), a stress-induced enzyme that shows cardioprotective properties. In our study, we aimed to investigate the role of inducing HO-1 in a cardiac hypertrophy model that expresses active NHE1 to determine whether HO-1 could protect against NHE1 induced cardiomyocyte hypertrophy. Methods: H9c2 cardiomyocytes were infected with the active form of the NHE1 adenovirus in the presence and absence of protoporphyrin (CoPP). Which was used to induce HO-1. Protein and mRNA expression of HO-1 were invested in H9c2 cardiomyocytes in the presence and absence of the expression of the active form of the NHE1 adenovirus. The effects of HO-1 induction on NHE1 protein expression and cardiomyocyte hypertrophic markers were measured respectively by western blotting and analyzing the cell surface area of H9c2. Results: Our results showed a significant decrease in HO-1 mRNA expression in cardiomyocytes expressing active NHE1 (74.84 ± 9.19 % vs. 100 % normal NHE1 expression, p<0.05). However, we did not see any changes in NHE1 protein expression following HO-1 induction. A trend towards decrease in cardiomyocyte hypertrophy was observed in H9c2 cardiomyoblasts infected with the active form of NHE1 following stimulation with HO-1 (NHE1, 154.93 ± 14.87 % vs. NHE1 + CoPP, 109 ± 16.44 %). Conclusion: In our model, HO-1 maybe a useful means to reduce NHE1 induced cardiomyocyte hypertrophy, although the mechanism by which it does that requires further investigation.
اللغةen
الناشرHamad bin Khalifa University Press (HBKU Press)
الموضوعHeme Oxygenase Isoform 1
Sodium Proton
Cardiomyocyte Hypertrophy
العنوانHeme Oxygenase Isoform 1 Regresses Cardiomyocyte Hypertrophy Through Regressing Sodium Proton Exchanger Isoform 1 Activity
النوعConference Paper
رقم العدد1
رقم المجلد2014
dc.accessType Open Access


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