ArticleRedox biology2015
Norepinephrine-induced apoptotic and hypertrophic responses in H9c2 cardiac myoblasts are characterized by different repertoire of reactive oxygen species generation.
Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Cardiac Mitochondrial Dysfunction Following Bleomycin-Induced Acute Lung Injury in Rats.bioRxiv : the preprint server for biology · 2026Article
- Blueberry extract attenuates norepinephrine-induced oxidative stress and apoptosis in H9c2 cardiac cells.Molecular and cellular biochemistry · 2022Article
- Andrographolide Attenuates Established Pulmonary Hypertension via Rescue of Vascular Remodeling.Biomolecules · 2021Article
- Stress hormones promote DNA damage in human oral keratinocytes.Scientific reports · 2021Article
- Mitoapocynin, a mitochondria targeted derivative of apocynin induces mitochondrial ROS generation and apoptosis in multiple cell types including cardiac myoblasts: a potential constraint to its therapeutic use.Molecular and cellular biochemistry · 2021Article
- Article
- Hydrogen Sulfide Ameliorates Angiotensin II-Induced Atrial Fibrosis Progression to Atrial Fibrillation Through Inhibition of the Warburg Effect and Endoplasmic Reticulum Stress.Frontiers in pharmacology · 2021Article
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Bucindolol Modulates Cardiac Remodeling by Attenuating Oxidative Stress in H9c2 Cardiac Cells Exposed to Norepinephrine.Oxidative medicine and cellular longevity · 2019Article
- Apocynin prevents isoproterenol-induced cardiac hypertrophy in rat.Molecular and cellular biochemistry · 2018Article
- An overview of the emerging interface between cardiac metabolism, redox biology and the circadian clock.Free radical biology & medicine · 2018Review
- Anti-hypotensive drug induced cardiotoxicity: an in vitro study.In vitro cellular & developmental biology. Animal · 2018Article
- Activation of adrenergic receptor in H9c2 cardiac myoblasts co-stimulates Nox2 and the derived ROS mediate the downstream responses.Molecular and cellular biochemistry · 2017Article
- Chickpea Ferritin CaFer1 Participates in Oxidative Stress Response, and Promotes Growth and Development.Scientific reports · 2016Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite recent advances, the role of ROS in mediating hypertrophic and apoptotic responses in cardiac myocytes elicited by norepinephrine (NE) is rather poorly understood. We demonstrate through our experiments that H9c2 cardiac myoblasts treated with 2 µM NE (hypertrophic dose) generate DCFH-DA positive ROS only for 2h; while those treated with 100 µM NE (apoptotic dose) sustains generation for 48 h, followed by apoptosis. Though the levels of DCFH fluorescence were comparable at early time points in the two treatment sets, its quenching by DPI, catalase and MnTmPyP suggested the existence of a different repertoire of ROS. Both doses of NE also induced moderate levels of H2O2 but with different kinetics. Sustained but intermittent generation of highly reactive species detectable by HPF was seen in both treatment sets but no peroxynitrite was generated in either conditions. Sustained generation of hydroxyl radicals with no appreciable differences were noticed in both treatment sets. Nevertheless, despite similar profile of ROS generation between the two conditions, extensive DNA damage as evident from the increase in 8-OH-dG content, formation of γ-H2AX and PARP cleavage was seen only in cells treated with the higher dose of NE. We therefore conclude that hypertrophic and apoptotic doses of NE generate distinct but comparable repertoire of ROS/RNS leading to two very distinct downstream responses.
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