Role of tRNA selenocysteine 1 associated protein 1 in the proliferation and apoptosis of cardiomyocyte-like H9c2 cells

Li, Meng-di; Cheng, Wanpeng; Shi, Min‑Xia; Ge, Tangdong; Zheng, Xiaolin; Wu, Dongyuan; Hu, Xiaoyan; Luo, Jincheng; Li, Fenglan

doi:10.3892/mmr.2016.6099

Cited by 6 publications

(3 citation statements)

References 36 publications

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“…Research investigating the aberrant molecular processes that occur during cardiac hypertrophy has used primary cardiomyocytes from neonatal rat hearts as the standard experimental in vitro system. In addition, some studies have made use of the H9C2 rat cardiomyoblast cell line ( 38 , 39 ), as it was found by Watkins et al ( 40 ) that the H9C2 cell line and primary neonatal cardiomyocyte cells exhibit similar hypertrophic responses in vitro . Therefore, the H9C2 cell line was selected for the present study, which also has the advantage of being an animal-free alternative.…”

Section: Discussionmentioning

confidence: 99%

Calcium inhibitor inhibits high glucose‑induced hypertrophy of H9C2 cells

Ruan

Tian

et al. 2020

Mol Med Rep

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The aim of the present study was to explore whether the hypertrophy of H9C2 cardiomyocytes was induced by high glucose, to investigate whether the calcium channel inhibitor (Norvasc) could inhibit this process and to clarify the possible signaling pathways. The morphology of H9C2 cells was observed under an optical microscope, and the cell surface area was measured by Image Pro Plus 6.1 software. Furthermore, fluorescence spectrophotometry was used to detect intracellular calcium concentration ([Ca 2+ ]i). ELISA was performed to detect calcineurin (CaN) activity; reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expression levels of CaN Aβ subunit (CnAβ), nuclear factor of activated T cells 3 (NFAT3) and β type myosin heavy chain (β-MHC). Cell size was increased with the increase in glucose concentration of culture medium at 48 and 72 h, respectively, and decreased with the addition of Norvasc compared with those without Norvasc (P<0.05). There was no significant difference in cell size with the addition of Norvasc compared with cells cultured with 5 mM glucose (P>0.05). The average [Ca 2+ ]i activity of single cells in the 48- and 72-h culture groups treated with 50 mM glucose was significantly higher than cells treated with 5 mM glucose (P<0.05); and the fluorescent value of average [Ca 2+ ]i activity of single cells was lower, following the addition of Norvasc than that without Norvasc (P<0.05). CaN activity in the 48- and 72-h culture group treated with 50 mM glucose was markedly higher than that treated with 5 mM glucose, and the activity of CaN notably decreased with the addition of Norvasc compared with those without Norvasc. The mRNA and protein expression levels of CnAβ, NFAT3 and β-MHC in the 48- and 72-h culture groups treated with 50 mM glucose were all significantly higher than those treated with 5 mM glucose (P<0.05). The mRNA and protein expression of CnAβ, NFAT3 and β-MHC cultured with 50 mM glucose were significantly decreased following the addition of Norvasc (P<0.05). Thus, the calcium channel inhibitor Norvasc may inhibit high glucose-induced hypertrophy of H9C2 cardiomyocytes by inhibiting the Ca 2+ -CaN-NFAT3 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Calcium inhibitor inhibits high glucose‑induced hypertrophy of H9C2 cells

Ruan

Tian

et al. 2020

Mol Med Rep

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“…According to these studies, Myc upregulates the expression of genes associated with RNA metabolism, protein metabolism, ribosome biogenesis and ribosome function (32). Additionally, Myc controls the expression of selenocysteine biosynthesis, ornithine decarboxylase and lactate dehydrogenase A, all of which promote cell proliferation in other cell types (146)(147)(148).…”

Section: From Harmful To Necessary: Myc Effects On Pancreatic β-Cell mentioning

confidence: 99%

The many lives of Myc in the pancreatic β-cell

Rosselot

Baumel-Alterzon

et al. 2021

Journal of Biological Chemistry

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Diabetes results from insufficient numbers of functional pancreatic β-cells. Thus, increasing the number of available functional β-cells ex vivo for transplantation, or regenerating them in situ in diabetic patients, is a major focus of diabetes research. The transcription factor, Myc, discovered decades ago, lies at the nexus of most, if not all, known proliferative pathways. Based on this, many studies in the 1990’s and early 2000’s explored the potential of harnessing Myc expression to expand β-cells for diabetes treatment. Nearly all these studies in β-cells used pathophysiological or supraphysiological levels of Myc and reported enhanced β-cell death, de-differentiation or the formation of insulinomas if co-overexpressed with Bcl-xL, an inhibitor of apoptosis. This obviously reduced the enthusiasm for Myc as a therapeutic target for β-cell regeneration. However, recent studies indicate that “gentle” induction of Myc expression enhances β-cell replication without induction of cell death or loss of insulin secretion, suggesting that appropriate levels of Myc could have therapeutic potential for β-cell regeneration. Furthermore, although it has been known for decades that Myc is induced by glucose in β-cells very little is known about how this essential anabolic transcription factor perceives and responds to nutrients and increased insulin demand in vivo. Here we summarize the previous and recent knowledge of Myc in the β-cell, its potential for β-cell regeneration and its physiological importance for neonatal and adaptive β-cell expansion.

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“…описано усиление каспаза-3-зависимого апоптоза в различных тканях позвоночных при селенодефиците [87]. [87,88]. Выход цитохрома с из митохондрий также зависит от активности каспаз -1 и -7.…”

Section: селенодефицит вызывает воспалениеunclassified

Selenium compounds in redox regulation of inflammation and apoptosis

et al. 2019

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Monocytes and macrophages play a key role in the development of inflammation: under the action of lipopolysaccharides (LPS), absorbed from the intestine, monocytes and macrophages form reactive oxygen species (ROS) and cytokines, this leads to the development of oxidative stress, inflammation and/or apoptosis in all types of tissues. In the cells LPS induce an “internal” TLR4-mediated MAP-kinase inflammatory signaling pathway and cytokines through the superfamily of tumor necrosis factor receptor (TNFR) and the “death domain” (DD) initiate an “external” caspase apoptosis cascade or necrosis activation that causes necroptosis. Many of the proteins involved in intracellular signaling cascades (MYD88, ASK1, IKKa/b, NF-kB, AP-1) are redox-sensitive and their activity is regulated by antioxidants thioredoxin, glutaredoxin, nitroredoxin, and glutathione. Oxidation of these signaling proteins induced by ROS enhances the development of inflammation and apoptosis, and their reduction with antioxidants, on the contrary, stabilizes the signaling cascades speed, preventing the vicious circle of oxidative stress, inflammation and apoptosis that follows it. Antioxidant (AO) enzymes thioredoxin reductase (TRXR), glutaredoxin reductase (GLRXR), glutathione reductase (GR) are required for reduction of non-enzymatic antioxidants (thioredoxin, glutaredoxin, nitroredoxin, glutathione), and AO enzymes (SOD, catalase, GPX) are required for ROS deactivation. The key AO enzymes (TRXR and GPX) are selenium-dependent; therefore selenium deficiency leads to a decrease in the body's antioxidant defense, the development of oxidative stress, inflammation, and/or apoptosis in various cell types. Nrf2-Keap1 signaling pathway activated by selenium deficiency and/or oxidative stress is necessary to restore redox homeostasis in the cell. In addition, expression of some genes is changed with selenium deficiency. Consequently, growth and proliferation of cells, their movement, development, death, and survival, as well as the interaction between cells, the redox regulation of intracellular signaling cascades of inflammation and apoptosis, depend on the selenium status of the body. Prophylactic administration of selenium-containing preparations (natural and synthetic (organic and inorganic)) is able to normalize the activity of AO enzymes and the general status of the body. Organic selenium compounds have a high bioavailability and, depending on their concentration, can act both as selenium donors to prevent selenium deficiency and as antitumor drugs due to their toxicity and participation in the regulation of signaling pathways of apoptosis. Known selenorganic compounds diphenyldiselenide and ethaselen share similarity with the Russian organo selenium compound, diacetophenonylselenide (DAPS-25), which serves as a source of bioavailable selenium, exhibits a wide range of biological activity, including antioxidant activity, that governs cell redox balance, inflammation and apoptosis regulation.

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Role of tRNA selenocysteine 1 associated protein 1 in the proliferation and apoptosis of cardiomyocyte-like H9c2 cells

Cited by 6 publications

References 36 publications

Calcium inhibitor inhibits high glucose‑induced hypertrophy of H9C2 cells

Calcium inhibitor inhibits high glucose‑induced hypertrophy of H9C2 cells

The many lives of Myc in the pancreatic β-cell

Selenium compounds in redox regulation of inflammation and apoptosis

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