Tyrosine phosphatase signalling in a lower plant: cell-cycle and oxidative stress-regulated expression of the Chlamydomonas eugametos VH-PTP13 gene

Background: Different cellular responses influence the progress of cancer. In this study, we have investigated the effect of hydrogen peroxide and quercetin induced changes on cell viability, apoptosis and oxidative stress in human hepatocellular carcinoma (HepG2) cells. Methods: The effects of hydrogen peroxide and quercetin on cell viability, cell cycle phases and oxidative stress related cellular changes were investigated. Cell viability was assessed by WST-1 assay. Apoptosis rate, cell cycle phase changes and oxidative stress were measured by flow cytometry. Protein expressions of p21, p27, p53, NF-Kβ-p50 and proteasome activity were determined by Western blot and fluorometry, respectively. Results: Hydrogen peroxide and quercetin treatment resulted in decreased cell viability and increased apoptosis in HepG2 cells. Proteasome activity was increased by hydrogen peroxide but decreased by quercetin treatment. Conclusion: Both agents resulted in decreased p53 protein expression and increased cell death by different mechanisms regarding proteostasis and cell cycle phases.

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Why should we study the plant cell cycle?

Journal of Experimental Botany ◽

10.1093/jxb/erg138 ◽

2003 ◽

Vol 54 (385) ◽

pp. 1125-1126 ◽

Cited By ~ 10

Author(s):

D. Inze

Keyword(s):

Cell Cycle ◽

Plant Cell ◽

Plant Cell Cycle

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Hypoxia-induced myocardial regeneration

Journal of Applied Physiology ◽

10.1152/japplphysiol.00328.2017 ◽

2017 ◽

Vol 123 (6) ◽

pp. 1676-1681 ◽

Cited By ~ 15

Author(s):

Wataru Kimura ◽

Yuji Nakada ◽

Hesham A. Sadek

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Systolic Heart Failure ◽

Cardiac Regeneration ◽

Oxygen Metabolism ◽

Functional Improvement ◽

Cardiomyocyte Proliferation ◽

Mammalian Heart ◽

Cell Cycle Reentry ◽

And Oxidative Stress

The underlying cause of systolic heart failure is the inability of the adult mammalian heart to regenerate damaged myocardium. In contrast, some vertebrate species and immature mammals are capable of full cardiac regeneration following multiple types of injury through cardiomyocyte proliferation. Little is known about what distinguishes proliferative cardiomyocytes from terminally differentiated, nonproliferative cardiomyocytes. Recently, several reports have suggested that oxygen metabolism and oxidative stress play a pivotal role in regulating the proliferative capacity of mammalian cardiomyocytes. Moreover, reducing oxygen metabolism in the adult mammalian heart can induce cardiomyocyte cell cycle reentry through blunting oxidative damage, which is sufficient for functional improvement following myocardial infarction. Here we concisely summarize recent findings that highlight the role of oxygen metabolism and oxidative stress in cardiomyocyte cell cycle regulation, and discuss future therapeutic approaches targeting oxidative metabolism to induce cardiac regeneration.

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