A systematic review of p53 regulation of oxidative stress in skeletal muscle

Beyfuss, Kaitlyn; Hood, David A.

doi:10.1080/13510002.2017.1416773

Cited by 185 publications

(134 citation statements)

References 121 publications

(299 reference statements)

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“…On the other hand, mean GSH and catalase values recorded a significant decrease, indicating oxidative stress. Going with, it was proved that oxidative stress facilitates increased cellular stress levels and initiates DNA fragmentation to induce apoptosis (29).…”

Section: Discussionmentioning

confidence: 99%

Effect of Stem Cells, Ascorbic Acid and SERCA1a Gene Transfected Stem Cells in Experimentally Induced Type I Diabetic Myopathy

Zickri

Sadek

Fares

et al. 2020

IJSC

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Background and Objectives: Sarco/endoplasmic reticulum Ca 2＋ -ATPase (SERCA) inhibition was proved in streptozotocin (STZ)-diabetic rats. The present study aimed at investigating and comparing the therapeutic effect of bone marrow mesenchymal stem cells (BMMSCs), BMMSCs combined with ascorbic acid (AA) and SERCA1a gene transfected BMMSCs in induced type I diabetic myopathy of male albino rat. Methods and Results: 54 rats were divided into donor group of 6 rats for isolation, propagation and characterization of BMMSCs and SERCA1a transfected BMMSCs, groups I∼V 48 rats. Group I of 8 control rats, group II (Diabetic) of 10 rats given STZ 50 mg/kg intraperitoneal, group III (BMMSCs) of 10 rats given STZ and BMMSCs intravenous (IV), group IV (BMMSCs and AA) of 10 rats given STZ, BMMSCs IV and AA 500 mg/kg and group V (SERCA 1a transfected BMMSCs) of 10 rats given STZ and SERCA1a transfected BMMSCs IV. The rats were sacrificed after 8 weeks. Gastrocnemius specimens were subjected to biochemical, histological, morphometric and statistical studies. Diabetic rats revealed inflammatory and degenerative muscle changes, a significant increase in blood glucose level, mean DNA fragmentation and mean MDA values and a significant decrease in mean GSH and catalase values, area of pale nuclei, area% of CD105 and CD34 ＋ve cells, SERCA1a protein and gene values. The morphological changes regressed by therapy. In group III significant decrease in DNA fragmentation and MDA, significant increase in GSH and catalase, significant increase in the mean area of pale nuclei, area % of CD105 and CD34 ＋ve cells versus diabetic group. In group IV, same findings as group III versus diabetic and BMMSCs groups. In group V, same findings as group IV versus diabetic and treated groups. Western blot and PCR proved a mean value of SERCA1a protein and gene comparable to the control group. Mean calcium concentration values revealed a significant increase in the diabetic group, in BMMSCs and AA group versus control and SERCA1a group. Conclusions: SERCA1a transfected BMMSCs proved a definite therapeutic effect, more remarkable than BMMSCs combined with AA. This effect was evidenced histologically and confirmed by significant changes in the biochemical tests indicating oxidative stress, muscle calcium concentration, morphometric parameters and PCR values of SERCA1a.

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Section: Discussionmentioning

confidence: 99%

Effect of Stem Cells, Ascorbic Acid and SERCA1a Gene Transfected Stem Cells in Experimentally Induced Type I Diabetic Myopathy

Zickri

Sadek

Fares

et al. 2020

IJSC

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“…Such a shift in the band might implicate protein hyperphosphorylation. In fact, p53 has multiple phosphorylation sites and is involved in regulating various cellular signalling pathways other than mitochondrial homeostasis (Beyfuss & Hood, ). Thus, further study is warranted to clarify the effect of the change in p53 expression in skeletal muscle metabolism under conditions of T2DM.…”

Section: Discussionmentioning

confidence: 99%

Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance training‐mediated myonuclear accretion and muscle mass gain in rats

Ato

Kido

Sato

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Type 2 diabetes mellitus (T2DM) causes skeletal muscle atrophy; does it affect resistance training (RT)‐mediated molecular adaptations and subsequent muscle hypertrophy? What is the main finding and its importance?Although skeletal muscle mass and regulation were not preserved under conditions of T2DM, the response of RT‐induced skeletal muscle hypertrophy was not impaired in T2DM rat skeletal muscle. These findings suggest that the capacity of RT‐mediated muscle mass gain is not diminished in the T2DM condition. Abstract Type 2 diabetes mellitus (T2DM) is known to cause skeletal muscle atrophy. However, it is not known whether T2DM affects resistance training (RT)‐mediated molecular adaptations and subsequent muscle hypertrophy. Therefore, we investigated the effect of T2DM on response of skeletal muscle hypertrophy to chronic RT using a rat resistance exercise mimetic model. T2DM and healthy control rats were subjected to 18 bouts (3 times per week) of chronic RT on unilateral lower legs. RT significantly increased gastrocnemius muscle mass and myonuclei in both T2DM and healthy control rats to the same extent, even though T2DM caused muscle atrophy in the resting condition. Further, T2DM significantly reduced mechanistic target of rapamycin complex 1 (mTORC1) activity (phosphorylation of p70S6KThr389 and 4E‐BP1Thr37/46) to insulin stimulation and the number of myonuclei in the untrained basal condition, but RT‐mediated adaptations were not affected by T2DM. These findings suggested that although the skeletal muscle mass and regulation were not preserved under basal conditions of T2DM, the response of RT‐induced skeletal muscle hypertrophy was not impaired in T2DM rat skeletal muscle.

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“…In various types of liver injury there are different degrees of oxidative stress that may impact directly liver specific enzymes, particularly glycogen synthase kinase (GSK) enzyme that regulate glycogen synthesis (25). Remarkably, oxidative stress can control hepatic cell proliferations and apoptosis, in part by regulating the activity of GSK (26)(27)(28), also by regulating several cell signalling pathways like β catenin/Wnt (29), p53 (30), NF-kB (nuclear factor kappa of activated B cells) (31), MAPK (mitogen-activated protein kinase) (32), and PI3K (phosphatidylinositide 3-kinase) (33). However, oxidative stress could be exacerbates hepatotoxicity by upstream the activity of GSK enzyme, and this fact may elucidate our result of high level of LGC in ND vaccinated groups at 7 and 15 days (see Table 2 and 3).…”

Section: Discussionmentioning

confidence: 99%

Effects of Newcastle disease vaccine on the liver and antioxidant enzymes of chicks

Mustafa¹

2019

IJVS

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Newcastle disease is a highly contagious disease of domestic and wild birds result in huge economic losses due to extreme morbidity and mortality. The aim of this paper is to explore the possibility of the harmful impact of Newcastle disease vaccine on certain biochemical profiles regarded to chicken liver. This study conducted during January-April 2014, one day old-53 chicks were divided into two groups; vaccinated (with Newcastle disease vaccine) group at the age of 1, 3, and 7 days and unvaccinated group. Results show damaging effects of vaccination on the liver glycogen and malondialdehyde concentrations, serum superoxide dismutase, catalase, glutathione peroxidase, gamma-glutamyl transferase, alanine transaminase, and aspartate transaminase activities. In contrast, studied parameters look to return to their usual range at the age of 30 days. From the convincing outcome of our investigation, it can be concluded that Newcastle disease vaccination has a detrimental influence on the liver of chickens, nonetheless this effect can be overwhelmed by the time.

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A systematic review of p53 regulation of oxidative stress in skeletal muscle

Cited by 185 publications

References 121 publications

Effect of Stem Cells, Ascorbic Acid and SERCA1a Gene Transfected Stem Cells in Experimentally Induced Type I Diabetic Myopathy

Effect of Stem Cells, Ascorbic Acid and SERCA1a Gene Transfected Stem Cells in Experimentally Induced Type I Diabetic Myopathy

Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance training‐mediated myonuclear accretion and muscle mass gain in rats

Effects of Newcastle disease vaccine on the liver and antioxidant enzymes of chicks

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