Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study

Erekat, Nour S.; Al-Jarrah, Muhammed

doi:10.12659/msmbr.910307

Cited by 15 publications

(7 citation statements)

References 67 publications

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“…Recent findings correlate PD and several apoptotic markers (the overexpression of p53 and active caspase-3 in the cardiac muscle) and the underexpression of the β-adrenergic receptor, which can potentially promote the cardiac dysfunction observed in PD patients. 20 Clinical and pathological studies have provided strong evidence of the involvement of cardiac sympathetic nerves in PD patients. [21][22][23][24] Our results demonstrate noradrenergic sympathetic loss (significant decrease in NA turnover in RV) in MPTP-treated monkeys.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys

et al. 2019

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Background Autonomic dysfunction is a well‐known dominant symptom in the advanced stages of Parkinson's disease. However, the role of cardiac sympathetic nerves still needs to be elucidated. Objectives To evaluate cardiac sympathetic response in Parkinsonian and dyskinetic monkeys. Methods Adult male monkeys were divided into 1 of the following 3 groups: controls, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine–treated monkeys, and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine+levodopa–treated animals. Noradrenaline, its metabolite normetanephrine, and phospho‐Heat shock proten 27 (p‐Hsp27) at serine 82 levels were analyzed in the left and right ventricles of the heart. Tyrosine hydroxylase immunohistochemistry was performed in the ventral mesencephalon. Results The results were the following: (1) 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine intoxication significantly increased normetanephrine levels and decreased noradrenaline turnover in the right ventricle without changes in the left ventricle; however, (2) levodopa treatment decreased noradrenaline levels and enhanced the normetanephrine/noradrenaline ratio in parallel with a very significant increase of Hsp27 activity in both ventricles. Conclusions Levodopa treatment could induce protective cardiac effects through the increased Hsp27 activity. © 2019 International Parkinson and Movement Disorder Society

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Section: Discussionmentioning

confidence: 99%

Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys

et al. 2019

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“…1 Several pieces of evidence suggest that dopamine-containing neurons' death may result from elevated reactive oxygen species levels, 1,[23][24][25] mitochondrial respiratory failure, 1,[26][27][28] and activation of the NF-κB and caspase pathways. 1,27,29,30 The development of inflammation and oxidative stress is often accompanied by dysbiosis or dysfunction of the gut microbiome. 31,32 The gut microbiome plays a vital role in human health and disease and is, therefore, a popular area of research.…”

Section: Introductionmentioning

confidence: 99%

Common Inflammatory Mechanisms in COVID-19 and Parkinson’s Diseases: The Role of Microbiome, Pharmabiotics and Postbiotics in Their Prevention

Даниленко¹,

Devyatkin²,

Марсова³

et al. 2021

JIR

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In the last decade, metagenomic studies have shown the key role of the gut microbiome in maintaining immune and neuroendocrine systems. Malfunction of the gut microbiome can induce inflammatory processes, oxidative stress, and cytokine storm. Dysfunction of the gut microbiome can be caused by short-term (virus infection and other infectious diseases) or long-term (environment, nutrition, and stress) factors. Here, we reviewed the inflammation and oxidative stress in neurodegenerative diseases and coronavirus infection (COVID-19). Here, we reviewed the renin-angiotensin-aldosterone system (RAAS) involved in the processes of formation of oxidative stress and inflammation in viral and neurodegenerative diseases. Moreover, the coronavirus uses ACE2 receptors of the RAAS to penetrate human cells. The coronavirus infection can be the trigger for neurodegenerative diseases by dysfunction of the RAAS. Pharmabiotics, postbiotics, and nextgeneration probiotics, are considered as a means to prevent oxidative stress, inflammatory processes, neurodegenerative and viral diseases through gut microbiome regulation.

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“…TNF-α initiates and promotes the cell surface death receptor-mediated apoptosis. [31][32][33] Previous studies have demonstrated TNF-α overexpression in many neurodegenerative diseases, such as PD, Alzheimer disease (AD), and amyotrophic lateral sclerosis (ALS). [34][35][36][37] In addition, elevated levels of TNF-α have been shown in the cerebellar PCs in many pathological conditions.…”

Section: Discussionmentioning

confidence: 99%

Cerebellar Upregulation of Cell Surface Death Receptor–Mediated Apoptotic Factors in Harmaline-Induced Tremor: An Immunohistochemistry Study

Erekat

2018

J�Cell Death

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Active caspase-3-mediated apoptosis has been implicated in the pathogenesis of harmaline-induced tremor. The aim of this study is to illustrate the impact of tremor induction on the expression of factors mediating the cell surface death receptor–dependent apoptosis. A total of 20 normal Wistar rats were randomly selected and equally divided into control and experimental groups. Tremor was induced in the experimental group by injecting the rats with a single dose of harmaline (50 mg/kg). After that, cerebellar tissues were evaluated by immunohistochemistry to examine the expression of tumor necrosis factor α (TNF-α) and active caspase-8 in the 2 groups of animals. TNF-α and active caspase-8 expression was significantly higher in cerebella from experimental rats compared with that in those from the control rats (P value < .01). Thus, our present data suggest the association of tremor induction with the cerebellar overexpression of TNF-α and active caspase-8, correlative with Purkinje cell (PC) loss indicated by loss of calbindin immunoreactivity, indicating the induction of the cell surface death receptor–mediated apoptosis.

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Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study

Cited by 15 publications

References 67 publications

Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys

Cardiac Noradrenaline Turnover and Heat Shock Protein 27 Phosphorylation in Dyskinetic Monkeys

Common Inflammatory Mechanisms in COVID-19 and Parkinson’s Diseases: The Role of Microbiome, Pharmabiotics and Postbiotics in Their Prevention

Cerebellar Upregulation of Cell Surface Death Receptor–Mediated Apoptotic Factors in Harmaline-Induced Tremor: An Immunohistochemistry Study

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