Major apoptotic mechanisms and genes involved in apoptosis

Kiraz, Yağmur; Adan, Aysun; Yandım, Melis Kartal; Baran, Yusuf

doi:10.1007/s13277-016-5035-9

Cited by 425 publications

(301 citation statements)

References 221 publications

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“…The mitochondrial apoptotic pathway is regulated by various apoptosis-related genes, such as Bax [47]. Bax is a pro-apoptotic protein residing in the cytosol but translocates to the mitochondria upon the induction of apoptosis [48].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Artemisia judaica against Doxorubicin-Induced Toxicity in Mice

Ahmed

Mabrouk

Hassanane

et al. 2017

ARRB

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Aim: The present study aimed to investigate the protective effect of Artemisia Judaica (A. Judaica) against doxorubicin (DOX)-induced toxicity in male mice. Place and Duration of Study: Department of Cell Biology, Genetic engineering and biotechnology division, National research centre, Egypt, between March 2016 and February 2017. Methodology: Male mice were divided into 7 groups (n=10) and treated as follow: the control group, the group treated with DMSO, the group injected (i.p.) with DOX , the groups treated with low and high dose of A. judaica extract and the groups injected (i.p.) with DOX and treated with low and high dose of A. judaica extract. Femur, testes and liver samples were collected for different analyses. Results: Our data showed that A. judaica significantly reversed the DOX-induced elevation of DNA fragmentation rate and MDA level in liver tissue, as well as declined chromosomal aberrations (CAs) either in the bone marrow cells or in the spermatocyte cells. Meanwhile, the expression of Ahmed et al.; ARRB, 18(3): 1-10, 2017; Article no.ARRB.35990 2 apoptosis-related genes (Bax and Caspase-3) in liver tissues was analyzed by quantitative real-time PCR (qRT-PCR) and results revealed that genes expression were up-regulated in DOX treated mice however; the administration of A. judaica didn't alter such increase. Conclusion: Overall, the findings indicated that A. judaica may attenuate the DOX-induced toxicity. However; further studies are required to confirm the protective effect of A. judaica extract against toxicity caused by DOX drug. Original Research Article

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Artemisia judaica against Doxorubicin-Induced Toxicity in Mice

Ahmed

Mabrouk

Hassanane

et al. 2017

ARRB

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“…Furthermore, the treatment with PEI/DOX-Duplex/ siRNA could obviously increase the activities of caspase-3 and caspase-9 and did not influence the caspase-8 activity ( Figure 10). The caspase-9 can target procaspase-3 in the mitochondrial apoptosis pathway, 38 which meant the ternary nanocomplex PEI/DOX-Duplex/siRNA could activate the mitochondria-mediated pathway. However, the nanocarrier had no profound effects on death receptor-mediated pathway, …”

Section: Zhang Et Almentioning

confidence: 99%

“…38 Similarly, more activation of caspase-3 and caspase-9 could be obtained in PEI/DOXDuplex/siRNA than in other groups. Finally, cell-cycle arrest assay indicated that PEI25K/siRNA did not induce obvious cell-cycle arrest, while the ternary nanocomplex could improve the G2 ratio (37.67%) and achieve the cell-cycle arrest at the G2 phase ( Figure 11).…”

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confidence: 90%

Inhibition of cell proliferation through an ATP-responsive co-delivery system of doxorubicin and Bcl-2 siRNA

Zhang¹,

Wang²,

Chen³

et al. 2017

IJN

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Herein, DNA duplex was constructed through the hybridization of adenosine triphosphate (ATP)-responsive aptamer and its cDNA in which GC-rich motif could be used to load doxorubicin (DOX), and then, cationic polymer PEI25K was used as a carrier to simultaneously condense DOX-Duplex and Bcl-2 siRNA to prepare the ternary nanocomplex polyethylenimine (PEI)/DOX-Duplex/siRNA. The ATP concentration gradient between the cytosol and extracellular environment could achieve the stable loading of DOX in duplex and the rapid drug release in an ATP-responsive manner. Using human prostate tumor cell line PC-3 as a model, an obvious induction of cell proliferation could be detected with a cell viability of 53.3%, which was stronger than single cargo delivery, indicating the synergistic effect between these two components. The enhanced anti-proliferative effect of ternary nanocomplex could be attributed to the improved induction of cell apoptosis in a mitochondria-mediated pathway and cell-cycle arrest at the G2 phase. Overall, the ATP-responsive nanocarrier for co-delivering DOX and Bcl-2 siRNA has been demonstrated to be a smart delivery system with favorable anti-proliferative effect, especially for solving the multidrug resistance of tumors.

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“…Recent studies suggest that AD pathology is associated with ERS 14 . ERS generates a toxic environment in neurons, which in turn activates endoplasmic reticulum pathways that ultimately cause apoptosis 15 . Thus, inhibition of ERS injury may be an effective strategy to prevent AD.…”

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confidence: 99%

Commentary: Protective Effects of Isorhamnetin on N2a Cell Against Endoplasmic Reticulum Stress-induced Injury Is Mediated by PKC?

Lu¹

2017

J Neurol Neuromedicine

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Neuronal apoptosis is an important pathophysiological factor of Alzheimer's disease (AD). Inhibition of endoplasmic reticulum stress (ERS)-induced neuronal apoptosis is an effective strategy to deal with AD. In this commentary, we summarize the relationship between AD and ERS injury-induced neuronal apoptosis, and highlight the protective effects and mechanism of isorhamnetin (Iso) against ERS-induced injury in N2a cells. Moreover, this commentary discusses the recent findings in the role of Iso in other diseases.Alzheimer's disease (AD) is a chronic neurodegenerative disease, and the fourth leading cause of death, behind heart disease, cancer and stroke 1. The clinical manifestations of AD include deteriorating cognitive function and memory, a decline in functioning in daily life activities, anda variety of neuropsychiatric symptoms and behavioral disorders 2,3 . The risk of AD gradually increases with age. There are more than 30 million AD patient living in the world today 4,5 .The etiology and pathogenesis of AD is not clear. AD is characterized by the accumulation of misfolded β-amyloid proteins caused by various genetic and environmental factors. These Aβ-plaques are associated with several pathological changes including the aggregation of misfolded proteins, formation of tissue precipitation, intracellular calcium disturbance, DNA fragmentation and lipid peroxidation. Together, these factors induce neuronal apoptosis and necrosis 6 . Thus, inhibiting neuron apoptosis is an effective way to prevent AD.The endoplasmic reticulum (ER) is theprincipal organelle for protein synthesis, protein folding and maintenance of calcium homeostasis 7 . Numerous stimuli, such as hypoxia and oxidative stress, can perturb calcium balance, and promote accumulation of unfolded and misfolded proteins in the ER lumen. This is known as endoplasmic reticulum stress (ERS) 8 . ERS is one of the key drivers of apoptosis. ERS induces apoptosis, through activation of the ASK and p38 MAPK signal pathway, trigger the kinase function of IRE1 [9][10][11] . Additionally, p38MAPK is reported to promote phosphorylation and activation of pro-apoptotic protein Bax 12,13 . Recent studies suggest that AD pathology is associated with ERS 14 . ERS generates a toxic environment in neurons, which in turn activates endoplasmic reticulum pathways that ultimately cause apoptosis 15 . Thus, inhibition of ERS injury may be an effective strategy to prevent AD.

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Major apoptotic mechanisms and genes involved in apoptosis

Cited by 425 publications

References 221 publications

Protective Effect of Artemisia judaica against Doxorubicin-Induced Toxicity in Mice

Protective Effect of Artemisia judaica against Doxorubicin-Induced Toxicity in Mice

Inhibition of cell proliferation through an ATP-responsive co-delivery system of doxorubicin and Bcl-2 siRNA

Commentary: Protective Effects of Isorhamnetin on N2a Cell Against Endoplasmic Reticulum Stress-induced Injury Is Mediated by PKC?

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