Apoptosis in health and disease and modulation of apoptosis for therapy: An overview

Singh, Neeta

doi:10.1007/bf02913307

Cited by 44 publications

(32 citation statements)

References 71 publications

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“…They were classified according to their various functions, the inflammatory caspases 1, 4, 5, 11, 12, 13, 14, the effector caspases 3, 6 and the initiator caspases 2, 8, 9, 10, (Singh, 2007). The apoptotic process that induced by mitochondrial pathway is triggered through intracellular stresses mainly in the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway

Wang

Zhang

et al. 2016

European Journal of Pharmacology

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Our former studies have suggested that taurochenodeoxycholic acid (TCDCA) as a signaling molecule shows obvious anti-inflammatory and immune regulation properties. In this research, we tentatively explored the potential effects and the possible mechanism that involve in the apoptotic process in NR8383 cells induced by TCDCA. Using flow cytometry analysis, we evaluated the apoptosis rate. Gene expression levels were determined by qPCR. The expressions of protein kinase C (PKC), Jun N-terminal kinase (JNK) and their phosphorylation were measured by Western Blot. We observed the activities of caspase-3 and caspase-8 with Caspase-Glo® regent. The results demonstrated that TCDCA dramatically improved the apoptosis rate of NR8383 cells in a concentration-dependent manner. In the meantime, PKC mRNA levels and activities were significantly augmented by TCDCA treatments. In addition, JNK, caspase-3 and caspase-8 mRNA expression levels and activities were increased by TCDCA, while they were markedly decreased by specific inhibitors. We conclude that TCDCA contributes to the apoptosis through the activation of the caspase cascade in NR8383 cells, and the PKC/JNK signaling pathway may be involved in this process. These results indicate that TCDCA may be a latent effective pharmaceutical product for apoptosis-related diseases.

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Section: Discussionmentioning

confidence: 99%

Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway

Wang

Zhang

et al. 2016

European Journal of Pharmacology

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“…Every day billions of cells are produced by mitosis and a similar number of cells die by apoptosis to maintain tissue homeostasis [3]. Physiological cell death occurs when a cell within an organism dies by a mechanism orchestrated by proteins encoded by the host's genome.…”

Section: Introductionmentioning

confidence: 99%

“…Apoptosis refers to both the initiation and execution of the events whereby a cell commits suicide and it is distinct from other forms of cell death [4]. It is a process of controlled cellular death whereby the activation of specific death-signaling pathways leads to deletion of cells from tissue [3]. It provides an efficient mechanism of eliminating unwanted cells during normal embryonic and adult development.…”

Section: Introductionmentioning

confidence: 99%

“…It provides an efficient mechanism of eliminating unwanted cells during normal embryonic and adult development. Physiologically, all multicellular organisms use apoptosis during development, homeostasis, defense, metamorphosis, terminal differentiation, immune response, cellular response to growth factors and hormones [3].…”

Section: Introductionmentioning

confidence: 99%

“…The loss of balance between cell division and cell death leads to cancer. It affects scattered individual cells, which have the following distinct morphological features such as Cell shrinkage, Chromatin condensation, Membrane blebbing, Formation of apoptotic bodies and Shows no inflammatory response [3]. Eventually the dying cell degrades into apoptotic bodies that are sub cellular membrane bound vesicles that are ultimately removed by phagocytosis [4].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Apoptosis-Biochemistry: A Mini Review

Jayakiran¹

2015

J Clin Exp Pathol

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Apoptosis or programmed cell death is a normal component of the development and health of multicellular organisms. Homeostasis is maintained through a balance between cell proliferation and cell death. It is a process of controlled cellular death whereby the activation of specific death-signaling pathways leads to deletion of cells from tissue. The distinct morphological features of apoptosis are Cell shrinkage, Chromatin condensation, Membrane blebbing and formation of apoptotic bodies, which are phagocytosed by neighbouring macrophages without any inflammatory response. Derailment of apoptosis in regulation can lead to several diseases or ailments with either too much or too little apoptosis. Understanding the molecular mechanism of apoptosis including death genes, death signals, surface receptors and signal pathways will provide new insights in developing strategies to regulate cell survival/death. The current knowledge on the molecular events of apoptotic cell death and their significance in health and disease is reviewed.

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Induction of macrophage cell‐cycle arrest and apoptosis by humic acid

Yang

Pei

Chen

et al. 2014

Environ and Mol Mutagen

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Humic acid (HA) in well water is associated with Blackfoot disease and various cancers. Previously, we reported that acute humic acid exposure (25–200 µg/mL for 24 hr) induces inflammation in RAW264.7 macrophages. In this study, we observed that prolonged (72 hr) HA exposure (25–200 µg/mL) induces cell‐cycle arrest and apoptosis in cultured RAW264.7 cells. We also observed that exposing macrophages to HA arrests cells in the G2/M phase of the cell cycle by reducing cyclin A/B1, Cdc2, and Cdc25C levels. Treating macrophages with HA triggers a sequence of events characteristic of apoptotic cell death including loss of cell viability, morphological changes, internucleosomal DNA fragmentation, sub‐G1 accumulation. Molecular markers of apoptosis associated with mitochondrial dysfunction were similarly observed, including cytochrome c release, caspase‐3 or caspase‐9 activation, and Bcl‐2/Bax dysregulation. In addition to the mitochondrial pathway, HA‐induced apoptosis may also be mediated through the death receptor and ER stress pathways, as evidence by induction of Fas, caspase‐8, caspase‐4, and caspase‐12 activity. HA also upregulates p53 expression and causes DNA damage as assessed by the comet assay. These findings yield new insight into the mechanisms by which HA exposure may trigger atherosclerosis through modulation of the macrophage‐mediated immune system. Environ. Mol. Mutagen. 55:741–750, 2014. © 2014 Wiley Periodicals, Inc.

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Apoptosis in health and disease and modulation of apoptosis for therapy: An overview

Abstract: ABSTRACT

Cited by 44 publications

References 71 publications

Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway

Taurochenodeoxycholic acid induces NR8383 cells apoptosis via PKC/JNK-dependent pathway

Apoptosis-Biochemistry: A Mini Review

Induction of macrophage cell‐cycle arrest and apoptosis by humic acid

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