apoptosis

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apoptosis

[‚ā·pō′tō·səs]
(cell and molecular biology)
Death of cells triggered by extracellular signals or genetically programmed events, carried out by processes within the cell, and characterized by systemic breakdown of cellular constituents, in particular chromosomal deoxyribonucleic acid; may be involved in normal development and aging, or may serve to eliminate defective or damaged cells. Also known as programmed cell death.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
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Live cells have a normal green nucleus; early apoptotic cells have bright green nucleus with condensed or fragmented chromatin; late apoptotic cells display condensed and fragmented chromatin and membrane blebbing (Canete et al., 2001; Adefolaju et al., 2015).
The expression level of activated caspase 3, another apoptotic marker, was also examined (Figure 4E).
Presence of apoptotic bodies among scattered clusters of granulusa cells indicates that apoptotic process was not fully completed.
Apoptotic index (%) values of 4a-d on HeLa cells Apoptotic Index (%) 4a Time (Hours) Control 160 [micro]M (*) 24 6.17[+ or -]0.06 (SD) 12.15[+ or -]0.02 48 7.21[+ or -]0.05 12.19[+ or -]0.03 72 7.96 [+ or -]0.09 14.33[+ or -]0.01 Apoptotic Index (%) 4b 4c 4d Time (Hours) 100 [micro]M (*) 80 [micro]M (*) 160 [micro]M (*) 24 8.16[+ or -]0.03 18.19[+ or -]0.11 10.23[+ or -]0.06 48 9.18[+ or -]0.04 19.01[+ or -]0.08 14.06[+ or -]0.03 72 10.12[+ or -]0.03 22.15[+ or -]0.03 15.04[+ or -]0.07 (*) Significantly different p<0.01 (SD): Standard deviation
The cells were palced in a 96 well plate forthe antiproliferative experiment at 30,000 cells/well; and to determine the apoptotic index, the cells were seeded in 12 well plate at 200,000 cells per well.
It is, therefore, suggested, that a detailed study with higher number of patients be commissioned, so that the exact role of apoptotic factors and caspases be delineated clearly.
Moreover, MCF-7 cells treated with 10, 20, and 80 xM atorvastatin revealed condensed nuclei of apoptotic cells.
Apoptotic and non-apoptotic programmed cardiomyocyte death in ventricular remodelling.
As illustrated in the Figure 1b, SRM 2786 significantly increases the percentage share of apoptotic cells at the dose of 31.25-500 [micro]g/ml (p < 0.05).
Targeting NF-kappa B in association with chemotherapy strongly enhances the apoptotic potential of the chemotherapy and is associated with suppression of angiogenesis and metastases in human prostate cancer.
Initiation of caspase-3 activation is known to be a crucial incident of apoptosis in the brain.10 It is well known that change in caspase-3 level in the brain changes the brain plasticity.11 It has been reported recently that metformin can interfere the apoptotic pathway by hindering the release of mitochondrial cytochrome-c and preventing neuronal loss and death.12 The clinical results are of great interest that by using metformin for both anti-hyperglycemic function and potent agent for the treatment of neurodegenerative disorders.

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