Apoptosis morphology

Williams et al. (2001) NO-NSAIDS Human colon cancer (HT2) Proliferation (PCNA) apoptosis (morphology and flow cytometry) Lowest IC50 1 [xM (NCX 4040) ... 

Telomerase Ribonucleoprotein Suppression of telomerase activity inhibition of cell proliferation change in morphology induction of apoptosis... 

Active caspases 8, 9 and 10 can convert caspase-3, the most abundant effector caspase from its pro-form to its active cleaved form. Cleavage of a number of different substrates by caspase-3 and also by caspase-6 and -7 which are two other executioner caspases besides caspase-3 then results in the typical morphology which is characteristic of apoptosis. Yet, the activation of caspase-3 and also of caspase-9 can be counteracted by IAPs, so called inhibitor of apoptosis proteins. However, concomitantly with cytochrome C also other proteins are released from mitochondria, including Smac/DIABLO. Smac/DIABLO and potentially other factors can interact with IAPs and thereby neutralize their caspase-inhibitory activity. This releases the breaks on the cell death program and allows apoptosis to ensue. 

Apoptosis is known as programmed cell death and represents also a control mechanism within the cell that reacts to the changes in its environment. This active cellular death process is characterized by distinctive morphological changes... 

Another morphological assay of apoptosis is done with acridine orange, a nuclear staining that reveals chromatin condensation under light and fluorescent microscope. 

Annexin V PT UOS staining is another procedure which allows to label the cells by allowing the observation of the morphological features of apoptosis. 

Visual imaging of cell population in vitro) using low signal-to-noise ratio phase contrast microscopy can enable systematic monitoring measurements of cell quality, development and apoptosis. In the present study, microscopic evaluations as seen in Fig. 11 did not reveal any significant alteration in cellular morphology upto 1000 ng/ml. 

When embryos treated as described above were left to develop, they reached the onset of gastrulation with no visible changes in morphology compared to untreated embryos. However, as they reached stage 10.5, the embryos underwent rapid and synchronous apoptosis. This rapid cell death had striking morphological characteristics individual cells from the embryo lost their cohesion and adhesiveness and rapidly lysed so that few or no intact cells were found in each embryo 20 minutes following the onset of apoptosis (Fig. IB). 

Many of the morphological and biochemical changes that occur in cells that die by necrosis are very different from those that occur in apoptosis 604... 

The morphological and biochemical characteristics of apoptosis are not always manifest in cells undergoing programmed cell death 612... 

Many of the morphological and biochemical changes that occur in cells that die by necrosis are very different from those that occur in apoptosis. During necrosis cells swell, mitochondria and endoplasmic reticulum lose their structure and become dysfunctional and the nuclear membrane becomes disrupted (Fig. 35-1). Necrotic death is independent of premitochondrial apoptotic proteins such as Bax, cytochrome c release and caspase activation. Necrosis is further distinguished from apoptosis by the fact that necrosis usually occurs as the result of a traumatic physical injury or stroke and cells die en masse, whereas apoptosis typically occurs in individual cells within a population of surviving neighbors. 

Slow-channel syndrome. Abnormally long-lived openings of mutant AChR channels result in prolonged endplate currents and potentials, which in turn elicit one or more repetitive muscle action potentials of lower amplitude that decrement. The morphologic consequences stem from prolonged activation of the AChR channel that causes cationic overload of the postsynaptic region - the endplate myopathy - with Ca2+ accumulation, destruction of the junctional folds, nuclear apoptosis, and vacuolar degeneration of the terminal. Some slow-channel mutations in the transmembrane domain of the AChR render the channel leaky by stabilization of the open state, which is populated even in the absence of ACh. Curiously, some slow-channel mutants can be opened by choline even at the concentrations that are normally present in serum. Quinidine, an open-channel blocker of the AchR, is used for therapy. 

Fig. 3.8 Protection of central nervous system (CNS) dopaminergic neurons from 6-OHDA-induced apoptosis by 8. Untreated top), 6-OHDA plus vehicle treatment middle) and 6-OHDA plus 250 pM 8 down) were stained with anti-tyrosine hydrolase antibody. The number of TH-immunoreactive cells clustered in dienecephalons was examined (arrows). After 250 pM 8 treatment, three of five animals showed a normal number of TH-immunoreactive cells with normal morphology (Reprinted from Beuerle, 2007. With friendly permission of Taylor Francis, http //www.informaworld.com)...

Tepper, A.D., Ruurs, P., Wiedmer, T, Sims, PJ., Borst, J. and van Bhtterswijk, W.J., 2000, Sphingomyelin hydrolysis to ceramide during the execution phase of apoptosis results from phospholipid scrambling and alters cell-surface morphology. J. Cell Biol., 150 F5-7. 

Capaccioh, S., and Orlandini, S. Z., 2000, Aponecrosis morphological and biochemical exploration of a syncretic process of cell death sharing apoptosis and necrosis, J. Cell Physiol. 182 41-49. 

In the previous paragraph changes occurring at the level of chromatin structure have been described. All these events cannot be considered from those taking place in the cytoplasm. Indeed, it is very likely that, albeit classical definition of apoptosis is based upon morphological criteria involving mainly the nucleus, cytoplasmic events are pivotal in determining the cellular fate after inadiation. 

---