Epithelium apoptosis

Seagle, B.L. et al., Melanin photoprotection in the human retinal pigment epithelium and its correlation with light-induced cell apoptosis, Proc. Natl. Acad. Sci. USA, 102, 8978, 2005. 

Sumantran, VN, Zhang, R, Lee, DS, and Wicha, MS, 2000. Differential regulation of apoptosis in normal versus transformed mammary epithelium by lutein and retinoic acid. Cancer Epidemiol Biomarkers Prev 9, 257-263. 

T cell and cytokine regulation of enterocyte apoptosis may also be important in the expulsion of nematodes, in particular T. spiralis and T. muris, which inhabit an intracellular niche. Certainly an increase in the number of apoptotic cells within the epithelium is observed around the period of expulsion of T. muris in resistant mouse strains (D. Artis, C.S. Potten and R.K. Grencis, unpublished). Apoptosis of host enterocytes may dislodge the nematode or perhaps expose vital feeding organs to immune attack, and so enhance expulsion. Whether enterocyte apoptosis results from the burrowing action of the worms or a tissue repair mechanism, or is involved in expulsion, remains to be investigated. 

D1 (10,17S-docosatriene) from DHA using tandem liquid chromatography-photodiode array-electrospray ionization-tandem mass spectrometry (LC-PDA-ESI-MS-MS)-based lipidomic analysis have been documented in ischemic brain [4] and retinal pigment epithelium [5], This new lipid is called neuroprotectin D1 (1) because of its neuro-protectiveproperties in brain ischemia-reperfusion [4] and in oxidative stress-challenged retinal pigment epithelial cells [5] (2) because of its potent ability to inactivate proapoptotic signaling (see apoptosis, Ch. 35) [5] and (3) because it is the first identified neuroprotective mediator derived from DHA. 

Ikeda H, Suzuki Y, Suzuki M, Koike M, Tamura J, Tong J, Nomura M, Itoh G (1998) Apoptosis is a major mode of cell death caused by ischaemia and ischaemia/reperfusion injury to the rat intestinal epithelium. Gut 42(4) 530-537... 

Gilbert, S., Loranger, A., Daigle, N., and Marceau, N. (2001). Simple epithelium keratins 8 and 18 provide resistance to Fas-mediated apoptosis. The protection occurs through a receptor-targeting modulation./. Cell Biol. 154, 763-774. 

Experimentally, the macrocyclic trichothecenes satra-toxin G, isosatratoxin F, and roridin A have been shown to cause nasal and pulmonary toxicity when administered intranasally or intratracheally to mice. Intranasal exposure of satratoxin G and roridin A induced apoptosis of olfactory sensory neurons resulting in atrophy of the olfactory epithelium and olfactory nerve layer of the olfactory bulb in the frontal brain (Islam et al, 2006, 2007). Alveolar-type II cells and alveolar macrophages were injured following intratracheal instillation of isosatratoxin F or Stachybotrys spores with marked changes in surfactant synthesis and secretion (Rand et al, 2002). 

Ortiz A, LorzC, Catalan MP, DanoffTM, Yamasaki Y,EgidoJ, and Neilson EG. Expression of apoptosis regulatory proteins in tubular epithelium stressed in culture or following acute renal failure. Kidney International 57 969-981, 2000. 

Potential direct nephrotoxicity and the underlying molecular mechanisms were analyzed by in vitro studies in renal proximal tubular cells exposed to IFNa. IFNa was shown to induce apoptosis in LLC-PKl renal proximal tubular like epithelium [216]. Caspase-8, a key player in death receptor signaling and caspase-9 that is involved in mitochondrial apoptosis were shown to be activated in addition to caspase-3. Furthermore, IFNa induced a breakdown of the inner mitochondrial membrane potential, further implying mitochondrial signahng in IFNa-induced apoptosis. The deafh receptor pathway and the mitochondrial pathway appear to both be necessary for efficient executor caspase activation by IFNa. The apoptotic signaling pathways activated by IFNa in proximal tubular cells, thus, resemble the pathways induced by IFNa in melanoma and bladder carcinoma cells [217, 218]. In addition to caspase activation, nuclear condensation, DNA fragmentation and a delayed LDH release were observed. DNA fragmentation and LDH release were partially prevented by caspase inhibition. Thus, caspase-inde-pendent death is also possible - albeit delayed and at a reduced extent [216]. 

Lechner J, Malloth N, SeppIT, Beer B, Jennings P, and Pfaller W. IFNfalpha induces barrier destabilization and apoptosis in renal proximal tubular epithelium. Am J Physiol Cell Physiol, 2007. 

The involvement of milk protein-derived cytomodulatory peptides to determine the viability of cancer cells is a field of great interest. Commercial yoghurt starter cultures hydrolyse casein to produce bioactive peptides that control colon cell kinetics in vitro. Bioactive sequences of casein modulate cell viability in different human cell cultures. Peptides from an extract of Gouda cheese inhibited growth of leukemia cells even at 1 pmol/L [223]. They were able to induce apoptosis in the tumor cells. Cancer cells are more reactive to peptide-induced apoptosis than non-malignant cells [224]. Casein-derived peptides could have a role in the prevention of colon cancer by blocking proliferation of the epithelium and by... 

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