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Intestinal Stem Cells (intestinal + stem_cell)
Selected AbstractsDegenerative and regenerative processes involved in midgut pseudotumor formation in the stick insect (Carausius morosus)JOURNAL OF MORPHOLOGY, Issue 12 2009Paul Hoffmann Abstract Spontaneous and experimentally induced pseudotumor formation in Carausius morosus impairs the midgut tissue homeostasis. Spontaneous pseudotumor formation begins by the break down of a single or a small group of columnar cells (CCs) and is followed by the degeneration of neighboring CCs. There are not only marked similarities but also decisive differences between normal dying CCs in healthy specimens and the degeneration of CCs leading to pseudotumors: in both cases, the apical cell parts with the nucleus are extruded into the midgut lumen, but only during of pseudotumor formation an "amorphous substance" originates from the basal parts of the CCs. Hemocytes are attracted to this substance and form a nodule-like aggregation, which is responsible for the phenotype of pseudotumors. Pseudotumor infestation has also an impact on the midgut nidi, which consist of an intestinal stem cell and several CC progenitor cells. In healthy specimens only one progenitor cell per nidus differentiates at a time, but, several to all progenitor cells differentiate simultaneously in pseudotumor-infested specimens. Extirpation of the ingluvial ganglion in healthy specimens results in an immediate onset of pseudotumor formation and a dramatic acceleration of pseudotumor growth. Importantly, the ultrastructural characteristics of spontaneous and experimentally induced pseudotumors are identical. This supports the idea that the stomatogastric nervous system plays an integral role in the maintenance of midgut tissue homeostasis. J. Morphol., 2009. © 2009 Wiley-Liss, Inc. [source] Correlation between Musashi-1 and c-hairy-1 expression and cell proliferation activity in the developing intestine and stomach of both chicken and mouseDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 8 2005Rieko Asai Musashi-1 (Msi-1) is an RNA-binding protein that plays key roles in the maintenance of neural stem cell states and in their differentiation into neural cells. Msi-1 has also been proposed as a candidate marker gene of mammalian intestinal stem cells and their immediate lineages. In this study, we examined Msi-1 expression in the small intestine and the stomach of both chicken and mouse during embryonic, fetal and postnatal development. In addition, we analyzed the expression of c-hairy-1, a chicken homologue of mouse Hes1, and assessed the proliferative activity of the cells expressing both of these factors. Significantly, during the development of these digestive organs in both species Msi-1 expression showed dynamic changes, suggesting that it is important for digestive organ development, particularly for epithelial differentiation. Based on our observations of the expression patterns of Msi-1 and c-hairy-1 in the adult small intestine, we speculate that Msi-1 is also a stem cell marker of the chicken small intestinal epithelium. [source] Proliferation and differentiation of intestinal stem cells during metamorphosis of the red flour beetle, Tribolium castaneumDEVELOPMENTAL DYNAMICS, Issue 4 2008R. Parthasarathy Abstract The insect midgut epithelium is remodeled during larval-pupal metamorphosis when larval polyploid cells (LPCs) are replaced by the daughters of intestinal stem cells (ISCs). We characterized the proliferation of ISCs during midgut remodeling in the red flour beetle, Tribolium castaneum. Midgut remodeling is initiated at 96 hr after ecdysis into the final instar larval stage. Immunocytochemistry with bromodeoxyuridine and phospho-histone H3 antibodies showed that the ISCs are the progenitors of the pupal/adult midgut epithelium and they undergo proliferation and differentiation to form new midgut epithelium. In vitro midgut culture experiments revealed that 20-hydroxyecdysone (20E) in the absence of juvenile hormone induces proliferation of ISCs. RNA interference (RNAi) mediated silencing of ecdysone receptors (EcRA and EcRB) and ultraspiracle (USP) identified EcRA and USP but not EcRB as the proteins involved in 20E regulation of ISCs proliferation. These data show that the proliferation of ISCs is under both developmental and endocrine regulation. Developmental Dynamics 237:893,908, 2008. © 2008 Wiley-Liss, Inc. [source] The role of NO synthases in arginine-dependent small intestinal and colonic carcinogenesisMOLECULAR CARCINOGENESIS, Issue 2 2006Hagit F. Yerushalmi Abstract Arginine is catabolized by NOS2 and other nitric oxide synthases to form nitric oxide. We evaluated the roles of dietary arginine and Nos2 in Apc -dependent intestinal tumorigenesis in Min mice with and without a functional Nos2 gene. NOS2 protein was expressed only in intestinal tissues of ApcMin/+Nos2+/+ mice. NOS3 expression was higher in intestinal tissues of mice lacking Nos2, mainly in the small intestine. When diet was supplemented with arginine (0.2% and 2% in drinking water), lack of Nos2 results in decreased tumorigenesis in both small intestine and colon. In Nos2 knockout mice, supplemental arginine (up to 2%) caused a decrease in small intestinal tumor number and size. The arginine-dependent decrease was associated with an increase in nitrotyrosine formation and apoptosis in the region of intestinal stem cells. Mice expressing Nos2 did not show these changes. These mice did, however, show an arginine-dependent increase in colon tumor number and incidence, while no effect on apoptosis was seen. These changes were associated with increased nitrotyrosine formation in epithelial cells. Mice lacking Nos2 did not show changes in tumorigenesis or nitrotyrosine formation, while demonstrating an arginine-dependent increase in apoptosis. These data suggest that Nos2 and dietary arginine have significant effects on intestinal and colonic tumorigenesis in Min mice. In both tissues, loss of Nos2 is associated with decreased tumorigenesis when mice are supplemented with dietary arginine. In the small intestine, Nos2 prevents the arginine-induced decrease in tumor number and size, which is associated with NOS3 expression and increased apoptosis. In the colon, Nos2 is required for the arginine-induced increase in tumor number and incidence. © 2005 Wiley-Liss, Inc. [source] Protective effect of phlorotannin components phloroglucinol and eckol on radiation-induced intestinal injury in micePHYTOTHERAPY RESEARCH, Issue 2 2008Changjong Moon Abstract Components of phlorotannin, which were extracted from Ecklonia species, have been reported to have in vitro radioprotective and antioxidative effects. The radioprotective effects of two of the components of phlorotannin, phloroglucinol and eckol, in intestinal stem cells were examined by evaluating their effects on jejunal crypt survival and apoptosis in gamma-irradiated mice. Pretreating the mice (i.p. 20 mg/kg of body weight at 12 and 36 h before irradiation) prior to irradiation with either phloroglucinol or eckol significantly improved the survival of the jejunal crypt (p < 0.001 and p < 0.01 vs irradiation controls at 3.5 days after 8 Gy irradiation, respectively). The administration of phloroglucinol and eckol prior to irradiation protected the intestinal crypts from radiation-induced apoptosis (p < 0.05 vs irradiation controls at 12 h after 1 Gy irradiation). Although the mechanism for this inhibitory effect remains unknown, these results showed that phloroglucinol and eckol might be useful radioprotectors that can defend intestinal stem cells against the oxidative damage caused by gamma-irradiation. Copyright © 2007 John Wiley & Sons, Ltd. [source] The stem cells of small intestinal crypts: where are they?CELL PROLIFERATION, Issue 6 2009C. S. Potten Recently, there has been resurgence of interest in the question of small intestinal stem cells, their precise location and numbers in the crypts. In this article, we attempt to re-assess the data, including historical information often omitted in recent studies on the subject. The conclusion we draw is that the evidence supports the concept that active murine small intestinal stem cells in steady state are few in number and are proliferative. There are two evolving, but divergent views on their location (which may be more related to scope of capability and reversibility than to location) several lineage labelling and stem cell self-renewing studies (based on Lgr5 expression) suggest a location intercalated between the Paneth cells (crypt base columnar cells (CBCCs)), or classical cell kinetic, label-retention and radiobiological evidence plus other recent studies, pointing to a location four cell positions luminally from the base of the crypt The latter is supported by recent lineage labelling of Bmi-1-expressing cells and by studies on expression of Wip-1 phosphatase. The situation in the human small intestine remains unclear, but recent mtDNA mutation studies suggest that the stem cells in humans are also located above the Paneth cell zone. There could be a distinct and as yet undiscovered relationship between these observed traits, with stem cell properties both in cells of the crypt base and those at cell position 4. [source] | |||||||||||||