scholarly journals Retinoid metabolism in the rat small intestine

2005 ◽  
Vol 93 (1) ◽  
pp. 59-63 ◽  
Author(s):  
Simmy Thomas ◽  
Ramamoorthy Prabhu ◽  
Kunissery A. Balasubramanian
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Epithelial Cell ◽  
Intestinal Epithelium ◽  
Reductase Activity ◽  
High Rate ◽  
Metabolizing Enzymes ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Differentiation And Proliferation

Vitamin A (retinol) is essential for epithelial cell growth, differentiation and proliferation. The absorption of retinol occurs in the small intestine, and the metabolism of this vitamin is not well studied in this organ. The intestinal epithelium has a high rate of cell proliferation and differentiation, and the present study looked at the level of retinoids and metabolizing enzymes involved in their interconversion along the villus–crypt axis under normal conditions. Intestine was removed from control rats, and enterocytes at various stages of maturation and differentiation were quantified by the metal chelation method. Using HPLC, various retinoid concentrations in the cell homogenate and the metabolizing enzymes in the cytosol were quantified. The proliferating crypt cells were found to have a higher level of retinoic acid as well as of the enzymes involved in its formation, such as retinaldehyde oxidase and retinol dehydrogenase, compared with the villus cells, suggesting a possible role for this compound in intestinal epithelial cell proliferation and differentiation. The high level of retinol and high retinaldehyde reductase activity in the villus cells suggest the important role played by this enzyme in the conversion of dietary β-carotene to retinol via retinaldehyde. In summary, this study has given for the first time a detailed analysis of the retinoid levels and metabolizing enzymes in different cell populations in the rat small intestinal epithelium.

scholarly journals Silencing hyperoxia-induced C/EBPα in neonatal mice improves lung architecture via enhanced proliferation of alveolar epithelial cells

2011 ◽  
Vol 301 (2) ◽  
pp. L187-L196 ◽  
Author(s):  
Guang Yang ◽  
Maurice D. Hinson ◽  
Jessica E. Bordner ◽  
Qing S. Lin ◽  
Amal P. Fernando ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Type I ◽  
Epithelial Cell Proliferation ◽  
Newborn Mice ◽  
Alveolar Epithelial ◽  
Lung Morphology ◽  
Cell Proliferation And Differentiation ◽  
Hyperoxic Exposure ◽  
Proliferation And Differentiation

Postnatal lung development requires proliferation and differentiation of specific cell types at precise times to promote proper alveolar formation. Hyperoxic exposure can disrupt alveolarization by inhibiting cell growth; however, it is not fully understood how this is mediated. The transcription factor CCAAT/enhancer binding protein-α (C/EBPα) is highly expressed in the lung and plays a role in cell proliferation and differentiation in many tissues. After 72 h of hyperoxia, C/EBPα expression was significantly enhanced in the lungs of newborn mice. The increased C/EBPα protein was predominantly located in alveolar type II cells. Silencing of C/EBPα with a transpulmonary injection of C/EBPα small interfering RNA (siRNA) prior to hyperoxic exposure reduced expression of markers of type I cell and differentiation typically observed after hyperoxia but did not rescue the altered lung morphology at 72 h. Nevertheless, when C/EBPα hyperoxia-exposed siRNA-injected mice were allowed to recover for 2 wk in room air, lung epithelial cell proliferation was increased and lung morphology was restored compared with hyperoxia-exposed control siRNA-injected mice. These data suggest that C/EBPα is an important regulator of postnatal alveolar epithelial cell proliferation and differentiation during injury and repair.

The Effect of LRAP on Enamel Organ Epithelial Cell Differentiation

2007 ◽  
Vol 86 (11) ◽  
pp. 1095-1099 ◽  
Author(s):  
T.Q. Le ◽  
Y. Zhang ◽  
W. Li ◽  
P.K. DenBesten
Keyword(s):  
Cell Proliferation ◽  
Cell Differentiation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Enamel Organ ◽  
E Coli ◽  
Cell Proliferation And Differentiation ◽  
Human Enamel ◽  
Proliferation And Differentiation ◽  
Alternatively Spliced

Leucine-rich amelogenin peptide (LRAP) is an alternatively spliced amelogenin found in the developing enamel organ. LRAP functions to regulate the development of mesenchymal-derived cells; however, its effect on cells of the enamel organ remains unclear. The hypothesis tested in this study is that LRAP also regulates human enamel organ epithelial cells. Recombinant human LRAP (rH58) was synthesized in E. coli, purified, and exogenously added to cultures of human primary enamel epithelial cells, which were analyzed for changes in cell proliferation and differentiation. rH58 had no effect on cell proliferation, but altered enamel epithelial cell morphology, resulting in larger, more rounded cells. Immunofluorescence showed that rH58 treatment increased amelogenin synthesis, but down-regulated Notch1 expression in enamel epithelial cells. LAMP-1, a membrane receptor for LRAP in mesenchymal cells, was identified and was up-regulated in the presence of rH58. These results suggest that rH58 promotes differentiation of human enamel organ epithelial cells.

Foxl1-deficient mice exhibit aberrant epithelial cell positioning resulting from dysregulated EphB/EphrinB expression in the small intestine

2006 ◽  
Vol 291 (1) ◽  
pp. G163-G170 ◽  
Author(s):  
Masumi Takano-Maruyama ◽  
Koji Hase ◽  
Hiroshi Fukamachi ◽  
Yasutaka Kato ◽  
Haruhiko Koseki ◽  
...  
Keyword(s):  
Small Intestine ◽  
Epithelial Cell ◽  
Paneth Cell ◽  
Real Time Quantitative Pcr ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Cell Positioning ◽  
Winged Helix Transcription Factor ◽  
Deficient Mice

The winged helix transcription factor Foxl1, expressed in the gut mesenchyme, regulates epithelial cell proliferation and differentiation through the Wnt/β-catenin pathway. To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice. The small intestine of Foxl1-deficient mice manifested aberrant crypt structure, including widely distributed Paneth cells, which coincided with the ectopic and increased expression of EphB2 and EphB3, which are key regulators of epithelial cell positioning. Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. Such an increase in Wnt expression was remarkable in the mesenchyme, where the aberrant Paneth cell positioning was observed by in situ hybridization. Foxl1 plays an important role in the maintenance of crypt architecture and epithelial cell positioning through the mesenchymal-epithelial interaction in the small intestine. This interaction is essential for the normal regulation of the Wnt/β-catenin pathway and the subsequent EphB/EphrinB expression.

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