Development of the structural components of the brush border in absorptive cells of the chick intestine

1979 ◽  
Vol 204 (3) ◽  
Author(s):  
Carolyn Chambers ◽  
RobertD. Grey
1970 ◽  
Vol 44 (1) ◽  
pp. 151-171 ◽  
Author(s):  
Mary A. Bonneville ◽  
Melvyn Weinstock

The differentiation of the brush border which makes up the apical free surface of intestinal absorptive cells has been studied by electron microscopy. Specimens of Xenopus small intestine were fixed at various stages during metamorphosis, the time when a new intestinal epithelium forms. The interpretation of details described herein emphasizes the role of "surface-forming" vesicles. These vesicles are thought to provide membrane both for the initial expansion of the apical surface and for the later elongation of the microvilli. The latter are believed to be "molded" around filamentous cores that appear early in differentiation. The cores are attached to the apical membrane and extend vertically into the supranuclear cytoplasm. This interpretation rests chiefly on (a) the resemblance, both in morphology and in staining properties with colloidal thorium, between the membrane that limits the vesicles and that which limits the microvilli and (b) the distribution and time of appearance of the vesicles with respect to development of the microvilli. According to this view, the specific properties of surface membrane reside in preformed units that arise within the supranuclear cytoplasm. This morphogenetic process probably involves participation of the Golgi region as the site where the complex macromolecular architecture of the cell surface is assembled.


2003 ◽  
Vol 67 (11) ◽  
pp. 2381-2387 ◽  
Author(s):  
Ikuo IKEDA ◽  
Kosuke MITSUI ◽  
Ryosuke MATSUOKA ◽  
Tadateru HAMADA ◽  
Sachiko IMABAYASHI ◽  
...  

2020 ◽  
Author(s):  
Barun Das ◽  
Kevin Okamoto ◽  
John Rabalais ◽  
Jocelyn Young ◽  
Kim E. Barrett ◽  
...  

AbstractBackground & AimsCongenital Tufting Enteropathy (CTE) is an intractable diarrheal disease of infancy caused by mutation of Epithelial Cell Adhesion Molecule (EpCAM). The cellular and molecular basis of CTE pathology has been elusive. We hypothesized that the loss of EpCAM in CTE results in altered lineage differentiation and defects in absorptive enterocytes thereby contributing to CTE pathogenesis.MethodsIntestine from CTE mice was evaluated for specific markers by RT-qPCR, western blotting and immunostaining. Body weight, blood glucose and intestinal enzyme activity were also investigated. A CTE enteroid model was used to assess whether the decreased census of secretory cells could be rescued.ResultsCTE mice exhibited alterations in brush-border function, disaccharidase activity and glucose absorption, potentially contributing to nutrient malabsorption and impaired weight gain. Altered cell differentiation in CTE mice led to decreased secretory cells and increased numbers of absorptive cells, though the absorptive enterocytes lacked key features, causing brush border malfunction. Further, treatment with Notch signaling inhibitor, DAPT, increased the numbers of major secretory cell types in CTE enteroids (Graphical abstract 1).ConclusionsAlterations in intestinal epithelial cell differentiation in CTE mice favor an increase in absorptive cells at the expense of secretory cells. Although the proportion of absorptive enterocytes is increased, they lack key functional properties. We conclude that these effects underlie pathogenic features of CTE such as malabsorption and diarrhea, and ultimately the failure to thrive seen in patients. The ability of DAPT to reverse aberrant differentiation suggests a possible therapeutic strategy.SynopsisA murine model of Congenital Tufting Enteropathy exhibits altered intestinal cell differentiation, leading to increased absorptive and decreased secretory cells, which can be reversed with DAPT. Absorptive enterocytes in these mice are also dysfunctional, contributing to disease pathogenesis.Graphical Abstract


1971 ◽  
Vol 233 (3) ◽  
pp. 550-561 ◽  
Author(s):  
Sander J. Robins ◽  
Donald M. Small ◽  
Jerry S. Trier ◽  
Robert M. Donaldson

1982 ◽  
Vol 9 (4) ◽  
pp. 424
Author(s):  
B.A.A. Scheven ◽  
J. Blok ◽  
A.A. Mulder-Stapel ◽  
L.A. Ginsel

1971 ◽  
Vol 223 (3) ◽  
pp. 550-561
Author(s):  
Sander J. Robins ◽  
Donald M. Small ◽  
Jerry S. Trier ◽  
Robert M. Donaldson

Author(s):  
John H. L. Watson ◽  
C. N. Sun

That the etiology of Whipple's disease could be bacterial was first suggested from electron micrographs in 1960. Evidence for binary fission of the bacteria, their phagocytosis by histiocytes in the lamina propria, their occurrence between and within the cells of the epithelium and on the brush border of the lumen were reported later. Scanning electron microscopy has been applied by us in an attempt to confirm the earlier observations by the new technique and to describe the bacterium further. Both transmission and scanning electron microscopy have been used concurrently to study the same biopsy specimens, and transmission observations have been used to confirm those made by scanning.The locations of the brush borders, the columnar epithelial cells, the basement membrane and the lamina propria beneath it were each easily identified by scanning electron microscopy. The lamina propria was completely filled with the wiener-shaped bacteria, Fig. 1.


Author(s):  
A. J. Tousimis

The elemental composition of amino acids is similar to that of the major structural components of the epithelial cells of the small intestine and other tissues. Therefore, their subcellular localization and concentration measurements are not possible by x-ray microanalysis. Radioactive isotope labeling: I131-tyrosine, Se75-methionine and S35-methionine have been successfully employed in numerous absorption and transport studies. The latter two have been utilized both in vitro and vivo, with similar results in the hamster and human small intestine. Non-radioactive Selenomethionine, since its absorption/transport behavior is assumed to be the same as that of Se75- methionine and S75-methionine could serve as a compound tracer for this amino acid.


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