Further evidence of species variation in mechanisms of epithelial cell loss in mammalian small intestine: ultrastructural studies on the reindeer ( Rangifer tarandus ) and seal ( Phoca groenlandica )

1998 ◽  
Vol 291 (3) ◽  
pp. 513-523 ◽  
Author(s):  
R. Myklebust ◽  
T. M. Mayhew
Gut ◽  
2014 ◽  
Vol 63 (Suppl 1) ◽  
pp. A157.1-A157 ◽  
Author(s):  
K Hughes ◽  
C Alcon-Giner ◽  
M Lawson ◽  
K McCoy ◽  
A Macpherson ◽  
...  

2021 ◽  
Vol 2 (4) ◽  
pp. 100963
Author(s):  
Sebastian Wurster ◽  
Oscar E. Ruiz ◽  
Alexander M. Tatara ◽  
Dimitrios P. Kontoyiannis ◽  
George T. Eisenhoffer

2020 ◽  
Vol 34 (7) ◽  
pp. 9450-9465
Author(s):  
Ayano Iwaki ◽  
Kenta Moriwaki ◽  
Tomoaki Sobajima ◽  
Manabu Taniguchi ◽  
Shin‐ichiro Yoshimura ◽  
...  

1997 ◽  
Vol 272 (6) ◽  
pp. L1031-L1045 ◽  
Author(s):  
B. D. Uhal

The type II alveolar epithelial cell has important metabolic and biosynthetic functions but also serves as the stem cell of the alveolar epithelium. Much of the evidence underlying this premise was obtained before 1980 and provided the basis for a working model that has not been reconsidered for more than fifteen years. With the exceptions to be discussed below, little evidence has accumulated in the interim to suggest that the model requires significant alteration. Important questions remain unanswered, however, and some components of the model need to be supplemented, particularly in light of recent investigations that have provided insights not possible in earlier work. In particular, in vitro studies have suggested that the relationship between the parent type II cell and its progeny may not be as straightforward as originally thought. In addition, the rate of epithelial cell loss was recognized long ago to be an important factor in the regulation of this system, but its kinetics and mechanisms have received little attention. These and other unresolved issues are critical to our understanding of the homeostasis of the alveolar epithelium under normal and pathological conditions.


1993 ◽  
Vol 264 (5) ◽  
pp. G921-G927 ◽  
Author(s):  
G. Cepinskas ◽  
R. D. Specian ◽  
P. R. Kvietys

Gastric mucosal injury induced by strong irritants can be dramatically reduced by pretreating the mucosa with mild forms of the same irritant. This phenomenon has been termed "adaptive cytoprotection." The aim of the present study was to use in vivo and in vitro approaches to study adaptive cytoprotection in the small intestine using physiologically relevant concentrations of oleic acid. Anesthetized rats were instrumented for perfusion of the proximal jejunum with 10 or 40 mM oleic acid (in 20 mM sodium taurocholate). Mucosal epithelial integrity was continuously monitored by measuring the blood-to-lumen clearance of 51Cr-labeled EDTA. Perfusion of the lumen with 40 mM oleic acid produced a 10-fold increase in 51Cr-EDTA clearance, which was not affected by a previous perfusion with 10 mM oleic acid, i.e., no adaptive cytoprotection. In another series of experiments, oleic acid was placed in the lumen rather than perfused, and mucosal epithelial integrity was assessed histologically. Intraluminal placement of 10 mM oleic acid resulted in the generation of a mucus layer over the epithelium. Subsequent placement of 40 mM oleic acid did not produce significant epithelial cell injury, i.e., adaptive cytoprotection. In in vitro studies, mucin (1, 5, and 10 mg/ml) was layered over confluent monolayers of Caco-2 cells prior to addition of 2 mM oleic acid in 4 mM sodium taurocholate. The epithelial cell injury induced by oleic acid was inhibited by mucin in a dose-dependent manner. Further studies indicate that mucin does not prevent, but simply delays, the onset of cell injury.(ABSTRACT TRUNCATED AT 250 WORDS)


1970 ◽  
Vol 283 (23) ◽  
pp. 1264-1271 ◽  
Author(s):  
Jerry D. Gardner ◽  
Michael S. Brown ◽  
Leonard Laster

1982 ◽  
Vol 203 (1) ◽  
pp. 129-146 ◽  
Author(s):  
J�ri Johannes Rumessen ◽  
Lars Thuneberg ◽  
Hanne Birte Mikkelsen

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