Dysregulation of intestinal crypt cell proliferation and villus cell migration in mice lacking Krüppel-like factor 9

2007 ◽  
Vol 292 (6) ◽  
pp. G1757-G1769 ◽  
Author(s):  
Frank A. Simmen ◽  
Rijin Xiao ◽  
Michael C. Velarde ◽  
Rachel D. Nicholson ◽  
Margaret T. Bowman ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Smooth Muscle ◽  
Cell Migration ◽  
Cell Fate ◽  
Crypt Cell ◽  
Cell Renewal ◽  
Crypt Cell Proliferation ◽  
Villus Cell ◽  
Null Mutant Mice ◽  
Intestinal Crypt Cell

Krüppel-like factor 9 (Klf9), a zinc-finger transcription factor, is implicated in the control of cell proliferation, cell differentiation, and cell fate. Using Klf9-null mutant mice, we have investigated the involvement of Klf9 in intestine crypt-villus cell renewal and lineage determination. We report the predominant expression of Klf9 gene in small and large intestine smooth muscle (muscularis externa). Jejunums null for Klf9 have shorter villi, reduced crypt stem/transit cell proliferation, and altered lineage determination as indicated by decreased and increased numbers of goblet and Paneth cells, respectively. A stimulatory role for Klf9 in villus cell migration was demonstrated by bromodeoxyuridine labeling. Results suggest that Klf9 controls the elaboration, from intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination and of villus cell migration.

scholarly journals The Effect of Ischemic Villus Cell Damage on Crypt Cell Proliferation in the Small Intestine

1976 ◽  
Vol 71 (5) ◽  
pp. 786-792 ◽  
Author(s):  
R.P.C. Rijke ◽  
W.R. Hanson ◽  
H.M. Plaisier ◽  
J.W. Osborne
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Cell Damage ◽  
Crypt Cell ◽  
Crypt Cell Proliferation ◽  
Villus Cell

A growth-stimulating activity derived from the proximal small intestine is associated with an adaptive response

1990 ◽  
Vol 68 (5) ◽  
pp. 646-649 ◽  
Author(s):  
V. L. Grey ◽  
C. L. Morin
Keyword(s):  
Cell Proliferation ◽  
Small Intestine ◽  
Thymidine Kinase ◽  
Kinase Activity ◽  
Crypt Cell ◽  
General Mechanism ◽  
Cell Renewal ◽  
Thymidine Kinase Activity ◽  
Crypt Cell Proliferation ◽  
Proximal Intestine

Luminal nutrition is important for the maintenance of small intestinal structure and function. The equilibrium between crypt cell production and villous cell loss in the mucosal epithelium of the small intestine is altered under certain conditions such as after a small bowel resection. Immediately after resection, there is a marked increase in crypt cell proliferation giving rise to an adaptive hyperplasia in the remnant intestine and for this response luminal nutrition is a critical factor. We have previously demonstrated the presence of a growth-stimulating (GS) activity in a heat-stable acidic extract of the rat proximal intestine 24, 48, and 96 h after resection, which is coincidental with an increase in crypt cell proliferation as measured by thymidine kinase activity. Eight days after resection when the GS activity is no longer detectable, the thymidine kinase activity returns to control values. The molecular weights of the peptides associated with this GS activity are 4500 and 1500, as determined by Sephadex gel filtration. Of note is that the oral intake of food is necessary for the appearance of the GS activity postoperatively. The presence of the GS activity has also been demonstrated upon refeeding after a fast, as well as at weaning in the rat, two physiological situations known to be associated with increased proliferation in the small intestine. This GS activity in the proximal intestine first detected in the resection model may represent a general mechanism by which food controls the cell renewal pattern of the small intestine.Key words: stimulating activity, proximal intestine, adaptation.

Gut Hypertrophy After Gastric Bypass Is Associated With Increased Glucagon-Like Peptide 2 and Intestinal Crypt Cell Proliferation

2010 ◽  
Vol 252 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Carel W. le Roux ◽  
Cynthia Borg ◽  
Katharina Wallis ◽  
Royce P. Vincent ◽  
Marco Bueter ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gastric Bypass ◽  
Crypt Cell ◽  
Intestinal Crypt ◽  
Crypt Cell Proliferation ◽  
Glucagon Like Peptide ◽  
Intestinal Crypt Cell

scholarly journals An Active Fraction of Trillium tschonoskii Promotes the Regeneration of Intestinal Epithelial Cells After Irradiation

2021 ◽  
Vol 9 ◽  
Author(s):  
Feiling Song ◽  
Sihan Wang ◽  
Xu Pang ◽  
Zeng Fan ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Crypt Cell ◽  
Oral Drug ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Active Fraction ◽  
Intestinal Crypt ◽  
Crypt Cell Proliferation ◽  
Trillium Tschonoskii ◽  
Intestinal Crypt Cell

Despite significant scientific advances toward the development of safe and effective radiation countermeasures, no drug has been approved for use in the clinic for prevention or treatment of radiation-induced acute gastrointestinal syndrome (AGS). Thus, there is an urgent need to develop potential drugs to accelerate the repair of injured intestinal tissue. In this study, we investigated that whether some fractions of Traditional Chinese Medicine (TCM) have the ability to regulate intestinal crypt cell proliferation and promotes crypt regeneration after radiation. By screening the different supplements from a TCM library, we found that an active fraction of the rhizomes of Trillium tschonoskii Maxim (TT), TT-2, strongly increased the colony-forming ability of irradiated rat intestinal epithelial cell line 6 (IEC-6) cells. TT-2 significantly promoted the proliferation and inhibited the apoptosis of irradiated IEC-6 cells. Furthermore, in a small intestinal organoid radiation model, TT-2 promoted irradiated intestinal organoid growth and increased Lgr5+ intestinal stem cell (ICS) numbers. More importantly, the oral administration of TT-2 remarkably enhanced intestinal crypt cell proliferation and promoted the repair of the intestinal epithelium of mice after abdominal irradiation (ABI). Mechanistically, TT-2 remarkably activated the expression of ICS-associated and proliferation-promoting genes and inhibited apoptosis-related gene expression. Our data indicate that active fraction of TT can be developed into a potential oral drug for improving the regeneration and repair of intestinal epithelia that have intestinal radiation damage.

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