scholarly journals Effect of cereal fibre source and processing on rectal epithelial cell proliferation

Gut ◽  
1997 ◽  
Vol 41 (2) ◽  
pp. 239-244 ◽  
Author(s):  
F A Macrae ◽  
D Kilias ◽  
L Selbie ◽  
M Abbott ◽  
K Sharpe ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Wheat Bran ◽  
Dietary Fibre ◽  
Nuclear Antigen ◽  
Epithelial Cell Proliferation ◽  
High Fat ◽  
Low Fat ◽  
Biopsy Specimens ◽  
Oat Bran

Background—Low fat and wheat bran interventions significantly reduced the growth of small to large adenomas and modestly suppressed rectal epithelial cell proliferation in the Australian Polyp Prevention Project.Aim—To study the effect of unprocessed wheat bran, unprocessed oat bran and processed wheat bran (Kellogg’s All Bran) on rectal epithelial cell proliferation.Patients—Twenty subjects with recent adenomas and a high fat background diet were recruited.Methods—Rectal biopsy specimens were taken at entry and at the end of three six-week periods of oat bran (64 g/day), wheat bran (25 g/day) and All Bran (38 g/day), all in association with a diet <25% energy as fat, in a randomised cross-over trial. Each of the bran supplements had a total of 11 g dietary fibre. The biopsy specimens were fixed in methacarn and stained immunohistochemically for presence of the proliferating cell nuclear antigen (PCNA). The kinetics used to measure proliferation were labelling index, whole distribution of labelled cells, and labelled cells in the top two-fifths of crypts using analysis of variance.Results—There were no significant differences in mean labelling indexes between the four diets or in the percentage of labelled cells in the top two-fifths (p=0.59), but activity in the top two-fifths of crypts was lowest with wheat bran. The mean (SD) labelling indexes were 2.23 (0.11)% for control, 2.13 (0.08)% for wheat bran, 2.19 (0.09)% for oat bran, and 2.12 (0.08)% for All Bran. The proportion in the top two-fifths of the crypts was 2.6 (0.6)% for control, 2.15 (0.5)% for wheat bran, 3.3 (0.9)% for oat bran, and 3.1 (0.9)% for All Bran. On analysis of whole distribution, there was no significant overall effect of diets but there was a difference between subjects. Analysis including total fibre intake also did not identify effects on proliferation.Conclusion—In this study of high risk subjects with initial high fat diets, dietary fibre in association with a low fat diet had no effect on rectal epithelial cell proliferation, although wheat bran had the greatest effect on percentage of labelled cells in the top two-fifths of crypts.

Cyclin kinase inhibitor p21CIP1/WAF1 limits interstitial cell proliferation following ureteric obstruction

1999 ◽  
Vol 277 (6) ◽  
pp. F948-F956 ◽  
Author(s):  
Jeremy Hughes ◽  
Paul Brown ◽  
Stuart J. Shankland
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Interstitial Cell ◽  
Tubular Epithelial Cell ◽  
Collagen I ◽  
Macrophage Infiltration ◽  
Nuclear Antigen ◽  
Epithelial Cell Proliferation ◽  
Ureteric Obstruction ◽  
Proliferation And Apoptosis

Tubulointerstitial renal injury induced by unilateral ureteric obstruction (UUO) is characterized by marked cell proliferation and apoptosis. Proliferation requires cell cycle transit that is positively regulated by cyclins and cyclin-dependent kinases (CDKs) and inhibited by the CIP/KIP family of cyclin-dependent kinase inhibitors (CKIs: p21, p27, and p57). We have shown that the absence of p27 results in markedly increased tubular epithelial cell proliferation and apoptosis following UUO (V. Ophascharoensuk, M. L. Fero, J. Hughes, J. M. Roberts, and S. J. Shankland. Nat. Med.4: 575–580, 1998). Since p21 mRNA is upregulated following UUO, we hypothesized that p21 would also serve to limit cell proliferation and apoptosis. We performed UUO in p21 +/+ and p21 −/− mice. Cell proliferation [bromodeoxyuridine (BrdU), proliferating cell nuclear antigen (PCNA)], apoptosis [terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method], interstitial myofibroblast accumulation (actin), macrophage infiltration (F4/80), and collagen I expression were quantified at days 3, 7, and 14. In contrast to p27 −/− mice, there was no difference in tubular epithelial cell proliferation or apoptosis between p21 −/− and p21 +/+ mice at any time point. However, interstitial cell proliferation at day 3 was significantly increased in p21 −/− mice [BrdU, 40.7 ± 1.9 cells/high-power field (cells/hpf) vs. 28.8 ± 2, P< 0.005], although, interestingly, no difference was seen in interstitial cell apoptosis. Actin/BrdU double staining demonstrated increased interstitial myofibroblast proliferation at day 3 in p21 −/− animals (10 ± 0.12 vs. 5.8 ± 0.11 cells/hpf, P < 0.05), which was followed by increased myofibroblast accumulation at day 7 in p21 −/− mice. No differences were detected in interstitial macrophage infiltration, collagen I deposition or transforming growth factor-β1 mRNA (in situ hybridization) expression. In conclusion p21, unlike p27, is not essential for the regulation of tubular epithelial cell proliferation and apoptosis following UUO, but p21 levels do serve to limit the magnitude of the early myofibroblast proliferation. This study demonstrates a differential role for the CKI p21 and p27 in this model.

Proliferation and repair of guinea pig tracheal epithelium after neuropeptide depletion and injury in vivo

1997 ◽  
Vol 273 (6) ◽  
pp. L1235-L1241 ◽  
Author(s):  
John S. Kim ◽  
Valerie S. McKinnis ◽  
Kimberly Adams ◽  
Steven R. White
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Mucosal Injury ◽  
Nuclear Antigen ◽  
Airway Epithelial ◽  
Epithelial Cell Proliferation ◽  
Injury Site ◽  
And Migration

Neuropeptides stimulate airway epithelial cell proliferation and migration in vitro, but the role of neuropeptides in the repair of the epithelium after injury in vivo is not clear. We studied epithelial proliferation and repair in 83 male Hartley guinea pigs. Animals received capsaicin weekly for 3 wk to deplete airway neuropeptides. One week later, the dorsal aspect of the trachea was injured with a metal stylette. Animals were killed 1 h to 1 wk later, after which epithelial cell proliferation was assessed for the presence of proliferating cell nuclear antigen (PCNA). PCNA labeling was <3% in noninjured animals. PCNA labeling increased substantially in the first 72 h after injury in control animals but was significantly decreased in capsaicin-treated animals within and adjacent to the site of injury. PCNA labeling increased opposite to the injury site in both control and capsaicin animals over the first 72 h. We conclude that neuropeptide depletion significantly attenuates both epithelial cell proliferation and repair in the first 72 h after mechanical injury to the trachea. However, neuropeptide depletion did not slow the ultimate repair of tracheal mucosal injury. Proliferation of epithelial cells in response to injury occurs throughout the airway, even away from the injury site.

Effects of Dietary Wheat Bran Fiber on Rectal Epithelial Cell Proliferation in Patients With Research for Colorectal Cancers

1990 ◽  
Vol 82 (15) ◽  
pp. 1280-1285 ◽  
Author(s):  
D. S. Alberts ◽  
J. Einspahr ◽  
S. Rees-McGee ◽  
P. Ramanujam ◽  
M. K. Buller ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Wheat Bran ◽  
Colorectal Cancers ◽  
Epithelial Cell Proliferation

scholarly journals Modulation of Abnormal Colonic Epithelial Cell Proliferation and Differentiation by Low-Fat Dairy Foods

JAMA ◽  
1998 ◽  
Vol 280 (12) ◽  
pp. 1074 ◽  
Author(s):  
Peter R. Holt ◽  
Evren O. Atillasoy ◽  
Jody Gilman ◽  
Janet Guss ◽  
Steven F. Moss ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cell Proliferation ◽  
Colonic Epithelial Cell ◽  
Low Fat ◽  
Dairy Foods ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

scholarly journals Progesterone Inhibits the Estrogen-Induced Phosphoinositide 3-Kinase→AKT→GSK-3β→Cyclin D1→pRB Pathway to Block Uterine Epithelial Cell Proliferation

2005 ◽  
Vol 19 (8) ◽  
pp. 1978-1990 ◽  
Author(s):  
Bo Chen ◽  
Haiyan Pan ◽  
Liyin Zhu ◽  
Yan Deng ◽  
Jeffrey W. Pollard
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Epithelial Cell ◽  
Cyclin D1 ◽  
Nuclear Accumulation ◽  
Nuclear Antigen ◽  
Epithelial Cell Proliferation ◽  
Uterine Epithelial Cell ◽  
Gsk 3Β ◽  
Phosphoinositide 3 Kinase

Abstract The mammalian cell cycle is regulated by the cyclin/cyclin-dependent kinase (CDK) phosphorylation of the retinoblastoma (pRB) family of proteins. Cyclin D1 with its CDK4/6 partners initiates the cell cycle and acts as the link between extracellular signals and the cell cycle machinery. Estradiol-17β (E2) stimulates uterine epithelial cell proliferation, a process that is completely inhibited by pretreatment with progesterone (P4). Previously, we identified cyclin D1 localization as a key point of regulation in these cells with E2 causing its nuclear accumulation and P4 retaining it in the cytoplasm with the resultant inhibition of pRB phosphorylation. Here we show that E2 stimulates phosphoinositide 3-kinase to activate phosphokinase B/AKT to effect an inhibitory phosphorylation of glycogen synthase kinase (GSK-3β). This pathway is suppressed by P4. Inhibition of the GSK-3β activity in P4-treated uteri by the specific inhibitor, LiCl, reversed the nuclear accumulation of cyclin D1 and in doing so, caused pRB phosphorylation and the induction of downstream genes, proliferating cell nuclear antigen and Ki67. Conversely, inhibition of phosphoinositide 3 kinase by LY294002 or Wortmanin reversed the E2-induced GSK-3β Ser9 inhibitory phosphorylation and blocked nuclear accumulation of cyclin D1. These data show the reciprocal actions of E2 and P4 on the phosphoinositide 3-kinase through to the GSK-3β pathway that in turn regulates cyclin D1 localization and cell cycle progression. These data reveal a novel signaling pathway that links E2 and P4 action to growth factor-mediated signaling in the uterus.

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