Purification and identification of intestinal mucosal cell proliferation-promoting peptides from Crassostrea hongkongensis

2018 ◽  
Vol 245 (3) ◽  
pp. 631-642
Author(s):  
Jianyu Pan ◽  
Peng Wan ◽  
Deke Chen ◽  
Hua Chen ◽  
Xin Chen ◽  
...  
2004 ◽  
Vol 91 (3) ◽  
pp. 357-365 ◽  
Author(s):  
Mahshid Dehghan-Kooshkghazi ◽  
John C. Mathers

Acarbose (Glucobay®; Bayer) is an α-glucosidase inhibitor used to treat diabetes and which may have a role in the prevention of type 2 diabetes. The present study investigated the effects of acarbose treatment on the site and extent of starch digestion, large-bowel fermentation and intestinal mucosal cell proliferation. Eighteen young male Wistar rats were fed ‘Westernised’ diets containing 0, 250 and 500mg acarbose/kg (six rats/diet) for 21d. For most variables measured, both acarbose doses had similar effects. Acarbose treatment suppressed starch digestion in the small bowel but there was compensatory salvage by bacterial fermentation in the large bowel. This was accompanied by a substantial hypertrophy of small- and large-bowel tissue and a consistent increase in crypt width along the intestine. Caecal total SCFA pool size was increased more than 4-fold, with even bigger increases for butyrate. These changes in butyrate were reflected in increased molar proportions of butyrate in blood from both the portal vein and heart. There was little effect of acarbose administration on crypt-cell proliferation (significant increase for mid-small intestine only). This is strong evidence against the hypothesis that increased fermentation and increased supply of butyrate enhances intestinal mucosal cell proliferation. In conclusion, apart from the increased faecal loss of starch, there was no evidence of adverse effects of acarbose on the aspects of large-bowel function investigated.


1998 ◽  
Vol 274 (5) ◽  
pp. G863-G870 ◽  
Author(s):  
Adhip P. N. Majumdar ◽  
James R. Goldenring

In Fischer 344 rats, induction of gastric mucosal proliferative activity, whether the result of aging or injury or occurring after administration of epidermal growth factor, gastrin, or bombesin, is associated with a rise in tyrosine kinase activity and tyrosine phosphorylation of several mucosal proteins, including a protein with a molecular mass of 53–55 kDa. We hypothesized that this phosphotyrosine membrane protein (referred to as pp55) may play a role in regulating gastric mucosal cell proliferation and differentiation. Purification and subsequent immunoprecipitation studies now show that pp55 is a tyrosine kinase. In addition, the enzyme activity in the gastric mucosa is found to be fourfold higher in aged rats than in young rats. Incubation of gastric mucosal membranes with transforming growth factor-α (2 × 10−8 M) stimulates tyrosine kinase activity of pp55. Immuolocalization studies reveal that pp55 immunoreactivity is predominantly present in mucous cells that are located just above the proliferative zone and spasmolytic peptide-immunoreactive mucous neck cells. Tyrosine kinase activity as well as expression of pp55 are also greatly increased in the gastric mucosa after hypertonic saline-induced injury, a condition that results in stimulation of surface mucosal cell proliferation and differentiation. Our current data suggest that pp55 is a tyrosine kinase, likely localized to pre-surface cells. The presence of pp55 in pre-surface mucous cells and the expression and tyrosine kinase activity of this protein, which can be stimulated during mucosal cell proliferation and differentiation, strongly suggest a role for pp55 in differentiation of gastric surface mucous cells.


1983 ◽  
Vol 245 (5) ◽  
pp. G656-G660 ◽  
Author(s):  
G. D. Luk ◽  
S. B. Baylin

Transient increases in the activities of ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase (SAM-DC), key enzymes in polyamine biosynthesis, may be critical to initiation of cell growth. We now report that such increases in ODC (X170) and SAM-DC (X83) activities, and their synthetic products putrescine (X4) and spermidine (X2), occur in rat ileal mucosa between days 1 and 4 after 50% intestinal resection. This is the time period of initiation of mucosal cell hyperplasia in intestinal adaptation after resection and is characterized by increased mucosal cell proliferation, as measured morphologically and biochemically. Intestinal weight increased by 76% and mucosal thickness by 48%. Mucosal DNA content increased by 67% and mucosal DNA synthesis by 104%. Increased intestinal crypt cell proliferation was manifested by a 120% increase in labeling per crypt and a 152% increase in crypt cell production rate (CCPR). The increase in ODC activity was closely associated with the increases in CCPR and rate of villus lengthening. Rates of mucosal cell proliferation, as measured by CCPR, and villus and crypt lengthening were significantly correlated with ODC activity (r = 0.97, 0.98, and 0.94, respectively; P less than 0.01 for all). Our results indicate that the increase in ODC activity, SAM-DC activity, and polyamine biosynthesis is closely associated with the process of adaptive postresectional crypt cell proliferation.


Gut ◽  
1989 ◽  
Vol 30 (3) ◽  
pp. 376-382 ◽  
Author(s):  
R C Gregoire ◽  
H S Stern ◽  
K S Yeung ◽  
J Stadler ◽  
S Langley ◽  
...  

2006 ◽  
Vol 17 (6) ◽  
pp. 396-401 ◽  
Author(s):  
Xiaoming Jia ◽  
Naoyuki Ebine ◽  
Yanwen Wang ◽  
Atif B. Awad ◽  
Peter J.H. Jones

Sign in / Sign up

Export Citation Format

Share Document