Basal nutrition promotes human intestinal epithelial (Caco-2) proliferation, brush border enzyme activity, and motility

Perdikis, Demetrios A.; Basson, Marc D.

doi:10.1097/00003246-199701000-00029

Cited by 36 publications

(17 citation statements)

References 48 publications

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“…However, the enterocyte can derive nutrition luminally or by submucosal perfusion [70, 71]. Moreover, cultured intestinal epithelial cells survive quite nicely in culture if supplied with basal nutrients, and indeed appear to differentiate and proliferate more readily than if nutrients are only supplied apically [72]. It was also postulated that glutamine might be a constitutive nutritional requirement for the small bowel mucosa, since the small bowel mucosa derives most of its caloric needs from enteral glutamine under normal circumstances.…”

Section: In Vivo Evidence That Mechanical Forces Might Act Upon Gi Mumentioning

confidence: 99%

Paradigms for Mechanical Signal Transduction in the Intestinal Epithelium

Basson¹

2003

Digestion

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Diverse physical forces including deformation or strain, pressure, and shear stress affect the intestinal mucosa during normal function, and mucosal biology is altered in pathological states in which these forces alter. Taken together with evidence in other tissues and cell types that physical forces can affect cell biology, this has led to the hypothesis that repetitively applied physical forces can initiate intracellular signals that alter intestinal epithelial proliferation and phenotype. This review outlines the nature of such forces and summarizes in vivo and in vitro evidence in support of the paradigm that repetitive force is trophic for the intestinal mucosa via a complex cascade of intracellular signals.

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Section: In Vivo Evidence That Mechanical Forces Might Act Upon Gi Mumentioning

confidence: 99%

Paradigms for Mechanical Signal Transduction in the Intestinal Epithelium

Basson¹

2003

Digestion

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“…associated with intracellular signals, 34 perhaps via integrin-mediated altered cell-matrix interaction. 35,36 The Ras and Raf-1 proto-oncogene products are key proteins in the transmission of a variety of intracellular proliferative and differentiation signals.…”

Section: Discussionmentioning

confidence: 99%

Activation of Raf-1 during Experimental Gastric Ulcer Healing Is Ras-Mediated and Protein Kinase C-Independent

Pai

Jones

Tomikawa

et al. 1999

The American Journal of Pathology

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Our previous study demonstrated increases in epidermal growth factor receptor (EGF-R) phosphorylation and receptor tyrosine kinase and extracellular signalregulated kinase (ERK1 and ERK2) activities in the ulcer margin of experimental gastric ulcer during healing. However , the intermediate steps linking activated receptor tyrosine kinase to ERKs during ulcer healing are as yet unknown. Raf-1 is upstream of mitogen-activated protein kinases (MAPK/ERK) and can be activated by Ras-dependent and/or Ras-independent mechanisms. Therefore , we studied Raf-1 activity , its potential activators protein kinase C (PKC) and Ras , and expression and associations of adapter proteins Shc , Grb2 , and Sos during experimental gastric ulcer healing. To investigate if Raf-1-ERK activation is attributable to the epithelial component of ulcer margins , we studied the effect of EGF on PKC, Ras , and ERK activities in a rat gastric epithelial cell line (RGM1). Our results demonstrate that gastric ulceration significantly increases Raf-1 kinase activity, Grb2 and Ras protein , and Shc-Grb2 and Grb2-Sos complex levels. In contrast , PKC activity and protein level were significantly decreased in the ulcer margins. In RGM1 cells , EGF significantly increased Ras and ERK2 activities without affecting PKC activity. These findings indicate that Raf-1 activation during gastric ulcer healing is Ras mediated , involves ShcGrb2-Sos , and is PKC-independent. (Am J Pathol 1999, 155:1759 -1766)

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“…All other reagents were obtained from Sigma or Baker Chemical (Phillipsburg, NJ) unless mentioned otherwise and were of the highest purity available. For studies of antibody effects on cell differentiation and proliferation, cells were seeded onto tissue culture inserts (BectonDickinson) precoated with laminin (Sigma, St. Louis) as previously described [14,41].…”

Section: Antibodies and Reagentsmentioning

confidence: 99%

Alpha Integrin Subunits Regulate Human (Caco-2) Intestinal Epithelial Proliferation and Phenotype

Basson

Emenaker

Sanders³

2000

Cell Physiol Biochem

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Background/Aims: Cell-matrix interactions influence intestinal epithelial biology, but the whether specific integrin heterodimers exert different effects is unclear. Methods: We used functional antibodies to investigate effects of the α2, α3, α5, and α6 integrin subunits on proliferation and differentiation of human intestinal Caco-2 cells on laminin. Cells seeded onto laminin-coated inserts in defibronectinized medium were treated with functional antibodies or normal IgG for 72 hrs and proliferation, alkaline phosphatase and dipeptidyl dipeptidase specific activity were measured. Results: Caco-2 adhesion to antibody to each α-integrin subunit stimulated tyrosine phosphorylation of Focal Adhesion Kinase and paxillin, suggesting that these antibodies intiate integrin-related tyrosine signalling. Proliferation was inhibited by anti-α2 and anti-α3, but stimulated by anti-α6. Alkaline phosphatase and dipeptidyl dipeptidase specific activity were promoted by α2 blockade but decreased after α6 blockade. Proliferative blockade using mitomycin C or hydroxyurea prevented the effects of α2 ligation on differentiation, but the decrease in alkaline phosphatase specific activity observed after α6 integrin subunit blockade was preserved even after proliferative blockade.Conclusion: Integrin heterodimers modulate human Caco-2 intestinal epithelial biology on laminin in an α-subunit specific manner. The different effects of anti-α2 and anti-α6 may reflect competitition by these antibodies with integrin subunit interactions with laminin as well as initiation of their own signals or different functions for the α6 integrin subunit.

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Basal nutrition promotes human intestinal epithelial (Caco-2) proliferation, brush border enzyme activity, and motility

Abstract: These results suggest that although apical nutrition may be critical for intestinal epithelial cell biology, nutrient delivery to the basal surface of intestinal epithelial cell membranes may also promote intestinal epithelial differentiation, proliferation, and mucosal healing.

Cited by 36 publications

References 48 publications

Paradigms for Mechanical Signal Transduction in the Intestinal Epithelium

Paradigms for Mechanical Signal Transduction in the Intestinal Epithelium

Activation of Raf-1 during Experimental Gastric Ulcer Healing Is Ras-Mediated and Protein Kinase C-Independent

Alpha Integrin Subunits Regulate Human (Caco-2) Intestinal Epithelial Proliferation and Phenotype

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