scholarly journals PPAR? agonists inhibit cell growth and suppress the expression of cyclin D1 and EGF-like growth factors in ras-transformed rat intestinal epithelial cells

2001 ◽  
Vol 94 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Shinji Kitamura ◽  
Yoshiji Miyazaki ◽  
Shintaro Hiraoka ◽  
Yutaka Nagasawa ◽  
Miyuki Toyota ◽  
...  
Keyword(s):  
Growth Factors ◽  
Cell Growth ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Inhibit Cell Growth ◽  
Ppar Agonists

Mechanisms of cyclin D1 regulation by PKC signaling in intestinal epithelial cells

2003 ◽  
Vol 124 (4) ◽  
pp. A599
Author(s):  
Aysen A. Hizli ◽  
Adrian R. Black ◽  
Jennifer D. Black
Keyword(s):  
Epithelial Cells ◽  
Cyclin D1 ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Pkc Signaling

Induction of endothelin-1 synthesis by IL-2 and its modulation of rat intestinal epithelial cell growth

1998 ◽  
Vol 275 (3) ◽  
pp. G556-G563 ◽  
Author(s):  
Takeharu Shigematsu ◽  
Soichiro Miura ◽  
Masahiko Hirokawa ◽  
Ryota Hokari ◽  
Hajime Higuchi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Lines ◽  
Proliferative Response ◽  
Intestinal Epithelial Cell ◽  
Culture Media ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Endothelin (ET), a vasoconstrictive peptide, is known to have a variety of biological actions. Although ET is released by vascular endothelial cells, other cell populations also have been reported to synthesize and release ET. In this study, we examined whether ET is synthesized by intestinal epithelial cells and whether it affects induction of epithelial cell proliferation by interleukin-2 (IL-2). Subconfluent monolayers of intestinal epithelial cells (IEC-6 and IEC-18) were maintained in serum-free medium before addition of rat IL-2. Both IEC-6 and IEC-18 cells released ET-1 into the medium under unstimulated conditions, as determined by a sandwich ELISA. IL-2 significantly enhanced ET-1 release in a time-dependent manner. ET-3 was not detectable in the culture media of either cell line. Expression of ET-1 and ET-3 mRNA in epithelial cells was assessed by competitive PCR. Both cell lines were shown to express ET-1 mRNA, but no ET-3 mRNA was detected. IL-2 treatment enhanced ET-1 mRNA expression by both IEC-6 and IEC-18 cells. Both cell lines also expressed mRNA for ETA and ETB receptor subtypes. When cell proliferation was assessed, exogenous ET-1 induced a slight proliferative response in both types of cells that was consistent and significant at low ET-1 concentrations; cell growth was inhibited at a higher concentration (10−7M). IL-2 produced a significant proliferative response in both cell lines. However, the addition of ET-1 (10−7 M) to culture media attenuated the IL-2-induced increase in cell proliferation. ETA-receptor antagonists significantly enhanced cellular proliferation, suggesting involvement of the ETA receptor in modulation of IL-2-induced intestinal epithelial cell growth.

Profile of IGF-binding proteins secreted by intestinal epithelial cells changes with differentiation

1994 ◽  
Vol 267 (5) ◽  
pp. G843-G850 ◽  
Author(s):  
S. Oguchi ◽  
W. A. Walker ◽  
I. R. Sanderson
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Binding Proteins ◽  
Egf Receptor ◽  
Transforming Growth Factor ◽  
Intestinal Epithelial Cells ◽  
Alpha Activity ◽  
Intestinal Epithelial ◽  
Igf I

Previous reports have shown that gastrointestinal epithelial cells produce insulin-like growth factor-binding proteins (IGF-BP), which modulate the actions of IGF. This study aims to examine the relationship between differentiation and IGF-BP secretion by human intestinal epithelial cells and the effect of growth factors on their production. Caco-2 cells were cultured in serum-free media. IGF-BP secretion into the incubation media was analyzed by Western ligand blotting and immunoblotting. Caco-2 cells produced IGF-BP-2, IGF-BP-3, and IGF-BP-4. Secretion of IGF-BP-2 and IGF-BP-3 increased with differentiation, but IGF-BP-4 secretion diminished. The effect of exogenous growth factors on IGF-BP secretion was maximal at earlier stages of differentiation. IGF-I stimulated mainly IGF-BP-3 production, but epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) stimulated predominantly IGF-BP-4 secretion. Adding an anti-EGF receptor antibody to block autocrine TGF-alpha activity inhibited IGF-BP-4 production but stimulated IGF-BP-2 and IGF-BP-3. In conclusion, the profile of IGF-BP secretion changes with differentiation. IGF-I and EGF (or TGF-alpha) stimulate different types of IGF-BP, with autocrine TGF-alpha activity being a factor affecting IGF-BP production during differentiation.

scholarly journals Protein Kinase C α Signaling Inhibits Cyclin D1 Translation in Intestinal Epithelial Cells

2006 ◽  
Vol 281 (21) ◽  
pp. 14596-14603 ◽  
Author(s):  
A. Asli Hizli ◽  
Adrian R. Black ◽  
Marybeth A. Pysz ◽  
Jennifer D. Black
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Kinase C

scholarly journals Intestinal cell kinase, a MAP kinase-related kinase, regulates proliferation and G1 cell cycle progression of intestinal epithelial cells

2009 ◽  
Vol 297 (4) ◽  
pp. G632-G640 ◽  
Author(s):  
Zheng Fu ◽  
Jungeun Kim ◽  
Alda Vidrich ◽  
Thomas W. Sturgill ◽  
Steven M. Cohn
Keyword(s):  
Cell Cycle ◽  
Epithelial Cells ◽  
Cyclin D1 ◽  
Intestinal Epithelial Cells ◽  
Protein Translation ◽  
Initiation Factor ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Altered Expression ◽  
Intestinal Cell Kinase

Intestinal cell kinase (ICK), originally cloned from the intestine and expressed in the intestinal crypt epithelium, is a highly conserved serine/threonine protein kinase that is similar to mitogen-activated protein kinases (MAPKs) in the catalytic domain and requires dual phosphorylation within a MAPK-like TDY motif for full activation. Despite these similarities to MAPKs, the biological functions of ICK remain unknown. In this study, we report that suppression of ICK expression in cultured intestinal epithelial cells by short hairpin RNA (shRNA) interference significantly impaired cellular proliferation and induced features of gene expression characteristic of colonic or enterocytic differentiation. Downregulation of ICK altered expression of cell cycle regulators (cyclin D1, c-Myc, and p21Cip1/WAF1) of G1-S transition, consistent with the G1 cell cycle delay induced by ICK shRNA. ICK deficiency also led to a significant decrease in the expression and/or activity of p70 ribosomal protein S6 kinase (S6K1) and eukaryotic initiation factor 4E (eIF4E), concomitant with reduced expression of their upstream regulators, the mammalian target of rapamycin (mTOR) and the regulatory associated protein of mTOR (Raptor). Furthermore, ICK interacts with the mTOR/Raptor complex in vivo and phosphorylates Raptor in vitro. These results suggest that disrupting ICK function may downregulate protein translation of specific downstream targets of eIF4E and S6K1 such as cyclin D1 and c-Myc through the mTOR/Raptor signaling pathway. Taken together, our findings demonstrate an important role for ICK in proliferation and differentiation of intestinal epithelial cells.

HGF-receptor C-met expression in intestinal epithelial cells is differentially regulated by cytokines and growth factors and is enhanced in the colon epithelium of IL-10m1Cgn mice

2001 ◽  
Vol 120 (5) ◽  
pp. A503-A503
Author(s):  
R HOPPE ◽  
M VEEN ◽  
E LIEBLERTENORIO ◽  
S OETJENS ◽  
F SCHMITZ ◽  
...  
Keyword(s):  
Growth Factors ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial

Cytokine regulation of fibroblast growth factor receptor 3 IIIb in intestinal epithelial cells

1997 ◽  
Vol 272 (4) ◽  
pp. G885-G893 ◽  
Author(s):  
M. Kanai ◽  
I. Rosenberg ◽  
D. K. Podolsky
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Fibroblast Growth Factor ◽  
Transforming Growth Factor ◽  
Intestinal Epithelial Cells ◽  
Interleukin 2 ◽  
Intestinal Epithelial ◽  
Fibroblast Growth ◽  
Fgf Receptor

Proliferation and function of the intestinal epithelium is modulated by a range of regulatory peptides, including cytokines and peptide growth factors. To define mechanisms integrating these regulatory systems, the effects of growth factors and cytokines on the expression of the fibroblast growth factor (FGF) receptor 3 (FGFR3) IIIb expressed on intestinal epithelial cells were examined in Caco-2 cells. Regulated expression of FGFR3 IIIb was associated with acquisition of the differentiated state. Keratinocyte growth factor (KGF), a ligand of another member of the FGF receptor family, enhanced expression of FGFR3 IIIb, but acidic FGF, the ligand for FGFR3 IIIb itself, had no effect. Epidermal growth factor and transforming growth factor-beta also markedly enhanced FGFR3 IIIb expression in a different temporal pattern. In addition, FGFR3 IIIb expression was increased 10-fold by the cytokine interleukin-2. These studies demonstrate integration between cytokines and growth factor ligand-receptor systems in intestinal epithelial cells.

HGF-receptor C-met expression in intestinal epithelial cells is differentially regulated by cytokines and growth factors and is enhanced in the colon epithelium of IL-10m1Cgn mice

2001 ◽  
Vol 120 (5) ◽  
pp. A503
Author(s):  
Ruediger Hoppe ◽  
Maike Veen ◽  
Elisabeth Liebler-Tenorio ◽  
Silvia Oetjens ◽  
Frank Schmitz ◽  
...  
Keyword(s):  
Growth Factors ◽  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial
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