Faculty Opinions recommendation of FAK regulates intestinal epithelial cell survival and proliferation during mucosal wound healing.

2011 ◽  
Author(s):  
Asma Nusrat ◽  
Stefan Koch
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Mucosal Wound ◽  
Cell Survival And Proliferation

scholarly journals FAK Regulates Intestinal Epithelial Cell Survival and Proliferation during Mucosal Wound Healing

PLoS ONE ◽  
2011 ◽  
Vol 6 (8) ◽  
pp. e23123 ◽  
Author(s):  
Katherine A. Owen ◽  
Michelle Y. Abshire ◽  
Robert W. Tilghman ◽  
James E. Casanova ◽  
Amy H. Bouton
Keyword(s):  
Wound Healing ◽  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Mucosal Wound ◽  
Cell Survival And Proliferation

Human intestinal epithelial cell survival: differentiation state-specific control mechanisms

2001 ◽  
Vol 280 (6) ◽  
pp. C1540-C1554 ◽  
Author(s):  
Rémy Gauthier ◽  
Charlène Harnois ◽  
Jean-François Drolet ◽  
John C. Reed ◽  
Anne Vézina ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
The State ◽  
Control Mechanisms ◽  
Intestinal Epithelial ◽  
Human Intestinal Epithelial Cell ◽  
Expression Levels ◽  
Specific Control

To investigate whether human intestinal epithelial cell survival involves distinct control mechanisms depending on the state of differentiation, we analyzed the in vitro effects of insulin, pharmacological inhibitors of Fak, MEK/Erk, and PI3-K/Akt, and integrin (β1, β4)-blocking antibodies on the survival of the well-established human Caco-2 enterocyte-like and HIEC-6 cryptlike cell models. In addition, relative expression levels of six Bcl-2 homologs (Bcl-2, Bcl-XL, Mcl-1, Bax, Bak, and Bad) and activation levels of Fak, Erk-2, and Akt were analyzed. Herein, we report that 1) the enterocytic differentiation process results in the establishment of distinct profiles of Bcl-2 homolog expression levels, as well as p125Fak, p42Erk-2, and p57Aktactivated levels; 2) the inhibition of Fak, of the MEK/Erk pathway, or of PI3-K, have distinct impacts on enterocytic cell survival in undifferentiated (subconfluent Caco-2, confluent HIEC-6) and differentiated (30 days postconfluent Caco-2) cells; 3) exposure to insulin and the inhibition of Fak, MEK, and PI3-K resulted in differentiation state-distinct modulations in the expression of each Bcl-2 homolog analyzed; and 4) Fak, β1 and β4 integrins, as well as the MEK/Erk and PI3-K/Akt pathways, are distinctively involved in cell survival depending on the state of cell differentiation. Taken together, these data indicate that human intestinal epithelial cell survival is regulated according to differentiation state-specific control mechanisms.

scholarly journals Lactobacillus gasseri SF1183 Affects Intestinal Epithelial Cell Survival and Growth

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e69102 ◽  
Author(s):  
Blanda Di Luccia ◽  
Nicola Manzo ◽  
Loredana Baccigalupi ◽  
Viola Calabrò ◽  
Elvira Crescenzi ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Lactobacillus Gasseri ◽  
Survival And Growth

Tu1831 MYPT1 Is a Critical Regulator of Intestinal Epithelial Cell Survival

2016 ◽  
Vol 150 (4) ◽  
pp. S955
Author(s):  
Juanmin Zha ◽  
Weiqi He ◽  
Matthew Odenwald ◽  
Jerrold Turner
Keyword(s):  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial

406 cFLIP Allows Intestinal Epithelial Cell Survival and Immune Homeostasis by Controlling the Activation Level of Caspase8

2013 ◽  
Vol 144 (5) ◽  
pp. S-79
Author(s):  
Nadine Wittkopf ◽  
Claudia Günther ◽  
Eva Martini ◽  
You-Wen He ◽  
Marcus Schuchmann ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Immune Homeostasis ◽  
Intestinal Epithelial ◽  
Activation Level

scholarly journals PTBP1/HNRNP I controls intestinal epithelial cell regeneration by maintaining stem cell survival and stemness

2021 ◽  
Author(s):  
Wesley Tung ◽  
Ullas Valiya Chembazhi ◽  
Jing Yang ◽  
Ka Lam Nguyen ◽  
Aryan Lalwani ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Epithelial Cell ◽  
Cell Survival ◽  
Intestinal Epithelial Cell ◽  
Intestinal Stem Cells ◽  
Intestinal Stem Cell ◽  
Cell Regeneration ◽  
Intestinal Epithelial ◽  
Stem Cell Survival

Properly controlled intestinal epithelial cell regeneration is not only vital for protection against insults from environmental hazards but also crucial for preventing intestinal cancer. Intestinal stem cells located in the crypt region provide the driving force for epithelial regeneration, and thus their survival and death must be precisely regulated. We show here that polypyrimidine tract binding protein 1 (PTBP1, also called heterogeneous nuclear ribonucleoprotein I, or HNRNP I), an RNA-binding protein that post-transcriptionally regulates gene expression, is critical for intestinal stem cell survival and stemness. Mechanistically, we show that PTBP1 inhibits the expression of PHLDA3, an AKT repressor, and thereby maintains AKT activity in the intestinal stem cell compartment to promote stem cell survival and proliferation. Furthermore, we show that PTBP1 inhibits the expression of PTBP2, a paralog of PTBP1 that is known to induce neuron differentiation, through repressing inclusion of alternative exon 10 to Ptbp2 transcript. Loss of PTBP1 results in a significant upregulation of PTBP2, which is accompanied by splicing changes in genes that are important for neuron cell development. This finding suggests that PTBP1 prevents aberrant differentiation of intestinal stem cells into neuronal cells through inhibiting PTBP2. Our results thus reveal a novel mechanism whereby PTBP1 maintains intestinal stem cell survival and stemness through the control of gene function post-transcriptionally.

CXCL12 activation of CXCR4 regulates mucosal host defense through stimulation of epithelial cell migration and promotion of intestinal barrier integrity

2005 ◽  
Vol 288 (2) ◽  
pp. G316-G326 ◽  
Author(s):  
Jennifer M. Smith ◽  
Priscilla A. Johanesen ◽  
Michael K. Wendt ◽  
David G. Binion ◽  
Michael B. Dwinell
Keyword(s):  
Wound Healing ◽  
Cell Migration ◽  
Epithelial Cell ◽  
Host Defense ◽  
Intestinal Epithelial Cell ◽  
Mucosal Barrier ◽  
Intestinal Epithelial ◽  
Barrier Integrity ◽  
Epithelial Migration ◽  
Epithelial Cell Migration

Intestinal epithelial cell migration plays a key role in gastrointestinal mucosal barrier formation, enterocyte development, differentiation, turnover, wound healing, and adenocarcinoma metastasis. Chemokines, through engagement of their corresponding receptors, are potent mediators of directed cell migration and are critical in the establishment and regulation of innate and adaptive immune responses. The aim of this study was to define the role for the chemokine CXCL12 and its sole cognate receptor CXCR4 in regulating intestinal epithelial cell migration and to determine its impact on barrier integrity. CXCL12 stimulated the dose-dependent chemotactic migration of human T84 colonic epithelial cells. Epithelial cell migration was inhibited by CXCR4 neutralizing antibody, pertussis toxin, LY-294002, and PD-98059, thereby implicating Gαi, phosphatidylinositol 3-kinase (PI3-kinase), and the ERK1/2 MAP kinase pathways in CXCR4-specific signaling. CXCL12 was also shown to increase barrier integrity, as defined by transepithelial resistance and paracellular flux across differentiating T84 monolayers. To determine whether CXCL12 regulated epithelial restitution, we used the normal nontransformed intestinal epithelial cell-6 (IEC-6) wound healing model. By using RT-PCR, immunoblot analysis, and immunofluorescence microscopy, we first showed expression of both CXCR4 and its ligand by IEC-6 cells. We then demonstrated that CXCL12 activated comparable signaling mechanisms to stimulate epithelial migration in the absence of proliferation in wounded IEC-6 monolayers. Taken together, these data indicate that CXCL12 signaling via CXCR4 directs intestinal epithelial cell migration, barrier maturation, and restitution, consistent with an important mechanistic role for these molecules in mucosal barrier integrity and innate host defense.

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