The repair of superficially damaged intestinal epithelium is initiated by restitution. Restitution is the covering of damaged area by the movement of neighboring epithelial cells without cell proliferation. Phenotypic switching of cells (epithelial-mesenchymal transition) is necessary for the cell movement and this process is controlled by complex intracellular signaling pathways conducting dynamic remodeling of actin cytoskeleton. Restitution is regulated by a variety of cytokines and growth factors, and is modulated by integrin-dependent interactions with the extracellular matrix. Understanding the restitution process suggests several possible therapeutic strategies to enhance gastrointestinal wound healing.
Cell Movement ; Humans ; Intestinal Mucosa/*physiology ; Regeneration/*physiology

The repair of superficially damaged intestinal epithelium is initiated by restitution. Restitution is the covering of damaged area by the movement of neighboring epithelial cells without cell proliferation. Phenotypic switching of cells (epithelial-mesenchymal transition) is necessary for the cell movement and this process is controlled by complex intracellular signaling pathways conducting dynamic remodeling of actin cytoskeleton. Restitution is regulated by a variety of cytokines and growth factors, and is modulated by integrin-dependent interactions with the extracellular matrix. Understanding the restitution process suggests several possible therapeutic strategies to enhance gastrointestinal wound healing.
Cell Movement ; Humans ; Intestinal Mucosa/*physiology ; Regeneration/*physiology

No abstract available.
Animals ; Apoptosis/*physiology ; Claudins/*metabolism ; Colitis/*physiopathology ; Intestinal Mucosa/*physiopathology ; Mannose-Binding Lectin/*immunology

This study was aimed to evaluate the cellular compatibility of the small intestinal submucosal(e) (SIS). Prepared by use of pig jejunum. SIS were cocultured with human embryonic periosteal osteoblasts (HEPOB), human embryonic skin fibroblasts (HESFB) and rabbit renal vascular endothelial cells (RRVEC) respectively. The cell growth, attachment, cell cycle, cell apoptosis rate were detected to evaluate the cellular compatibility of SIS. The three kinds of cells attached onto SIS and grew well. SIS accelerated the growth of RRVEC. No effects of SIS were detected on cell cycle and cell apoptosis rate in the three kinds of cells. SIS has good cellular compatibility without cytotoxicity. The porous structure of SIS is suited for the growth of HEPOB, HESFB and RRVEC in three dimensions in the scaffold. SIS is a good bio-derived material of tissue engineering.
Animals ; Cell Differentiation ; physiology ; Cell Division ; physiology ; Cells, Cultured ; Coculture Techniques ; Extracellular Matrix ; physiology ; Histocompatibility ; Intestinal Mucosa ; cytology ; Jejunum ; cytology ; Osteoblasts ; cytology ; physiology ; Swine ; Tissue Engineering

Animals ; Gene Expression Regulation ; physiology ; Gills ; metabolism ; Intestinal Mucosa ; metabolism ; Lancelets ; genetics ; metabolism ; Liver ; metabolism ; MicroRNAs ; biosynthesis ; genetics

Bacterial Translocation ; physiology ; Humans ; Intestinal Mucosa ; pathology ; physiology ; Lipopolysaccharides ; metabolism ; physiology ; Liver Failure, Acute ; etiology ; immunology ; physiopathology ; Lymphocytes ; immunology ; metabolism ; Macrophages ; immunology ; metabolism ; Signal Transduction ; genetics ; physiology ; Toll-Like Receptor 4 ; metabolism ; physiology

Epithelial cells line the gastrointestinal (GI) mucosa and form an important barrier that protects the subepithelial tissue against a wide array of noxious substances, allergens, viruses, and luminal microbial pathogens. Restoration of mucosal integrity following injury requires epithelial cell decisions that regulate signaling networks controlling gene expression, survival, migration, and proliferation. Over the past few years, polyamines have been shown to play a critical role in GI mucosal repair, and the control of cellular polyamines is a central convergence point for the multiple signaling pathways. Both the function of polyamines in rapid intestinal mucosal epithelial restitution and the underlying mechanism, especially the implication of K(+) channel activity, are the subject of this mini-review article.
Animals ; Cell Movement ; Epithelial Cells ; metabolism ; pathology ; physiology ; Gene Expression Regulation ; Humans ; Intestinal Mucosa ; cytology ; pathology ; physiology ; Membrane Potentials ; Polyamines ; metabolism ; Potassium Channels ; physiology ; Signal Transduction ; Wound Healing ; physiology

OBJECTIVETo investigate the role of integrin α4β7 in the development of ulcerative colitis (UC) in rats.

METHODSSixty Sprague-Dawley rats were randomly divided into the control group (acetone enema), the model group (2,4-dinitrochlorobenzene, DNCB enema), and the α4 intervention group. Colonic mucosa of different groups was observed and compared in terms of pathology and cytokine changes(IL-2 and IL-6) using ELISA. Semi-quantitative RT-PCR was used to detect the colon α4β7 expression. Integrin α4β7(+) lymphocytes in the portal vein of rats were determined by flow cytometry.

RESULTSThe expression of α4 mRNA was 0.68±0.24 in the model group and 0.58±0.37 in the intervention group, and the expression of β7 mRNA was 0.84±0.37 in the model group and 0.65±0.30 in the intervention group, which were all significantly higher as compared to those in the control group(0.15±0.13 for α4 and 0.24±0.62 for β7, P<0.01). The proportions of integrin α4β7 positive lymphocytes in the portal vein in the model group and intervention group were significantly higher than that in the control group [(76.7±8.2)% and (68.2±7.6)% vs. (14.7±6.7)%, P<0.01]. The expression of IL-2 and IL-6 and the result of macroscopic and microscopic scores in the intervention group were lower than those in the model group(P<0.05).

CONCLUSIONSHigh expression of α4β7 may play an important role in experimental colon mucosa inflammation in rats with ulcerative colitis. The blockade of integrin α4β7 may be a potential target to reduce colonic mucosa inflammation.

Animals ; Colitis, Ulcerative ; metabolism ; pathology ; Colon ; metabolism ; pathology ; Disease Models, Animal ; Female ; Integrins ; metabolism ; physiology ; Interleukin-2 ; metabolism ; Interleukin-6 ; metabolism ; Intestinal Mucosa ; pathology ; Rats

OBJECTIVETo investigate the protective effects of small dose of dopamine on the intestinal mucosa of scalded rats in shock stage.

METHODSWistar rats inflicted by 30% TBSA of III degree scalding were employed as the model. The rats were pre-placed with cardiac catheter before and were resuscitated intravenously after injury. The scalded rats were treated by routine (control) and small dose of dopamine (3 micro g.kg(-1).min(-1)), respectively. The changes of rat serum levels of diamine oxidase (DAO), malondialdehyde (MDA) and lactic acid (LA) were observed after treatment. And the pathomorphological changes of the intestine were scored.

RESULTSThe general condition of the rats with dopamine treatment in shock stage was better than that in control group. The rat serum levels of MDA, LA and DAO decreased obviously, especially during 3 to 12 postburn hours (PBHs) after treatment by small dose of dopamine. The pathomorphological scoring of ileum in dopamine treating group was better than that in control.

CONCLUSIONThe intestinal mucosa of severely scalded rats in shock stage could be well protected by small dose of dopamine.

Animals ; Burns ; pathology ; Disease Models, Animal ; Dopamine ; administration & dosage ; pharmacology ; Intestinal Mucosa ; drug effects ; physiology ; Male ; Protective Agents ; administration & dosage ; pharmacology ; Rats ; Rats, Wistar

Severe burn injury is often accompanied by intestinal epithelial tight junction barrier dysfunction, which is believed to be closely associated with postburn shock, inflammation, hypermetabolism, infection, organ dysfunction etc. Recent studies have documented the critical role of tight junction-associated protein regulation in intestinal epithelial barrier dysfunction induced by severe burn injury. Myosin light chain (MLC) phosphorylation regulated by both myosin light chain kinase, which can phosphorylate MLC directly, and Rho-associated kinase, which can inhibit MLC phosphatase and then induce MLC phosphorylation indirectly, play a critical role in intestinal epithelial tight junction barrier dysfunction which occurs in severe burn injury. Recent advances have provided new insights into the mechanisms and the therapeutic strategies of intestinal epithelial tight junction barrier dysfunction following severe burn injury.
Burns ; metabolism ; physiopathology ; Humans ; Intestinal Mucosa ; metabolism ; physiopathology ; Myosin-Light-Chain Kinase ; metabolism ; Permeability ; Phosphorylation ; Tight Junctions ; metabolism ; physiology ; rho-Associated Kinases ; metabolism