1.Mucosal Restitution.
The Korean Journal of Gastroenterology 2006;47(6):409-412
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
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Humans
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Intestinal Mucosa/*physiology
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Regeneration/*physiology
2.Mucosal Restitution.
The Korean Journal of Gastroenterology 2006;47(6):409-412
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
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Humans
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Intestinal Mucosa/*physiology
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Regeneration/*physiology
3.The Role of Barrier Dysfunction and Change of Claudin Expression in Inflammatory Bowel Disease.
Gut and Liver 2015;9(6):699-700
No abstract available.
Animals
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Apoptosis/*physiology
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Claudins/*metabolism
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Colitis/*physiopathology
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Intestinal Mucosa/*physiopathology
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Mannose-Binding Lectin/*immunology
4.Cellular compatibility of small intestinal submucosa in vitro.
Jingcong LUO ; Zhiming YANG ; Xiuqun LI ; Li DENG
Journal of Biomedical Engineering 2004;21(5):800-804
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
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Cell Differentiation
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physiology
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Cell Division
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physiology
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Cells, Cultured
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Coculture Techniques
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Extracellular Matrix
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physiology
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Histocompatibility
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Intestinal Mucosa
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cytology
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Jejunum
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cytology
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Osteoblasts
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cytology
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physiology
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Swine
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Tissue Engineering
5.Identification of microRNA expression profiles in the gill, intestine and hepatic caecum of Branchiostoma belcheri.
Xin LIAO ; Liu YANG ; Xi CHEN ; Junyuan CHEN
Protein & Cell 2017;8(4):302-307
Animals
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Gene Expression Regulation
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physiology
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Gills
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metabolism
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Intestinal Mucosa
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metabolism
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Lancelets
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genetics
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metabolism
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Liver
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metabolism
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MicroRNAs
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biosynthesis
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genetics
6.The role of LPS/TLR4 interaction on the pathogenesis of acute on chronic liver failure.
Chinese Journal of Hepatology 2010;18(1):78-80
Bacterial Translocation
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physiology
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Humans
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Intestinal Mucosa
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pathology
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physiology
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Lipopolysaccharides
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metabolism
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physiology
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Liver Failure, Acute
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etiology
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immunology
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physiopathology
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Lymphocytes
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immunology
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metabolism
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Macrophages
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immunology
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metabolism
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Signal Transduction
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genetics
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physiology
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Toll-Like Receptor 4
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metabolism
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physiology
7.Cellular signaling in rapid intestinal epithelial restitution: implication of polyamines and K+ channels.
Acta Physiologica Sinica 2003;55(4):365-372
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
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Cell Movement
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Epithelial Cells
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metabolism
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pathology
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physiology
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Gene Expression Regulation
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Humans
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Intestinal Mucosa
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cytology
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pathology
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physiology
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Membrane Potentials
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Polyamines
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metabolism
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Potassium Channels
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physiology
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Signal Transduction
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Wound Healing
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physiology
8.Research on intestinal tight junction barrier dysfunction should be emphasized in burn injury.
Chinese Journal of Burns 2010;26(5):331-333
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
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metabolism
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physiopathology
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Humans
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Intestinal Mucosa
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metabolism
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physiopathology
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Myosin-Light-Chain Kinase
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metabolism
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Permeability
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Phosphorylation
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Tight Junctions
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metabolism
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physiology
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rho-Associated Kinases
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metabolism
9.Small intestine submucosa as a scaffold for cartilage reconstruction in vitro.
Qingquan KONG ; Bo GAO ; Rong XING ; Zhou XIANG ; Zhiming YANG ; Jingcong LUO ; Xiuqun LI
Journal of Biomedical Engineering 2011;28(3):521-525
This paper is aimed to investigate the feasibility of applying the small intestine submucosa (SIS) as the scaffold in constructing tissue engineering cartilage in vitro. We obtained SIS from the small intestine of specific pathogen-free pigs. Then we isolated tunica submucosa layer from the mucosal, muscular, and serosal layers by gentle mechanic abrasion. The SIS was made acellular by combination of detergent and enzyme digestion. The chondrocytes were seeded onto the SIS and were cultured for 3 weeks. The cell growth, attachment and distribution were detected by histochemical stain, immunohistochemical stain and scan electron microscope. The chondrocytes could adhere and grow well on the matrix surface, and synthesize a large of the GAG and type U collagen. However, the chondrocytes grew only on the surface andsuperficial layer of the scaffold, they did not move into the inner part of the scaffold. It could be concluded that SIS has good cellular compatibility without cytotoxicity and provides temporary substrate to which these anchorage-dependent cells can adhere, and stimulate the chondrocytes anchored on the scaffold to proliferate and keep differentiated phenotype. Further study will be needed to promote the ability of chondrocyte chemotaxis in order to distribute the chondrocytes into the whole scaffold uniformly.
Animals
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Cell Adhesion
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Cell Culture Techniques
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Cell Proliferation
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Chondrocytes
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cytology
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Chondrogenesis
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physiology
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Intestinal Mucosa
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cytology
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Intestine, Small
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cytology
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Swine
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Tissue Engineering
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methods
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Tissue Scaffolds
10.Bifidobacterial supplement enhances the expression and excretion of intestinal sIgA in severely burned rats.
Zhong-tang WANG ; Yong-ming YAO ; Guang-xia XIAO ; Wei-hong CAO ; Zhi-yong SHENG
Chinese Journal of Surgery 2003;41(5):385-388
OBJECTIVETo investigate the potential effect of bifidobacterial supplement on intestinal mucosal immunity associated with severe burns.
METHODSWistar rats were randomly divided into burn control group (BC group, n = 30), treatment group (BT group, n = 30), and sham-burn group (NC group, n = 10). Rats in BT group were fed bifidobacterial preparation (5 x 10(9) CFU/ml) after 30% total body surface area full-thickness burns, 1.5 ml, twice daily. Rats in BC group and NC group were fed normal saline, 1.5 ml, twice daily. Samples were taken on post-burn 1-, 3-, and 5-day. The incidence of bacterial translocation and bifidobacteria counts in the cecum mucosa were determined with standard methods. The sIgA levels in the mucus of the small intestine were measured by RIA. The positive sIgA expression in the lamina propria was detected by immunohistochemical staining.
RESULTSThe incidence of bacterial translocation was 42% and 16% in BC and BT groups on post-burn day 3 (P = 0.004), 30% and 8% on day 5 (P = 0.002), respectively. Plasma endotoxin levels were markedly higher in BC and BT groups than in NC group at the early stage post-burn. There was a significant decrease between BT group and BC group on post-burn day 1 (P = 0.0412). Bifidobacteria counts in cecum mucosa were reduced by 10- to 60-fold after thermal injury, but there was a remarkable increase in bifidobacteria counts in animals fed with bifidobacteria. sIgA levels in the intestinal mucus were significantly decreased in group BC, but they returned to normal range in BT group on post-burn day 5. Similarly, sIgA expression in the lamina propria was also weakened after burns, and had a tendency to recover after prescription of a 5-day bifidobacteria-supplemented formula. A strong positive correlation was observed between the counts of bifidobacteria in the cecal mucosa and the levels of sIgA in the intestinal mucus (r = 0.7534, P = 0.0000).
CONCLUSIONSThe expression and excretion of sIgA in the intestine appear to be markedly inhibited following a severe thermal injury. The supplement of exogenous bifidobacteria could improve sIgA formation in the small intestine, thereby reducing the incidence of bacterial/endotoxin translocation secondary to major burns.
Animals ; Bacterial Translocation ; Bifidobacterium ; physiology ; Burns ; immunology ; microbiology ; Disease Models, Animal ; Female ; Immunoglobulin A, Secretory ; biosynthesis ; Intestinal Mucosa ; immunology ; microbiology ; Male ; Probiotics ; Random Allocation ; Rats ; Rats, Wistar