Evidence for the involvement of NOD2 in regulating colonic epithelial cell growth and survival
AIM： To investigate the function of NOD2 in colonic epithelial cells （CEC）. METHODS： A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA inte...
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| Veröffentlicht in: | World journal of gastroenterology : WJG 2008-10, Vol.14 (38), p.5834-5841 |
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| container_title | World journal of gastroenterology : WJG |
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| creator | Cruickshank, Sheena-M Wakenshaw, Louise Cardone, John Howdle, Peter-D Murray, Peter-J Carding, Simon-R |
| description | AIM： To investigate the function of NOD2 in colonic epithelial cells （CEC）. METHODS： A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA interference was also used to investigate the consequences of knocking down NOD2 gene expression on the growth and survival of colorectal carcinoma cell lines. RESULTS： In the colonic mucosa the highest levels of NOD2 expression were in proliferating crypt epithelial cells. Muramyl dipeptide （MDP）, that is recognized by NOD2, promoted CEC growth in vitro. By contrast,the growth of NOD2-deficient CECs was impaired. In vivo CEC proliferation was also reduced and apoptosis increased in Nod2^-/- mice, which were also evident following enteric Salmonella infection. Furthermore, neutralization of NOD2 mRNA expression in human colonic carcinoma cells by shRNA interference resulted in decreased survival due to increased levels of apoptosis. CONCLUSION： These findings are consistent with the involvement of NOD2 protein in promoting CEC growth and survival. Defects in proliferation by CECs in cases of CD may contribute to the underlying pathology of disrupted intestinal homeostasis and excessive inflammation. |
| doi_str_mv | 10.3748/wjg.14.5834 |
| format | Article |
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METHODS： A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA interference was also used to investigate the consequences of knocking down NOD2 gene expression on the growth and survival of colorectal carcinoma cell lines. RESULTS： In the colonic mucosa the highest levels of NOD2 expression were in proliferating crypt epithelial cells. Muramyl dipeptide （MDP）, that is recognized by NOD2, promoted CEC growth in vitro. By contrast,the growth of NOD2-deficient CECs was impaired. In vivo CEC proliferation was also reduced and apoptosis increased in Nod2^-/- mice, which were also evident following enteric Salmonella infection. Furthermore, neutralization of NOD2 mRNA expression in human colonic carcinoma cells by shRNA interference resulted in decreased survival due to increased levels of apoptosis. CONCLUSION： These findings are consistent with the involvement of NOD2 protein in promoting CEC growth and survival. Defects in proliferation by CECs in cases of CD may contribute to the underlying pathology of disrupted intestinal homeostasis and excessive inflammation.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.14.5834</identifier><identifier>PMID: 18855982</identifier><language>eng</language><publisher>United States: The Institute of Food Research, Norwich Research Park, Norwich NR4 7UA, United Kingdom%Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom%Section of Medicine, Surgery & Anaesthesia, Leeds Institute of Molecular Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom%Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105, United States</publisher><subject>Acetylmuramyl-Alanyl-Isoglutamine - pharmacology ; Animals ; Apoptosis ; Basic Research ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival ; Colon - drug effects ; Colon - metabolism ; Colon - microbiology ; Colon - pathology ; Disease Models, Animal ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Epithelial Cells - microbiology ; Epithelial Cells - pathology ; Humans ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - microbiology ; Intestinal Mucosa - pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NOD2 ; Nod2 Signaling Adaptor Protein - deficiency ; Nod2 Signaling Adaptor Protein - genetics ; Nod2 Signaling Adaptor Protein - metabolism ; RNA Interference ; RNA, Small Interfering - metabolism ; Salmonella Infections - metabolism ; Salmonella Infections - microbiology ; Salmonella Infections - pathology ; Salmonella typhimurium ; Time Factors ; 上皮细胞 ; 功能蛋白 ; 细胞生长</subject><ispartof>World journal of gastroenterology : WJG, 2008-10, Vol.14 (38), p.5834-5841</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>2008 The WJG Press and Baishideng. All rights reserved. 2008</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-c794b7c7d3de32fbefc557a596cccb278ba8842b4dbe1990ce95e8ef591c976a3</citedby><cites>FETCH-LOGICAL-c435t-c794b7c7d3de32fbefc557a596cccb278ba8842b4dbe1990ce95e8ef591c976a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/84123X/84123X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751893/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2751893/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18855982$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cruickshank, Sheena-M</creatorcontrib><creatorcontrib>Wakenshaw, Louise</creatorcontrib><creatorcontrib>Cardone, John</creatorcontrib><creatorcontrib>Howdle, Peter-D</creatorcontrib><creatorcontrib>Murray, Peter-J</creatorcontrib><creatorcontrib>Carding, Simon-R</creatorcontrib><title>Evidence for the involvement of NOD2 in regulating colonic epithelial cell growth and survival</title><title>World journal of gastroenterology : WJG</title><addtitle>World Journal of Gastroenterology</addtitle><description>AIM： To investigate the function of NOD2 in colonic epithelial cells （CEC）. METHODS： A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA interference was also used to investigate the consequences of knocking down NOD2 gene expression on the growth and survival of colorectal carcinoma cell lines. RESULTS： In the colonic mucosa the highest levels of NOD2 expression were in proliferating crypt epithelial cells. Muramyl dipeptide （MDP）, that is recognized by NOD2, promoted CEC growth in vitro. By contrast,the growth of NOD2-deficient CECs was impaired. In vivo CEC proliferation was also reduced and apoptosis increased in Nod2^-/- mice, which were also evident following enteric Salmonella infection. Furthermore, neutralization of NOD2 mRNA expression in human colonic carcinoma cells by shRNA interference resulted in decreased survival due to increased levels of apoptosis. CONCLUSION： These findings are consistent with the involvement of NOD2 protein in promoting CEC growth and survival. Defects in proliferation by CECs in cases of CD may contribute to the underlying pathology of disrupted intestinal homeostasis and excessive inflammation.</description><subject>Acetylmuramyl-Alanyl-Isoglutamine - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Basic Research</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival</subject><subject>Colon - drug effects</subject><subject>Colon - metabolism</subject><subject>Colon - microbiology</subject><subject>Colon - pathology</subject><subject>Disease Models, Animal</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - microbiology</subject><subject>Epithelial Cells - pathology</subject><subject>Humans</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - microbiology</subject><subject>Intestinal Mucosa - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>NOD2</subject><subject>Nod2 Signaling Adaptor Protein - deficiency</subject><subject>Nod2 Signaling Adaptor Protein - genetics</subject><subject>Nod2 Signaling Adaptor Protein - metabolism</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Salmonella Infections - metabolism</subject><subject>Salmonella Infections - microbiology</subject><subject>Salmonella Infections - pathology</subject><subject>Salmonella typhimurium</subject><subject>Time Factors</subject><subject>上皮细胞</subject><subject>功能蛋白</subject><subject>细胞生长</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUuvEyEYhonReGp15d4QY9yYVq4zsDExx-MlOfFsdCthmG-mVAo9zKXx38ukjZcNJPDw8MKL0HNKtrwW6u1p32-p2ErFxQO0YozqDVOCPEQrSki90ZzVV-jJMOwJYZxL9hhdUaWk1Iqt0I-b2bcQHeAuZTzuAPs4pzDDAeKIU4e_3n1gZQ1n6KdgRx977FJI0TsMR18OBG8DdhAC7nM6jTtsY4uHKc9-tuEpetTZMMCzy7xG3z_efLv-vLm9-_Tl-v3txgkux42rtWhqV7e8Bc66BjonZW2lrpxzDatVY5USrBFtA1Rr4kBLUNBJTZ2uK8vX6N3Ze5yaA7SuhM82mGP2B5t_mWS9-X8n-p3p02xYLanSvAhenQUnGzsbe7NPU44lsinfywhRXC3DGr2-3JPT_QTDaA5-WB5vI6RpMJWuKqokK-CbM-hyGoYM3Z8slJiltsVrqDBLbYV-8W_8v-ylpwK8vOh2Kfb3pQXTWPez8wEMU7KqhOT8NyKLoRM</recordid><startdate>20081014</startdate><enddate>20081014</enddate><creator>Cruickshank, Sheena-M</creator><creator>Wakenshaw, Louise</creator><creator>Cardone, John</creator><creator>Howdle, Peter-D</creator><creator>Murray, Peter-J</creator><creator>Carding, Simon-R</creator><general>The Institute of Food Research, Norwich Research Park, Norwich NR4 7UA, United Kingdom%Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom%Section of Medicine, Surgery & Anaesthesia, Leeds Institute of Molecular Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom%Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105, United States</general><general>Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom</general><general>Faculty of Life Sciences, University of Manchester, Manchester M 13 9PT, United Kingdom%Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom</general><general>The WJG Press and Baishideng</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W91</scope><scope>~WA</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20081014</creationdate><title>Evidence for the involvement of NOD2 in regulating colonic epithelial cell growth and survival</title><author>Cruickshank, Sheena-M ; 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METHODS： A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA interference was also used to investigate the consequences of knocking down NOD2 gene expression on the growth and survival of colorectal carcinoma cell lines. RESULTS： In the colonic mucosa the highest levels of NOD2 expression were in proliferating crypt epithelial cells. Muramyl dipeptide （MDP）, that is recognized by NOD2, promoted CEC growth in vitro. By contrast,the growth of NOD2-deficient CECs was impaired. In vivo CEC proliferation was also reduced and apoptosis increased in Nod2^-/- mice, which were also evident following enteric Salmonella infection. Furthermore, neutralization of NOD2 mRNA expression in human colonic carcinoma cells by shRNA interference resulted in decreased survival due to increased levels of apoptosis. CONCLUSION： These findings are consistent with the involvement of NOD2 protein in promoting CEC growth and survival. Defects in proliferation by CECs in cases of CD may contribute to the underlying pathology of disrupted intestinal homeostasis and excessive inflammation.</abstract><cop>United States</cop><pub>The Institute of Food Research, Norwich Research Park, Norwich NR4 7UA, United Kingdom%Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom%Section of Medicine, Surgery & Anaesthesia, Leeds Institute of Molecular Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom%Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis TN 38105, United States</pub><pmid>18855982</pmid><doi>10.3748/wjg.14.5834</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Baishideng "World Journal of" online journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Acetylmuramyl-Alanyl-Isoglutamine - pharmacology Animals Apoptosis Basic Research Cell Line, Tumor Cell Proliferation - drug effects Cell Survival Colon - drug effects Colon - metabolism Colon - microbiology Colon - pathology Disease Models, Animal Epithelial Cells - drug effects Epithelial Cells - metabolism Epithelial Cells - microbiology Epithelial Cells - pathology Humans Intestinal Mucosa - drug effects Intestinal Mucosa - metabolism Intestinal Mucosa - microbiology Intestinal Mucosa - pathology Mice Mice, Inbred C57BL Mice, Knockout NOD2 Nod2 Signaling Adaptor Protein - deficiency Nod2 Signaling Adaptor Protein - genetics Nod2 Signaling Adaptor Protein - metabolism RNA Interference RNA, Small Interfering - metabolism Salmonella Infections - metabolism Salmonella Infections - microbiology Salmonella Infections - pathology Salmonella typhimurium Time Factors 上皮细胞 功能蛋白 细胞生长 |
| title | Evidence for the involvement of NOD2 in regulating colonic epithelial cell growth and survival |
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