Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway
Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution pat...
Gespeichert in:
| Veröffentlicht in: | Cell biology international 2014-10, Vol.38 (10), p.1194-1204 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1204 |
|---|---|
| container_issue | 10 |
| container_start_page | 1194 |
| container_title | Cell biology international |
| container_volume | 38 |
| creator | Min, Xiao-Hui Yu, Tao Qing, Qing Yuan, Yu-Hong Zhong, Wa Chen, Guang-Cheng Zhao, Li-Na Deng, Na Zhang, Li-Fa Chen, Qi-Kui |
| description | Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D‐lactate was raised in diabetic mice (P |
| doi_str_mv | 10.1002/cbin.10323 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1616479643</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1616479643</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4653-bafbe651e511e4115552af77e242ea3d936d54a242e09f53ab7bb74a0e8ecdc53</originalsourceid><addsrcrecordid>eNp9kc9u1DAQhyMEoqVw4QGQJS6oUqj_Z3Nsl7JdqVoOgFbiYtnOhHVJnGAnWva9eECcpl0hDpw8o_nms61flr0m-D3BmF5Y43yqGGVPslOCS5EvmBBPp1qKXJalOMlexHiHMSF8IZ9nJ5QvSlxScZr9vjS-C61uUOXqGgL4wenBdR51NXJ-gDg4n6bQu2EHjRtbpH3198ToEBwEVB1iPXp7v-t80mkDg7OodRaQjrGzSQwV2icRqqAPEGNqN91gdxeb9fIDGoL2sRqPinl0A5Gg6L5Pd_V62O314WX2rNZNhFcP51n29eP1l-VNfvtptV5e3uaWS8Fyo2sDUhAQhAAnRAhBdV0UQDkFzaqSyUpwPXW4rAXTpjCm4BrDAmxlBTvL3s3ePnQ_x_Rh1bpooWm0h26MikgieVFKzhL69h_0rhtDevNEcVkUdEFpos5nyoYuxgC16oNrdTgogtWUpZqyVPdZJvjNg3I0LVRH9DG8BJAZ2LsGDv9RqeXVevMozecdFwf4ddzR4YeSBSuE2m5W6ops6Up-_qa27A_5gryZ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1646772822</pqid></control><display><type>article</type><title>Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway</title><source>Wiley Online Library - AutoHoldings Journals</source><source>MEDLINE</source><creator>Min, Xiao-Hui ; Yu, Tao ; Qing, Qing ; Yuan, Yu-Hong ; Zhong, Wa ; Chen, Guang-Cheng ; Zhao, Li-Na ; Deng, Na ; Zhang, Li-Fa ; Chen, Qi-Kui</creator><creatorcontrib>Min, Xiao-Hui ; Yu, Tao ; Qing, Qing ; Yuan, Yu-Hong ; Zhong, Wa ; Chen, Guang-Cheng ; Zhao, Li-Na ; Deng, Na ; Zhang, Li-Fa ; Chen, Qi-Kui</creatorcontrib><description>Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D‐lactate was raised in diabetic mice (P < 0.05). The expression of Zo1 and Ocln in the small intestine of diabetic mice were lower, while the markers for absorptive cell (SI) and Paneth cell (Lyz1) were significantly higher than in control mice (P < 0.05). The expression of Msi1, Notch1, and Dll1 in small intestine gradually increased throughout the course of hyperglycemia in diabetic mice (P < 0.05). However, the expression of NICD, RBP‐jκ, Math1, and Hes1 had a reverse trend compared with Msi1 and Notch1. Intestinal absorptive cells and Paneth cells had a high proliferation rate in diabetic mice. However, the intestinal barrier dysfunction associated with the decreased expressions of Zo1 and Ocln was detected throughout hyperglycemia. In conclusion, downregulation of Notch/Hes1 signal pathway caused by depressed Notch/NICD transduction is associated with the abnormal differentiation of IECs and intestinal barrier dysfunction in diabetic mice.</description><identifier>ISSN: 1065-6995</identifier><identifier>EISSN: 1095-8355</identifier><identifier>DOI: 10.1002/cbin.10323</identifier><identifier>PMID: 24890925</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Basic Helix-Loop-Helix Transcription Factors - metabolism ; Cell Differentiation ; Cell Membrane Permeability ; Diabetes ; diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - pathology ; differentiation ; Down-Regulation ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; intestinal barrier function ; intestinal epithelial cells ; Intestinal Mucosa - cytology ; Intestinal Mucosa - metabolism ; Intestinal Mucosa - pathology ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Notch pathway ; Receptor, Notch1 - genetics ; Receptor, Notch1 - metabolism ; RNA-Binding Proteins - genetics ; RNA-Binding Proteins - metabolism ; Rodents ; Signal Transduction ; Small intestine ; Transcription Factor HES-1</subject><ispartof>Cell biology international, 2014-10, Vol.38 (10), p.1194-1204</ispartof><rights>2014 International Federation for Cell Biology</rights><rights>2014 International Federation for Cell Biology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4653-bafbe651e511e4115552af77e242ea3d936d54a242e09f53ab7bb74a0e8ecdc53</citedby><cites>FETCH-LOGICAL-c4653-bafbe651e511e4115552af77e242ea3d936d54a242e09f53ab7bb74a0e8ecdc53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcbin.10323$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcbin.10323$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24890925$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Min, Xiao-Hui</creatorcontrib><creatorcontrib>Yu, Tao</creatorcontrib><creatorcontrib>Qing, Qing</creatorcontrib><creatorcontrib>Yuan, Yu-Hong</creatorcontrib><creatorcontrib>Zhong, Wa</creatorcontrib><creatorcontrib>Chen, Guang-Cheng</creatorcontrib><creatorcontrib>Zhao, Li-Na</creatorcontrib><creatorcontrib>Deng, Na</creatorcontrib><creatorcontrib>Zhang, Li-Fa</creatorcontrib><creatorcontrib>Chen, Qi-Kui</creatorcontrib><title>Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway</title><title>Cell biology international</title><addtitle>Cell Biol Int</addtitle><description>Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D‐lactate was raised in diabetic mice (P < 0.05). The expression of Zo1 and Ocln in the small intestine of diabetic mice were lower, while the markers for absorptive cell (SI) and Paneth cell (Lyz1) were significantly higher than in control mice (P < 0.05). The expression of Msi1, Notch1, and Dll1 in small intestine gradually increased throughout the course of hyperglycemia in diabetic mice (P < 0.05). However, the expression of NICD, RBP‐jκ, Math1, and Hes1 had a reverse trend compared with Msi1 and Notch1. Intestinal absorptive cells and Paneth cells had a high proliferation rate in diabetic mice. However, the intestinal barrier dysfunction associated with the decreased expressions of Zo1 and Ocln was detected throughout hyperglycemia. In conclusion, downregulation of Notch/Hes1 signal pathway caused by depressed Notch/NICD transduction is associated with the abnormal differentiation of IECs and intestinal barrier dysfunction in diabetic mice.</description><subject>Animals</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Basic Helix-Loop-Helix Transcription Factors - metabolism</subject><subject>Cell Differentiation</subject><subject>Cell Membrane Permeability</subject><subject>Diabetes</subject><subject>diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>differentiation</subject><subject>Down-Regulation</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>intestinal barrier function</subject><subject>intestinal epithelial cells</subject><subject>Intestinal Mucosa - cytology</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestinal Mucosa - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Notch pathway</subject><subject>Receptor, Notch1 - genetics</subject><subject>Receptor, Notch1 - metabolism</subject><subject>RNA-Binding Proteins - genetics</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Small intestine</subject><subject>Transcription Factor HES-1</subject><issn>1065-6995</issn><issn>1095-8355</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9u1DAQhyMEoqVw4QGQJS6oUqj_Z3Nsl7JdqVoOgFbiYtnOhHVJnGAnWva9eECcpl0hDpw8o_nms61flr0m-D3BmF5Y43yqGGVPslOCS5EvmBBPp1qKXJalOMlexHiHMSF8IZ9nJ5QvSlxScZr9vjS-C61uUOXqGgL4wenBdR51NXJ-gDg4n6bQu2EHjRtbpH3198ToEBwEVB1iPXp7v-t80mkDg7OodRaQjrGzSQwV2icRqqAPEGNqN91gdxeb9fIDGoL2sRqPinl0A5Gg6L5Pd_V62O314WX2rNZNhFcP51n29eP1l-VNfvtptV5e3uaWS8Fyo2sDUhAQhAAnRAhBdV0UQDkFzaqSyUpwPXW4rAXTpjCm4BrDAmxlBTvL3s3ePnQ_x_Rh1bpooWm0h26MikgieVFKzhL69h_0rhtDevNEcVkUdEFpos5nyoYuxgC16oNrdTgogtWUpZqyVPdZJvjNg3I0LVRH9DG8BJAZ2LsGDv9RqeXVevMozecdFwf4ddzR4YeSBSuE2m5W6ops6Up-_qa27A_5gryZ</recordid><startdate>201410</startdate><enddate>201410</enddate><creator>Min, Xiao-Hui</creator><creator>Yu, Tao</creator><creator>Qing, Qing</creator><creator>Yuan, Yu-Hong</creator><creator>Zhong, Wa</creator><creator>Chen, Guang-Cheng</creator><creator>Zhao, Li-Na</creator><creator>Deng, Na</creator><creator>Zhang, Li-Fa</creator><creator>Chen, Qi-Kui</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201410</creationdate><title>Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway</title><author>Min, Xiao-Hui ; Yu, Tao ; Qing, Qing ; Yuan, Yu-Hong ; Zhong, Wa ; Chen, Guang-Cheng ; Zhao, Li-Na ; Deng, Na ; Zhang, Li-Fa ; Chen, Qi-Kui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4653-bafbe651e511e4115552af77e242ea3d936d54a242e09f53ab7bb74a0e8ecdc53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Basic Helix-Loop-Helix Transcription Factors - genetics</topic><topic>Basic Helix-Loop-Helix Transcription Factors - metabolism</topic><topic>Cell Differentiation</topic><topic>Cell Membrane Permeability</topic><topic>Diabetes</topic><topic>diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>differentiation</topic><topic>Down-Regulation</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - metabolism</topic><topic>intestinal barrier function</topic><topic>intestinal epithelial cells</topic><topic>Intestinal Mucosa - cytology</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestinal Mucosa - pathology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Notch pathway</topic><topic>Receptor, Notch1 - genetics</topic><topic>Receptor, Notch1 - metabolism</topic><topic>RNA-Binding Proteins - genetics</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Small intestine</topic><topic>Transcription Factor HES-1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Min, Xiao-Hui</creatorcontrib><creatorcontrib>Yu, Tao</creatorcontrib><creatorcontrib>Qing, Qing</creatorcontrib><creatorcontrib>Yuan, Yu-Hong</creatorcontrib><creatorcontrib>Zhong, Wa</creatorcontrib><creatorcontrib>Chen, Guang-Cheng</creatorcontrib><creatorcontrib>Zhao, Li-Na</creatorcontrib><creatorcontrib>Deng, Na</creatorcontrib><creatorcontrib>Zhang, Li-Fa</creatorcontrib><creatorcontrib>Chen, Qi-Kui</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Min, Xiao-Hui</au><au>Yu, Tao</au><au>Qing, Qing</au><au>Yuan, Yu-Hong</au><au>Zhong, Wa</au><au>Chen, Guang-Cheng</au><au>Zhao, Li-Na</au><au>Deng, Na</au><au>Zhang, Li-Fa</au><au>Chen, Qi-Kui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway</atitle><jtitle>Cell biology international</jtitle><addtitle>Cell Biol Int</addtitle><date>2014-10</date><risdate>2014</risdate><volume>38</volume><issue>10</issue><spage>1194</spage><epage>1204</epage><pages>1194-1204</pages><issn>1065-6995</issn><eissn>1095-8355</eissn><abstract>Proliferative change and intestinal barrier dysfunction in intestinal mucosa of diabetes have been described, but the differentiation characteristics of intestinal epithelial cells (IECs) and the mechanisms in the IECs development remain unclear. To explore the intestinal epithelial constitution patterns and barrier function, the diabetic mouse model was induced by streptozotocin. Tight junctions between IECs were significantly damaged and the serum level of D‐lactate was raised in diabetic mice (P < 0.05). The expression of Zo1 and Ocln in the small intestine of diabetic mice were lower, while the markers for absorptive cell (SI) and Paneth cell (Lyz1) were significantly higher than in control mice (P < 0.05). The expression of Msi1, Notch1, and Dll1 in small intestine gradually increased throughout the course of hyperglycemia in diabetic mice (P < 0.05). However, the expression of NICD, RBP‐jκ, Math1, and Hes1 had a reverse trend compared with Msi1 and Notch1. Intestinal absorptive cells and Paneth cells had a high proliferation rate in diabetic mice. However, the intestinal barrier dysfunction associated with the decreased expressions of Zo1 and Ocln was detected throughout hyperglycemia. In conclusion, downregulation of Notch/Hes1 signal pathway caused by depressed Notch/NICD transduction is associated with the abnormal differentiation of IECs and intestinal barrier dysfunction in diabetic mice.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24890925</pmid><doi>10.1002/cbin.10323</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1065-6995 |
| ispartof | Cell biology international, 2014-10, Vol.38 (10), p.1194-1204 |
| issn | 1065-6995 1095-8355 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1616479643 |
| source | Wiley Online Library - AutoHoldings Journals; MEDLINE |
| subjects | Animals Basic Helix-Loop-Helix Transcription Factors - genetics Basic Helix-Loop-Helix Transcription Factors - metabolism Cell Differentiation Cell Membrane Permeability Diabetes diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - pathology differentiation Down-Regulation Homeodomain Proteins - genetics Homeodomain Proteins - metabolism intestinal barrier function intestinal epithelial cells Intestinal Mucosa - cytology Intestinal Mucosa - metabolism Intestinal Mucosa - pathology Mice Mice, Inbred C57BL Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Notch pathway Receptor, Notch1 - genetics Receptor, Notch1 - metabolism RNA-Binding Proteins - genetics RNA-Binding Proteins - metabolism Rodents Signal Transduction Small intestine Transcription Factor HES-1 |
| title | Abnormal differentiation of intestinal epithelium and intestinal barrier dysfunction in diabetic mice associated with depressed Notch/NICD transduction in Notch/Hes1 signal pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T22%3A42%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Abnormal%20differentiation%20of%20intestinal%20epithelium%20and%20intestinal%20barrier%20dysfunction%20in%20diabetic%20mice%20associated%20with%20depressed%20Notch/NICD%20transduction%20in%20Notch/Hes1%20signal%20pathway&rft.jtitle=Cell%20biology%20international&rft.au=Min,%20Xiao-Hui&rft.date=2014-10&rft.volume=38&rft.issue=10&rft.spage=1194&rft.epage=1204&rft.pages=1194-1204&rft.issn=1065-6995&rft.eissn=1095-8355&rft_id=info:doi/10.1002/cbin.10323&rft_dat=%3Cproquest_cross%3E1616479643%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1646772822&rft_id=info:pmid/24890925&rfr_iscdi=true |