Exendin‑4 promotes osteogenic differentiation of adipose‑derived stem cells and facilitates bone repair
Inflammation‑related bone defects pose a heavy burden on patients and orthopedic surgeons. Although stem‑cell‑based bone repair has developed rapidly, it is of great significance to characterize bio‑active molecules that facilitate bone regeneration. It is reported that a glucagon‑like peptide 1 rec...
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Veröffentlicht in: | Molecular medicine reports 2019-12, Vol.20 (6), p.4933-4942 |
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creator | Deng, Banglian Zhu, Wenzhong Duan, Yansheng Hu, Yuqian Chen, Xuefeng Song, Shuang Yi, Zian Song, Yingliang |
description | Inflammation‑related bone defects pose a heavy burden on patients and orthopedic surgeons. Although stem‑cell‑based bone repair has developed rapidly, it is of great significance to characterize bio‑active molecules that facilitate bone regeneration. It is reported that a glucagon‑like peptide 1 receptor agonist, exendin‑4, promoted bone regeneration mediated by the transplantation of adipose‑derived stem cells in a metaphyseal defect mouse model of femur injury. However, the underlying mechanism is unclear. Bone imaging, immunohistochemistry real‑time PCR and western blot analysis were used in the present study, and the results revealed that exendin‑4 increased the transcription of the osteogenic differentiation‑related genes and induced osteogenic differentiation in situ. Furthermore, the present data obtained from sorted adipose‑derived stem cells revealed that exendin‑4 promoted osteogenic differentiation and inhibited adipogenic differentiation in vitro. These findings indicated that exendin‑4 facilitates osteogenic differentiation of transplanted adipose‑derived stem cells for bone repair and illuminated clinical prospects of both adipose‑derived stem cells and exendin‑4 in stem‑cell‑based bone defect repair. |
doi_str_mv | 10.3892/mmr.2019.10764 |
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Although stem‑cell‑based bone repair has developed rapidly, it is of great significance to characterize bio‑active molecules that facilitate bone regeneration. It is reported that a glucagon‑like peptide 1 receptor agonist, exendin‑4, promoted bone regeneration mediated by the transplantation of adipose‑derived stem cells in a metaphyseal defect mouse model of femur injury. However, the underlying mechanism is unclear. Bone imaging, immunohistochemistry real‑time PCR and western blot analysis were used in the present study, and the results revealed that exendin‑4 increased the transcription of the osteogenic differentiation‑related genes and induced osteogenic differentiation in situ. Furthermore, the present data obtained from sorted adipose‑derived stem cells revealed that exendin‑4 promoted osteogenic differentiation and inhibited adipogenic differentiation in vitro. These findings indicated that exendin‑4 facilitates osteogenic differentiation of transplanted adipose‑derived stem cells for bone repair and illuminated clinical prospects of both adipose‑derived stem cells and exendin‑4 in stem‑cell‑based bone defect repair.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2019.10764</identifier><identifier>PMID: 31661134</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Animals ; Bone growth ; Bone healing ; Bone imaging ; Bone Regeneration - drug effects ; Bones ; Cell differentiation ; Cells, Cultured ; Defects ; Exenatide ; Exenatide - pharmacology ; Exenatide - therapeutic use ; Experiments ; Femur ; Femur - drug effects ; Femur - injuries ; Femur - metabolism ; Femur - pathology ; Genes ; Glucagon ; Glucagon-like peptide 1 ; Glucagon-Like Peptide-1 Receptor - agonists ; Immunohistochemistry ; Inflammation ; Kinases ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells - cytology ; Mesenchymal Stem Cells - drug effects ; Mesenchymal Stem Cells - metabolism ; Mice, Inbred C57BL ; Osteogenesis - drug effects ; Peptides ; Pharmaceutical industry ; Proteins ; Regeneration ; Scientific equipment industry ; Stem cell transplantation ; Stem cells ; Surgeons ; Surgery ; Tetracyclines ; Tissue engineering ; Transcription ; Transcription (Genetics) ; Transcriptional Activation - drug effects ; Type 2 diabetes</subject><ispartof>Molecular medicine reports, 2019-12, Vol.20 (6), p.4933-4942</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><rights>Copyright: © Deng et al. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-d1010f9b0f0360c44fbccdd1e3335e62d8d031a2adbff4bc390570f1385afe023</citedby><cites>FETCH-LOGICAL-c485t-d1010f9b0f0360c44fbccdd1e3335e62d8d031a2adbff4bc390570f1385afe023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,778,782,883,27907,27908</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31661134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Deng, Banglian</creatorcontrib><creatorcontrib>Zhu, Wenzhong</creatorcontrib><creatorcontrib>Duan, Yansheng</creatorcontrib><creatorcontrib>Hu, Yuqian</creatorcontrib><creatorcontrib>Chen, Xuefeng</creatorcontrib><creatorcontrib>Song, Shuang</creatorcontrib><creatorcontrib>Yi, Zian</creatorcontrib><creatorcontrib>Song, Yingliang</creatorcontrib><title>Exendin‑4 promotes osteogenic differentiation of adipose‑derived stem cells and facilitates bone repair</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Inflammation‑related bone defects pose a heavy burden on patients and orthopedic surgeons. Although stem‑cell‑based bone repair has developed rapidly, it is of great significance to characterize bio‑active molecules that facilitate bone regeneration. It is reported that a glucagon‑like peptide 1 receptor agonist, exendin‑4, promoted bone regeneration mediated by the transplantation of adipose‑derived stem cells in a metaphyseal defect mouse model of femur injury. However, the underlying mechanism is unclear. Bone imaging, immunohistochemistry real‑time PCR and western blot analysis were used in the present study, and the results revealed that exendin‑4 increased the transcription of the osteogenic differentiation‑related genes and induced osteogenic differentiation in situ. Furthermore, the present data obtained from sorted adipose‑derived stem cells revealed that exendin‑4 promoted osteogenic differentiation and inhibited adipogenic differentiation in vitro. These findings indicated that exendin‑4 facilitates osteogenic differentiation of transplanted adipose‑derived stem cells for bone repair and illuminated clinical prospects of both adipose‑derived stem cells and exendin‑4 in stem‑cell‑based bone defect repair.</description><subject>Animals</subject><subject>Bone growth</subject><subject>Bone healing</subject><subject>Bone imaging</subject><subject>Bone Regeneration - drug effects</subject><subject>Bones</subject><subject>Cell differentiation</subject><subject>Cells, Cultured</subject><subject>Defects</subject><subject>Exenatide</subject><subject>Exenatide - pharmacology</subject><subject>Exenatide - therapeutic use</subject><subject>Experiments</subject><subject>Femur</subject><subject>Femur - drug effects</subject><subject>Femur - injuries</subject><subject>Femur - metabolism</subject><subject>Femur - pathology</subject><subject>Genes</subject><subject>Glucagon</subject><subject>Glucagon-like peptide 1</subject><subject>Glucagon-Like Peptide-1 Receptor - agonists</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Male</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal Stem Cells - cytology</subject><subject>Mesenchymal Stem Cells - drug effects</subject><subject>Mesenchymal Stem Cells - metabolism</subject><subject>Mice, Inbred C57BL</subject><subject>Osteogenesis - drug effects</subject><subject>Peptides</subject><subject>Pharmaceutical industry</subject><subject>Proteins</subject><subject>Regeneration</subject><subject>Scientific equipment industry</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Surgeons</subject><subject>Surgery</subject><subject>Tetracyclines</subject><subject>Tissue engineering</subject><subject>Transcription</subject><subject>Transcription (Genetics)</subject><subject>Transcriptional Activation - drug effects</subject><subject>Type 2 diabetes</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkstu1TAQhi0EoqWwZYkssenmHMaXOMkGqarKRarEBtaWY48PLokd7JwKdn0FXpEnwYFDuajywpb9zT_-Rz8hTxlsRdfzF9OUtxxYv2XQKnmPHLO2ZxsBIO8fzrzv2yPyqJQrANXwpn9IjgRTijEhj8mniy8YXYjfb75JOuc0pQULTWXBtMMYLHXBe8wYl2CWkCJNnhoX5lSwljjM4RodrfhELY5joSY66o0NY1jMKjWkiDTjbEJ-TB54MxZ8cthPyIdXF-_P32wu371-e352ubGya5aNY8DA9wN4EAqslH6w1jmGQogGFXedA8EMN27wXg5W9NC04JnoGuMRuDghL3_pzvthQmfr57MZ9ZzDZPJXnUzQ_77E8FHv0rVWXSMb2VaB04NATp_3WBY9hbLaMxHTvmguGPBeslZV9Pl_6FXa51jtrZQSneCc_6F2ZkQdok-1r11F9Zli0EnRgajU9g6qLodTsHWOPtT7uwpsTqVk9LceGeg1HrrGQ6_x0D_jUQue_T2ZW_x3HsQPQJG49Q</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Deng, Banglian</creator><creator>Zhu, Wenzhong</creator><creator>Duan, Yansheng</creator><creator>Hu, Yuqian</creator><creator>Chen, Xuefeng</creator><creator>Song, Shuang</creator><creator>Yi, Zian</creator><creator>Song, Yingliang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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drug effects</topic><topic>Bones</topic><topic>Cell differentiation</topic><topic>Cells, Cultured</topic><topic>Defects</topic><topic>Exenatide</topic><topic>Exenatide - pharmacology</topic><topic>Exenatide - therapeutic use</topic><topic>Experiments</topic><topic>Femur</topic><topic>Femur - drug effects</topic><topic>Femur - injuries</topic><topic>Femur - metabolism</topic><topic>Femur - pathology</topic><topic>Genes</topic><topic>Glucagon</topic><topic>Glucagon-like peptide 1</topic><topic>Glucagon-Like Peptide-1 Receptor - agonists</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Male</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal Stem Cells - cytology</topic><topic>Mesenchymal Stem Cells - drug effects</topic><topic>Mesenchymal Stem Cells - metabolism</topic><topic>Mice, Inbred C57BL</topic><topic>Osteogenesis - drug effects</topic><topic>Peptides</topic><topic>Pharmaceutical industry</topic><topic>Proteins</topic><topic>Regeneration</topic><topic>Scientific equipment industry</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Surgeons</topic><topic>Surgery</topic><topic>Tetracyclines</topic><topic>Tissue engineering</topic><topic>Transcription</topic><topic>Transcription (Genetics)</topic><topic>Transcriptional Activation - drug effects</topic><topic>Type 2 diabetes</topic><toplevel>online_resources</toplevel><creatorcontrib>Deng, Banglian</creatorcontrib><creatorcontrib>Zhu, Wenzhong</creatorcontrib><creatorcontrib>Duan, Yansheng</creatorcontrib><creatorcontrib>Hu, Yuqian</creatorcontrib><creatorcontrib>Chen, Xuefeng</creatorcontrib><creatorcontrib>Song, Shuang</creatorcontrib><creatorcontrib>Yi, Zian</creatorcontrib><creatorcontrib>Song, Yingliang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Deng, Banglian</au><au>Zhu, Wenzhong</au><au>Duan, Yansheng</au><au>Hu, Yuqian</au><au>Chen, Xuefeng</au><au>Song, Shuang</au><au>Yi, Zian</au><au>Song, Yingliang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exendin‑4 promotes osteogenic differentiation of adipose‑derived stem cells and facilitates bone repair</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2019-12-01</date><risdate>2019</risdate><volume>20</volume><issue>6</issue><spage>4933</spage><epage>4942</epage><pages>4933-4942</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Inflammation‑related bone defects pose a heavy burden on patients and orthopedic surgeons. Although stem‑cell‑based bone repair has developed rapidly, it is of great significance to characterize bio‑active molecules that facilitate bone regeneration. It is reported that a glucagon‑like peptide 1 receptor agonist, exendin‑4, promoted bone regeneration mediated by the transplantation of adipose‑derived stem cells in a metaphyseal defect mouse model of femur injury. However, the underlying mechanism is unclear. Bone imaging, immunohistochemistry real‑time PCR and western blot analysis were used in the present study, and the results revealed that exendin‑4 increased the transcription of the osteogenic differentiation‑related genes and induced osteogenic differentiation in situ. Furthermore, the present data obtained from sorted adipose‑derived stem cells revealed that exendin‑4 promoted osteogenic differentiation and inhibited adipogenic differentiation in vitro. These findings indicated that exendin‑4 facilitates osteogenic differentiation of transplanted adipose‑derived stem cells for bone repair and illuminated clinical prospects of both adipose‑derived stem cells and exendin‑4 in stem‑cell‑based bone defect repair.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>31661134</pmid><doi>10.3892/mmr.2019.10764</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Bone growth Bone healing Bone imaging Bone Regeneration - drug effects Bones Cell differentiation Cells, Cultured Defects Exenatide Exenatide - pharmacology Exenatide - therapeutic use Experiments Femur Femur - drug effects Femur - injuries Femur - metabolism Femur - pathology Genes Glucagon Glucagon-like peptide 1 Glucagon-Like Peptide-1 Receptor - agonists Immunohistochemistry Inflammation Kinases Male Mesenchymal Stem Cell Transplantation Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Mice, Inbred C57BL Osteogenesis - drug effects Peptides Pharmaceutical industry Proteins Regeneration Scientific equipment industry Stem cell transplantation Stem cells Surgeons Surgery Tetracyclines Tissue engineering Transcription Transcription (Genetics) Transcriptional Activation - drug effects Type 2 diabetes |
title | Exendin‑4 promotes osteogenic differentiation of adipose‑derived stem cells and facilitates bone repair |
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