Annexin A2 functions downstream of c‑Jun N‑terminal kinase to promote skin fibroblast cell migration
Delayed healing of skin wounds is one of the outcomes of diabetes mellitus (DM), a condition that affects a significant number of patients worldwide. However, the underlying mechanisms remain unknown. In order to examine proteome alterations in DM, a rat model of type 1 diabetes was developed using...
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| Veröffentlicht in: | Molecular medicine reports 2017-06, Vol.15 (6), p.4207-4216 |
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| creator | Wang, Youpei Wu, Xinmei Wang, Qing Zheng, Meiqin Pang, Lingxia |
| description | Delayed healing of skin wounds is one of the outcomes of diabetes mellitus (DM), a condition that affects a significant number of patients worldwide. However, the underlying mechanisms remain unknown. In order to examine proteome alterations in DM, a rat model of type 1 diabetes was developed using streptozotocin injections. The proteomic responses of normal and DM rat skin were analyzed by two‑dimensional electrophoresis, and differentially expressed proteins were identified using a liquid chromatography/mass spectrometry system. DM induced 36 and repressed 41 differentially expressed proteins, respectively. Altered proteins were involved in a number of biological processes, including RNA and protein metabolism, the tricarboxylic acid cycle, glycolysis, cytoskeleton regulation, hydrogen detoxification and calcium‑mediated signal transduction. In addition, overexpression of annexin A2, one of the signaling proteins altered by DM, accelerated the rate of human skin fibroblast cell migration. Application of SP600125, an inhibitor of a key regulator of cell migration c‑Jun N‑terminal kinase (JNK), inhibited the migration of normal cells. By contrast, SP600125 treatment did not inhibit the migration of annexin A2‑overexpressed cells, indicating that annexin A2 may function downstream of JNK. In conclusion, the results of the present study reveal the potential proteomic responses to DM in skin tissues, and demonstrate a positive functional role of annexin A2 in fibroblast cell migration. |
| doi_str_mv | 10.3892/mmr.2017.6535 |
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However, the underlying mechanisms remain unknown. In order to examine proteome alterations in DM, a rat model of type 1 diabetes was developed using streptozotocin injections. The proteomic responses of normal and DM rat skin were analyzed by two‑dimensional electrophoresis, and differentially expressed proteins were identified using a liquid chromatography/mass spectrometry system. DM induced 36 and repressed 41 differentially expressed proteins, respectively. Altered proteins were involved in a number of biological processes, including RNA and protein metabolism, the tricarboxylic acid cycle, glycolysis, cytoskeleton regulation, hydrogen detoxification and calcium‑mediated signal transduction. In addition, overexpression of annexin A2, one of the signaling proteins altered by DM, accelerated the rate of human skin fibroblast cell migration. Application of SP600125, an inhibitor of a key regulator of cell migration c‑Jun N‑terminal kinase (JNK), inhibited the migration of normal cells. By contrast, SP600125 treatment did not inhibit the migration of annexin A2‑overexpressed cells, indicating that annexin A2 may function downstream of JNK. In conclusion, the results of the present study reveal the potential proteomic responses to DM in skin tissues, and demonstrate a positive functional role of annexin A2 in fibroblast cell migration.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6535</identifier><identifier>PMID: 28487977</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Angiogenesis ; Animals ; Annexin A2 - metabolism ; Apoptosis ; c-Jun protein ; Calcium signalling ; Carbon ; Cell adhesion & migration ; Cell growth ; Cell migration ; Cell Movement - physiology ; Cells, Cultured ; Citric Acid Cycle - physiology ; Collagen ; Cytoskeleton ; Dehydrogenases ; Detoxification ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetes Mellitus, Type 1 - metabolism ; Diabetes Mellitus, Type 1 - pathology ; Disease Models, Animal ; Extracellular matrix ; Fibroblasts ; Fibroblasts - metabolism ; Fibroblasts - pathology ; Glycolysis ; Glycolysis - physiology ; Health aspects ; Humans ; Inflammation ; JNK Mitogen-Activated Protein Kinases - metabolism ; JNK protein ; Kinases ; Lipids ; Liquid chromatography ; Mass spectroscopy ; Metabolism ; Phosphotransferases ; Protein folding ; Protein turnover ; Proteome - metabolism ; Proteomics - methods ; Rats ; Ribonucleic acid ; RNA ; Rodents ; Signal transduction ; Signal Transduction - physiology ; Skin ; Skin - metabolism ; Skin - pathology ; Streptozocin ; Transcription factors ; Tricarboxylic acid cycle ; Ulcers ; Wound healing ; Wound Healing - physiology</subject><ispartof>Molecular medicine reports, 2017-06, Vol.15 (6), p.4207-4216</ispartof><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-96f635150a099b30aa41262795f0a4818a4a60bef438818c880fa3ea5f3760e53</citedby><cites>FETCH-LOGICAL-c427t-96f635150a099b30aa41262795f0a4818a4a60bef438818c880fa3ea5f3760e53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28487977$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Youpei</creatorcontrib><creatorcontrib>Wu, Xinmei</creatorcontrib><creatorcontrib>Wang, Qing</creatorcontrib><creatorcontrib>Zheng, Meiqin</creatorcontrib><creatorcontrib>Pang, Lingxia</creatorcontrib><title>Annexin A2 functions downstream of c‑Jun N‑terminal kinase to promote skin fibroblast cell migration</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Delayed healing of skin wounds is one of the outcomes of diabetes mellitus (DM), a condition that affects a significant number of patients worldwide. However, the underlying mechanisms remain unknown. In order to examine proteome alterations in DM, a rat model of type 1 diabetes was developed using streptozotocin injections. The proteomic responses of normal and DM rat skin were analyzed by two‑dimensional electrophoresis, and differentially expressed proteins were identified using a liquid chromatography/mass spectrometry system. DM induced 36 and repressed 41 differentially expressed proteins, respectively. Altered proteins were involved in a number of biological processes, including RNA and protein metabolism, the tricarboxylic acid cycle, glycolysis, cytoskeleton regulation, hydrogen detoxification and calcium‑mediated signal transduction. In addition, overexpression of annexin A2, one of the signaling proteins altered by DM, accelerated the rate of human skin fibroblast cell migration. Application of SP600125, an inhibitor of a key regulator of cell migration c‑Jun N‑terminal kinase (JNK), inhibited the migration of normal cells. By contrast, SP600125 treatment did not inhibit the migration of annexin A2‑overexpressed cells, indicating that annexin A2 may function downstream of JNK. In conclusion, the results of the present study reveal the potential proteomic responses to DM in skin tissues, and demonstrate a positive functional role of annexin A2 in fibroblast cell migration.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Annexin A2 - metabolism</subject><subject>Apoptosis</subject><subject>c-Jun protein</subject><subject>Calcium signalling</subject><subject>Carbon</subject><subject>Cell adhesion & migration</subject><subject>Cell growth</subject><subject>Cell migration</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Citric Acid Cycle - physiology</subject><subject>Collagen</subject><subject>Cytoskeleton</subject><subject>Dehydrogenases</subject><subject>Detoxification</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes Mellitus, Type 1 - metabolism</subject><subject>Diabetes Mellitus, Type 1 - pathology</subject><subject>Disease Models, Animal</subject><subject>Extracellular matrix</subject><subject>Fibroblasts</subject><subject>Fibroblasts - metabolism</subject><subject>Fibroblasts - pathology</subject><subject>Glycolysis</subject><subject>Glycolysis - physiology</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Inflammation</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Liquid chromatography</subject><subject>Mass spectroscopy</subject><subject>Metabolism</subject><subject>Phosphotransferases</subject><subject>Protein folding</subject><subject>Protein turnover</subject><subject>Proteome - metabolism</subject><subject>Proteomics - methods</subject><subject>Rats</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Skin</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>Streptozocin</subject><subject>Transcription factors</subject><subject>Tricarboxylic acid cycle</subject><subject>Ulcers</subject><subject>Wound healing</subject><subject>Wound Healing - physiology</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkctuVSEUhonR2FodOm1InHSyj9wvw5PGW9PoRMeEvQ9U2g20wI466yv0FX0S2enRRmNIWLDyrT8__AC8xGhDlSavYywbgrDcCE75I3CIpcYDRYg93p-J1vIAPKv1EiHBCddPwQFRTEkt5SH4uk3JfQ8Jbgn0S5payKnCXf6WaivORpg9nH7e3p0tCX7stbkSQ7IzvOp7dbBleF1yzM3B2lvQh7Hkcba1wcnNM4zhothV9Dl44u1c3Yt9PQJf3r75fPp-OP_07sPp9nyYGJFt0MILyjFHFmk9UmQtw0QQqblHlimsLLMCjc4zqvptUgp5S53lnkqBHKdH4ORet9u6WVxtJoa6WrHJ5aUarLTGGBMlOvrqH_QyL6U_rlNaEK5Y_7EH6sLOzoTkcyt2WkXNlmlFFUEEdWrzH6qvnYthysn50Pt_DQz3A1PJtRbnzXUJ0ZYfBiOzJmt6smZN1qzJdv54b3YZo9v9oX9HSX8BOAqeWg</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Wang, Youpei</creator><creator>Wu, Xinmei</creator><creator>Wang, Qing</creator><creator>Zheng, Meiqin</creator><creator>Pang, Lingxia</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170601</creationdate><title>Annexin A2 functions downstream of c‑Jun N‑terminal kinase to promote skin fibroblast cell migration</title><author>Wang, Youpei ; Wu, Xinmei ; Wang, Qing ; Zheng, Meiqin ; Pang, Lingxia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-96f635150a099b30aa41262795f0a4818a4a60bef438818c880fa3ea5f3760e53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Annexin A2 - metabolism</topic><topic>Apoptosis</topic><topic>c-Jun protein</topic><topic>Calcium signalling</topic><topic>Carbon</topic><topic>Cell adhesion & migration</topic><topic>Cell growth</topic><topic>Cell migration</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Citric Acid Cycle - physiology</topic><topic>Collagen</topic><topic>Cytoskeleton</topic><topic>Dehydrogenases</topic><topic>Detoxification</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes Mellitus, Type 1 - metabolism</topic><topic>Diabetes Mellitus, Type 1 - pathology</topic><topic>Disease Models, Animal</topic><topic>Extracellular matrix</topic><topic>Fibroblasts</topic><topic>Fibroblasts - metabolism</topic><topic>Fibroblasts - pathology</topic><topic>Glycolysis</topic><topic>Glycolysis - physiology</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Inflammation</topic><topic>JNK Mitogen-Activated Protein Kinases - 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Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Youpei</au><au>Wu, Xinmei</au><au>Wang, Qing</au><au>Zheng, Meiqin</au><au>Pang, Lingxia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Annexin A2 functions downstream of c‑Jun N‑terminal kinase to promote skin fibroblast cell migration</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>15</volume><issue>6</issue><spage>4207</spage><epage>4216</epage><pages>4207-4216</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Delayed healing of skin wounds is one of the outcomes of diabetes mellitus (DM), a condition that affects a significant number of patients worldwide. However, the underlying mechanisms remain unknown. In order to examine proteome alterations in DM, a rat model of type 1 diabetes was developed using streptozotocin injections. The proteomic responses of normal and DM rat skin were analyzed by two‑dimensional electrophoresis, and differentially expressed proteins were identified using a liquid chromatography/mass spectrometry system. DM induced 36 and repressed 41 differentially expressed proteins, respectively. Altered proteins were involved in a number of biological processes, including RNA and protein metabolism, the tricarboxylic acid cycle, glycolysis, cytoskeleton regulation, hydrogen detoxification and calcium‑mediated signal transduction. In addition, overexpression of annexin A2, one of the signaling proteins altered by DM, accelerated the rate of human skin fibroblast cell migration. Application of SP600125, an inhibitor of a key regulator of cell migration c‑Jun N‑terminal kinase (JNK), inhibited the migration of normal cells. By contrast, SP600125 treatment did not inhibit the migration of annexin A2‑overexpressed cells, indicating that annexin A2 may function downstream of JNK. In conclusion, the results of the present study reveal the potential proteomic responses to DM in skin tissues, and demonstrate a positive functional role of annexin A2 in fibroblast cell migration.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>28487977</pmid><doi>10.3892/mmr.2017.6535</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Animals Annexin A2 - metabolism Apoptosis c-Jun protein Calcium signalling Carbon Cell adhesion & migration Cell growth Cell migration Cell Movement - physiology Cells, Cultured Citric Acid Cycle - physiology Collagen Cytoskeleton Dehydrogenases Detoxification Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes Mellitus, Type 1 - metabolism Diabetes Mellitus, Type 1 - pathology Disease Models, Animal Extracellular matrix Fibroblasts Fibroblasts - metabolism Fibroblasts - pathology Glycolysis Glycolysis - physiology Health aspects Humans Inflammation JNK Mitogen-Activated Protein Kinases - metabolism JNK protein Kinases Lipids Liquid chromatography Mass spectroscopy Metabolism Phosphotransferases Protein folding Protein turnover Proteome - metabolism Proteomics - methods Rats Ribonucleic acid RNA Rodents Signal transduction Signal Transduction - physiology Skin Skin - metabolism Skin - pathology Streptozocin Transcription factors Tricarboxylic acid cycle Ulcers Wound healing Wound Healing - physiology |
| title | Annexin A2 functions downstream of c‑Jun N‑terminal kinase to promote skin fibroblast cell migration |
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