Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat
To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by...
Gespeichert in:
| Veröffentlicht in: | Molecular and cellular biochemistry 2012-02, Vol.361 (1-2), p.305-314 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 314 |
|---|---|
| container_issue | 1-2 |
| container_start_page | 305 |
| container_title | Molecular and cellular biochemistry |
| container_volume | 361 |
| creator | Xie, Shuyang Xie, Ning Li, Youjie Wang, Pingyu Zhang, Chao Li, Qiang Liu, Xiaolin Deng, Jingti Zhang, Can Lv, Changjun |
| description | To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by immunohistochemistry, ELISA, reverse transcription-polymerase chain reaction (RT-PCR), and real-time PCR detection. GFP expression in RAOEC cells (rat vascular aortic endothelial cell)were detected by flow cytometry and fluorescent microscope. TRB2 gene expression was increased in endothelia cell and the adventitia of Goto-Kakizaki (GK) rat compared with Wistar rat. Next, studies using RAOEC cells showed that the TRB2 expression was inhibited by the treatment of miR-98. We further showed that the expression of miR-98 was significantly decreased in the adventitia and endomembrane at different degrees in GK rats compared with control. Finally, we validated the changes in TRB2 by studying one of the TRB2’s substrates, Akt, in animal models. We expected a corresponding change in the levels of phosphorylated Akt. Indeed, our results showed that the phosphorylation of Akt at Thr 308 in the endothelial cells and phosphorylation of Akt at Ser 473 in adventitia was decreased in GK rats, compared with Wistar control. TRB2 plays important roles in the pathogenesis of diabetic-2 large artery complications at early stage, and these effects may be modulated by miR-98. Thus, targeting TRB2 and miR-98 could be considered as novel therapeutic strategies for the early large artery deficits in diabetic-2. |
| doi_str_mv | 10.1007/s11010-011-1116-7 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_913032488</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A358998701</galeid><sourcerecordid>A358998701</sourcerecordid><originalsourceid>FETCH-LOGICAL-c577t-52e9a2aca95b81b78694fb80adc555cf41fe4f0b0ac7822cffe0aead70fbb3be3</originalsourceid><addsrcrecordid>eNp10c-L1TAQB_Agivtc_QO8SNCDp6wzafuSHtfFX7AgLLvnkKSTZ5a-9pm0h_73pnRVFCWHkOQzw4QvYy8RLhBAvcuIgCAAUSDiXqhHbIeNqkTdYvuY7aACEBqVOmPPcr6Hgot9ys6kBJR7rHbM3Z0SHebeTnEc-Bj47c17yePQzZ467hZ-jDei1eWGT9-Ik039wnvKReeV9zYdiNs0UVrW87ScSEjeRetoip4nOz1nT4LtM7142M_Z3ccPt1efxfXXT1-uLq-Fb5SaRCOptdJ62zZOo1N639bBabCdb5rGhxoD1QEcWK-0lD4EAku2UxCcqxxV5-zt1veUxu8z5ckcY_bU93agcc6mxQoqWWtd5Ou_5P04p6EMV5DUKOumLujNhg62JxOHME7J-rWluawa3bZaARZ18Q9VVkfH6MeBQiz3fxTgVuDTmHOiYE4pHm1aDIJZUzVbqqYkZdZUjSo1rx7mnd2Rul8VP2MsQG4gl6fhQOn3h_7f9Qebb6pJ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>912812454</pqid></control><display><type>article</type><title>Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat</title><source>MEDLINE</source><source>Springer Online Journals Complete</source><creator>Xie, Shuyang ; Xie, Ning ; Li, Youjie ; Wang, Pingyu ; Zhang, Chao ; Li, Qiang ; Liu, Xiaolin ; Deng, Jingti ; Zhang, Can ; Lv, Changjun</creator><creatorcontrib>Xie, Shuyang ; Xie, Ning ; Li, Youjie ; Wang, Pingyu ; Zhang, Chao ; Li, Qiang ; Liu, Xiaolin ; Deng, Jingti ; Zhang, Can ; Lv, Changjun</creatorcontrib><description>To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by immunohistochemistry, ELISA, reverse transcription-polymerase chain reaction (RT-PCR), and real-time PCR detection. GFP expression in RAOEC cells (rat vascular aortic endothelial cell)were detected by flow cytometry and fluorescent microscope. TRB2 gene expression was increased in endothelia cell and the adventitia of Goto-Kakizaki (GK) rat compared with Wistar rat. Next, studies using RAOEC cells showed that the TRB2 expression was inhibited by the treatment of miR-98. We further showed that the expression of miR-98 was significantly decreased in the adventitia and endomembrane at different degrees in GK rats compared with control. Finally, we validated the changes in TRB2 by studying one of the TRB2’s substrates, Akt, in animal models. We expected a corresponding change in the levels of phosphorylated Akt. Indeed, our results showed that the phosphorylation of Akt at Thr 308 in the endothelial cells and phosphorylation of Akt at Ser 473 in adventitia was decreased in GK rats, compared with Wistar control. TRB2 plays important roles in the pathogenesis of diabetic-2 large artery complications at early stage, and these effects may be modulated by miR-98. Thus, targeting TRB2 and miR-98 could be considered as novel therapeutic strategies for the early large artery deficits in diabetic-2.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-011-1116-7</identifier><identifier>PMID: 22012613</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>3' Untranslated Regions ; Animal models ; Animals ; Aorta - metabolism ; Aorta - pathology ; Aortic Diseases - etiology ; Aortic Diseases - genetics ; Aortic Diseases - metabolism ; Atherosclerosis - etiology ; Atherosclerosis - genetics ; Atherosclerosis - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cells, Cultured ; Comparative analysis ; Complications and side effects ; Diabetes ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetic Angiopathies - etiology ; Diabetic Angiopathies - genetics ; Diabetic Angiopathies - metabolism ; Endothelial Cells - metabolism ; Enzyme-linked immunosorbent assay ; Gene Expression ; Gene Expression Regulation ; Genes, Reporter ; Green Fluorescent Proteins - biosynthesis ; Green Fluorescent Proteins - genetics ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Life Sciences ; Male ; Medical Biochemistry ; MicroRNA ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Oncology ; Proto-Oncogene Proteins c-akt - metabolism ; Rats ; Rats, Wistar ; Ribonucleic acid ; RNA ; Rodents ; Up-Regulation ; Veins & arteries</subject><ispartof>Molecular and cellular biochemistry, 2012-02, Vol.361 (1-2), p.305-314</ispartof><rights>Springer Science+Business Media, LLC. 2011</rights><rights>COPYRIGHT 2012 Springer</rights><rights>Springer Science+Business Media, LLC. 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c577t-52e9a2aca95b81b78694fb80adc555cf41fe4f0b0ac7822cffe0aead70fbb3be3</citedby><cites>FETCH-LOGICAL-c577t-52e9a2aca95b81b78694fb80adc555cf41fe4f0b0ac7822cffe0aead70fbb3be3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-011-1116-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-011-1116-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22012613$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xie, Shuyang</creatorcontrib><creatorcontrib>Xie, Ning</creatorcontrib><creatorcontrib>Li, Youjie</creatorcontrib><creatorcontrib>Wang, Pingyu</creatorcontrib><creatorcontrib>Zhang, Chao</creatorcontrib><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Liu, Xiaolin</creatorcontrib><creatorcontrib>Deng, Jingti</creatorcontrib><creatorcontrib>Zhang, Can</creatorcontrib><creatorcontrib>Lv, Changjun</creatorcontrib><title>Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by immunohistochemistry, ELISA, reverse transcription-polymerase chain reaction (RT-PCR), and real-time PCR detection. GFP expression in RAOEC cells (rat vascular aortic endothelial cell)were detected by flow cytometry and fluorescent microscope. TRB2 gene expression was increased in endothelia cell and the adventitia of Goto-Kakizaki (GK) rat compared with Wistar rat. Next, studies using RAOEC cells showed that the TRB2 expression was inhibited by the treatment of miR-98. We further showed that the expression of miR-98 was significantly decreased in the adventitia and endomembrane at different degrees in GK rats compared with control. Finally, we validated the changes in TRB2 by studying one of the TRB2’s substrates, Akt, in animal models. We expected a corresponding change in the levels of phosphorylated Akt. Indeed, our results showed that the phosphorylation of Akt at Thr 308 in the endothelial cells and phosphorylation of Akt at Ser 473 in adventitia was decreased in GK rats, compared with Wistar control. TRB2 plays important roles in the pathogenesis of diabetic-2 large artery complications at early stage, and these effects may be modulated by miR-98. Thus, targeting TRB2 and miR-98 could be considered as novel therapeutic strategies for the early large artery deficits in diabetic-2.</description><subject>3' Untranslated Regions</subject><subject>Animal models</subject><subject>Animals</subject><subject>Aorta - metabolism</subject><subject>Aorta - pathology</subject><subject>Aortic Diseases - etiology</subject><subject>Aortic Diseases - genetics</subject><subject>Aortic Diseases - metabolism</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cells, Cultured</subject><subject>Comparative analysis</subject><subject>Complications and side effects</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetic Angiopathies - etiology</subject><subject>Diabetic Angiopathies - genetics</subject><subject>Diabetic Angiopathies - metabolism</subject><subject>Endothelial Cells - metabolism</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation</subject><subject>Genes, Reporter</subject><subject>Green Fluorescent Proteins - biosynthesis</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Oncology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Up-Regulation</subject><subject>Veins & arteries</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</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>eNp10c-L1TAQB_Agivtc_QO8SNCDp6wzafuSHtfFX7AgLLvnkKSTZ5a-9pm0h_73pnRVFCWHkOQzw4QvYy8RLhBAvcuIgCAAUSDiXqhHbIeNqkTdYvuY7aACEBqVOmPPcr6Hgot9ys6kBJR7rHbM3Z0SHebeTnEc-Bj47c17yePQzZ467hZ-jDei1eWGT9-Ik039wnvKReeV9zYdiNs0UVrW87ScSEjeRetoip4nOz1nT4LtM7142M_Z3ccPt1efxfXXT1-uLq-Fb5SaRCOptdJ62zZOo1N639bBabCdb5rGhxoD1QEcWK-0lD4EAku2UxCcqxxV5-zt1veUxu8z5ckcY_bU93agcc6mxQoqWWtd5Ou_5P04p6EMV5DUKOumLujNhg62JxOHME7J-rWluawa3bZaARZ18Q9VVkfH6MeBQiz3fxTgVuDTmHOiYE4pHm1aDIJZUzVbqqYkZdZUjSo1rx7mnd2Rul8VP2MsQG4gl6fhQOn3h_7f9Qebb6pJ</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Xie, Shuyang</creator><creator>Xie, Ning</creator><creator>Li, Youjie</creator><creator>Wang, Pingyu</creator><creator>Zhang, Chao</creator><creator>Li, Qiang</creator><creator>Liu, Xiaolin</creator><creator>Deng, Jingti</creator><creator>Zhang, Can</creator><creator>Lv, Changjun</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20120201</creationdate><title>Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat</title><author>Xie, Shuyang ; Xie, Ning ; Li, Youjie ; Wang, Pingyu ; Zhang, Chao ; Li, Qiang ; Liu, Xiaolin ; Deng, Jingti ; Zhang, Can ; Lv, Changjun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-52e9a2aca95b81b78694fb80adc555cf41fe4f0b0ac7822cffe0aead70fbb3be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>3' Untranslated Regions</topic><topic>Animal models</topic><topic>Animals</topic><topic>Aorta - metabolism</topic><topic>Aorta - pathology</topic><topic>Aortic Diseases - etiology</topic><topic>Aortic Diseases - genetics</topic><topic>Aortic Diseases - metabolism</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cells, Cultured</topic><topic>Comparative analysis</topic><topic>Complications and side effects</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetic Angiopathies - etiology</topic><topic>Diabetic Angiopathies - genetics</topic><topic>Diabetic Angiopathies - metabolism</topic><topic>Endothelial Cells - metabolism</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation</topic><topic>Genes, Reporter</topic><topic>Green Fluorescent Proteins - biosynthesis</topic><topic>Green Fluorescent Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical Biochemistry</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Oncology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Rodents</topic><topic>Up-Regulation</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xie, Shuyang</creatorcontrib><creatorcontrib>Xie, Ning</creatorcontrib><creatorcontrib>Li, Youjie</creatorcontrib><creatorcontrib>Wang, Pingyu</creatorcontrib><creatorcontrib>Zhang, Chao</creatorcontrib><creatorcontrib>Li, Qiang</creatorcontrib><creatorcontrib>Liu, Xiaolin</creatorcontrib><creatorcontrib>Deng, Jingti</creatorcontrib><creatorcontrib>Zhang, Can</creatorcontrib><creatorcontrib>Lv, Changjun</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xie, Shuyang</au><au>Xie, Ning</au><au>Li, Youjie</au><au>Wang, Pingyu</au><au>Zhang, Chao</au><au>Li, Qiang</au><au>Liu, Xiaolin</au><au>Deng, Jingti</au><au>Zhang, Can</au><au>Lv, Changjun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>361</volume><issue>1-2</issue><spage>305</spage><epage>314</epage><pages>305-314</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>To characterize the roles of tribble 2 (TRB2) and its targeted microRNAs (miRNAs) in the pathogenesis of the early vascular injury involved in diabetic-2 rat. Goto-Kakizaki (GK) rat and Wistar rat were used as the animal models. Each eligible rat was killed and the rat aorta tissues were analyzed by immunohistochemistry, ELISA, reverse transcription-polymerase chain reaction (RT-PCR), and real-time PCR detection. GFP expression in RAOEC cells (rat vascular aortic endothelial cell)were detected by flow cytometry and fluorescent microscope. TRB2 gene expression was increased in endothelia cell and the adventitia of Goto-Kakizaki (GK) rat compared with Wistar rat. Next, studies using RAOEC cells showed that the TRB2 expression was inhibited by the treatment of miR-98. We further showed that the expression of miR-98 was significantly decreased in the adventitia and endomembrane at different degrees in GK rats compared with control. Finally, we validated the changes in TRB2 by studying one of the TRB2’s substrates, Akt, in animal models. We expected a corresponding change in the levels of phosphorylated Akt. Indeed, our results showed that the phosphorylation of Akt at Thr 308 in the endothelial cells and phosphorylation of Akt at Ser 473 in adventitia was decreased in GK rats, compared with Wistar control. TRB2 plays important roles in the pathogenesis of diabetic-2 large artery complications at early stage, and these effects may be modulated by miR-98. Thus, targeting TRB2 and miR-98 could be considered as novel therapeutic strategies for the early large artery deficits in diabetic-2.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>22012613</pmid><doi>10.1007/s11010-011-1116-7</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-8177 |
| ispartof | Molecular and cellular biochemistry, 2012-02, Vol.361 (1-2), p.305-314 |
| issn | 0300-8177 1573-4919 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_913032488 |
| source | MEDLINE; Springer Online Journals Complete |
| subjects | 3' Untranslated Regions Animal models Animals Aorta - metabolism Aorta - pathology Aortic Diseases - etiology Aortic Diseases - genetics Aortic Diseases - metabolism Atherosclerosis - etiology Atherosclerosis - genetics Atherosclerosis - metabolism Biochemistry Biomedical and Life Sciences Cardiology Cells, Cultured Comparative analysis Complications and side effects Diabetes Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetic Angiopathies - etiology Diabetic Angiopathies - genetics Diabetic Angiopathies - metabolism Endothelial Cells - metabolism Enzyme-linked immunosorbent assay Gene Expression Gene Expression Regulation Genes, Reporter Green Fluorescent Proteins - biosynthesis Green Fluorescent Proteins - genetics Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Life Sciences Male Medical Biochemistry MicroRNA MicroRNAs - genetics MicroRNAs - metabolism Oncology Proto-Oncogene Proteins c-akt - metabolism Rats Rats, Wistar Ribonucleic acid RNA Rodents Up-Regulation Veins & arteries |
| title | Upregulation of TRB2 induced by miR-98 in the early lesions of large artery of type-2 diabetic rat |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T02%3A59%3A11IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Upregulation%20of%20TRB2%20induced%20by%20miR-98%20in%20the%20early%20lesions%20of%20large%20artery%20of%20type-2%20diabetic%20rat&rft.jtitle=Molecular%20and%20cellular%20biochemistry&rft.au=Xie,%20Shuyang&rft.date=2012-02-01&rft.volume=361&rft.issue=1-2&rft.spage=305&rft.epage=314&rft.pages=305-314&rft.issn=0300-8177&rft.eissn=1573-4919&rft_id=info:doi/10.1007/s11010-011-1116-7&rft_dat=%3Cgale_proqu%3EA358998701%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=912812454&rft_id=info:pmid/22012613&rft_galeid=A358998701&rfr_iscdi=true |