miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2
The present study aimed to investigate the expression status of miRNA-199a-3p in patients with diabetic neuropathy (DN) and the mechanism by which this miRNA is involved in the genesis of DN. The expression of miRNA-199a-3p in plasma of peripheral blood was compared between patients with diabetes an...
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| Veröffentlicht in: | Molecular medicine reports 2017-09, Vol.16 (3), p.2417-2424 |
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| creator | Li, Ying-Bo Wu, Qun Liu, Jie Fan, Yong-Zhi Yu, Kai-Feng Cai, Yi |
| description | The present study aimed to investigate the expression status of miRNA-199a-3p in patients with diabetic neuropathy (DN) and the mechanism by which this miRNA is involved in the genesis of DN. The expression of miRNA-199a-3p in plasma of peripheral blood was compared between patients with diabetes and a family history of diabetes and control volunteers by reverse transcription-quantitative polymerase chain reaction (RT-qPCR); in 60 diabetes patients, 45 (75%) demosntrated upregulated miR-199a-3p expression compared with control volunteer plasma. RT-qPCR was also used to detect miRNA-199a-3p expression in paired lower limb skin tissues from 30 patients with DN and 20 control volunteers; miR-199a-3p expression in patients with DN was significantly higher than in the control group. Next miR-199a-3p expression levels were evaluated with respect to the clinic-pathological parameters of diabetes; increased expression of miR-199a-3p was significantly associated with increased disease duration (P=0.041), glycated hemoglobin (HbA1C) levels (P=0.033), and fibrinogen levels (P=0.003). Finally, the effects on downstream mRNA expression levels were investigated as a result of manipulating miR-199a-3p levels. miR-199a-3p overexpression inhibited the expression of the extracellular serine protease inhibitor E2 (SerpinE2). Therefore, it may be hypothesized that miR-199a-3p can induce DN via promoting coagulation in skin peripheral circulation, through the downregulation of SerpinE2. The present findings suggested that miR-199a-3p may have potential as a novel therapeutic target for the treatment of patients with DN. |
| doi_str_mv | 10.3892/mmr.2017.6874 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5547973</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A511672852</galeid><sourcerecordid>A511672852</sourcerecordid><originalsourceid>FETCH-LOGICAL-c558t-5fec903b8be8da525f3496710db559d67b69c8754a57286fbc12f5cadb6d8bf83</originalsourceid><addsrcrecordid>eNptks2P1CAYxhujcdfVo1fTxINeGPkoUC4mm836kWxi4seZUHjbYdNChXY2-9_LZMbRNYYDhPf3PvDAU1UvCd6wVtF305Q2FBO5Ea1sHlXnRCqCGMbN4-OaKiXPqmc532IsOOXqaXVGWyGlZPy8Wif_FRGlDGJz7XPtwy6OO3BlUS9bqGezbOMAAXIpmuDqOcUhQc4-hjr2tfOmg8XbOsCa4p6-L30prsO2dvEuJBjW0SxH-huk2Ydr-rx60psxw4vjfFH9-HD9_eoTuvny8fPV5Q2ynLcL4j1YhVnXdtA6U-7es0YJSbDrOFdOyE4o20reGC6Lpb6zhPbcGtcJ13Z9yy6q9wfdee0mcBbCksyo5-Qnk-51NF4_rAS_1UPcac4bqSQrAm-PAin-XCEvevLZwjiaAHHNmigiWCEVKejrf9DbuKZQ7BWqoYRTocQfajAjaB_6WM61e1F9yQkRxQenhdr8hyrDweRtDND7sv-gAR0abIo5J-hPHgnW-5zokhO9z4ne56Twr_5-mBP9OxgFeHMA8lx-3buYT0xRQkQgzBBtiGS_ALFyxtM</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1942152696</pqid></control><display><type>article</type><title>miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Li, Ying-Bo ; Wu, Qun ; Liu, Jie ; Fan, Yong-Zhi ; Yu, Kai-Feng ; Cai, Yi</creator><creatorcontrib>Li, Ying-Bo ; Wu, Qun ; Liu, Jie ; Fan, Yong-Zhi ; Yu, Kai-Feng ; Cai, Yi</creatorcontrib><description>The present study aimed to investigate the expression status of miRNA-199a-3p in patients with diabetic neuropathy (DN) and the mechanism by which this miRNA is involved in the genesis of DN. The expression of miRNA-199a-3p in plasma of peripheral blood was compared between patients with diabetes and a family history of diabetes and control volunteers by reverse transcription-quantitative polymerase chain reaction (RT-qPCR); in 60 diabetes patients, 45 (75%) demosntrated upregulated miR-199a-3p expression compared with control volunteer plasma. RT-qPCR was also used to detect miRNA-199a-3p expression in paired lower limb skin tissues from 30 patients with DN and 20 control volunteers; miR-199a-3p expression in patients with DN was significantly higher than in the control group. Next miR-199a-3p expression levels were evaluated with respect to the clinic-pathological parameters of diabetes; increased expression of miR-199a-3p was significantly associated with increased disease duration (P=0.041), glycated hemoglobin (HbA1C) levels (P=0.033), and fibrinogen levels (P=0.003). Finally, the effects on downstream mRNA expression levels were investigated as a result of manipulating miR-199a-3p levels. miR-199a-3p overexpression inhibited the expression of the extracellular serine protease inhibitor E2 (SerpinE2). Therefore, it may be hypothesized that miR-199a-3p can induce DN via promoting coagulation in skin peripheral circulation, through the downregulation of SerpinE2. The present findings suggested that miR-199a-3p may have potential as a novel therapeutic target for the treatment of patients with DN.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.6874</identifier><identifier>PMID: 28677735</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Adult ; Aged ; Blood Coagulation ; Care and treatment ; Cell Line ; Cellular proteins ; coagulation ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Type 2 - blood ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - genetics ; Diabetic neuropathies ; Diabetic Neuropathies - blood ; Diabetic Neuropathies - genetics ; Diabetic neuropathy ; diabetic peripheral neuropathy ; Disease ; Disease Progression ; Down-Regulation ; Female ; Fibrinogen ; Gene expression ; Genetic aspects ; Health aspects ; Hemoglobin ; Humans ; Male ; MicroRNA ; MicroRNAs ; MicroRNAs - blood ; MicroRNAs - genetics ; Middle Aged ; miR-199a-3p ; miRNA ; Pathogenesis ; Peripheral blood ; Plasma ; Polymerase chain reaction ; Protein expression ; Proteins ; Reverse transcription ; Rodents ; Serine ; Serine proteinase ; Serpin E2 - genetics ; SerpinE2 ; Skin ; Up-Regulation</subject><ispartof>Molecular medicine reports, 2017-09, Vol.16 (3), p.2417-2424</ispartof><rights>Copyright: © Li et al.</rights><rights>COPYRIGHT 2017 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright: © Li et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-5fec903b8be8da525f3496710db559d67b69c8754a57286fbc12f5cadb6d8bf83</citedby><cites>FETCH-LOGICAL-c558t-5fec903b8be8da525f3496710db559d67b69c8754a57286fbc12f5cadb6d8bf83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28677735$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Ying-Bo</creatorcontrib><creatorcontrib>Wu, Qun</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Fan, Yong-Zhi</creatorcontrib><creatorcontrib>Yu, Kai-Feng</creatorcontrib><creatorcontrib>Cai, Yi</creatorcontrib><title>miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>The present study aimed to investigate the expression status of miRNA-199a-3p in patients with diabetic neuropathy (DN) and the mechanism by which this miRNA is involved in the genesis of DN. The expression of miRNA-199a-3p in plasma of peripheral blood was compared between patients with diabetes and a family history of diabetes and control volunteers by reverse transcription-quantitative polymerase chain reaction (RT-qPCR); in 60 diabetes patients, 45 (75%) demosntrated upregulated miR-199a-3p expression compared with control volunteer plasma. RT-qPCR was also used to detect miRNA-199a-3p expression in paired lower limb skin tissues from 30 patients with DN and 20 control volunteers; miR-199a-3p expression in patients with DN was significantly higher than in the control group. Next miR-199a-3p expression levels were evaluated with respect to the clinic-pathological parameters of diabetes; increased expression of miR-199a-3p was significantly associated with increased disease duration (P=0.041), glycated hemoglobin (HbA1C) levels (P=0.033), and fibrinogen levels (P=0.003). Finally, the effects on downstream mRNA expression levels were investigated as a result of manipulating miR-199a-3p levels. miR-199a-3p overexpression inhibited the expression of the extracellular serine protease inhibitor E2 (SerpinE2). Therefore, it may be hypothesized that miR-199a-3p can induce DN via promoting coagulation in skin peripheral circulation, through the downregulation of SerpinE2. The present findings suggested that miR-199a-3p may have potential as a novel therapeutic target for the treatment of patients with DN.</description><subject>Adult</subject><subject>Aged</subject><subject>Blood Coagulation</subject><subject>Care and treatment</subject><subject>Cell Line</subject><subject>Cellular proteins</subject><subject>coagulation</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Type 2 - blood</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetic neuropathies</subject><subject>Diabetic Neuropathies - blood</subject><subject>Diabetic Neuropathies - genetics</subject><subject>Diabetic neuropathy</subject><subject>diabetic peripheral neuropathy</subject><subject>Disease</subject><subject>Disease Progression</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Fibrinogen</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Male</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - blood</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miR-199a-3p</subject><subject>miRNA</subject><subject>Pathogenesis</subject><subject>Peripheral blood</subject><subject>Plasma</subject><subject>Polymerase chain reaction</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reverse transcription</subject><subject>Rodents</subject><subject>Serine</subject><subject>Serine proteinase</subject><subject>Serpin E2 - genetics</subject><subject>SerpinE2</subject><subject>Skin</subject><subject>Up-Regulation</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>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptks2P1CAYxhujcdfVo1fTxINeGPkoUC4mm836kWxi4seZUHjbYdNChXY2-9_LZMbRNYYDhPf3PvDAU1UvCd6wVtF305Q2FBO5Ea1sHlXnRCqCGMbN4-OaKiXPqmc532IsOOXqaXVGWyGlZPy8Wif_FRGlDGJz7XPtwy6OO3BlUS9bqGezbOMAAXIpmuDqOcUhQc4-hjr2tfOmg8XbOsCa4p6-L30prsO2dvEuJBjW0SxH-huk2Ydr-rx60psxw4vjfFH9-HD9_eoTuvny8fPV5Q2ynLcL4j1YhVnXdtA6U-7es0YJSbDrOFdOyE4o20reGC6Lpb6zhPbcGtcJ13Z9yy6q9wfdee0mcBbCksyo5-Qnk-51NF4_rAS_1UPcac4bqSQrAm-PAin-XCEvevLZwjiaAHHNmigiWCEVKejrf9DbuKZQ7BWqoYRTocQfajAjaB_6WM61e1F9yQkRxQenhdr8hyrDweRtDND7sv-gAR0abIo5J-hPHgnW-5zokhO9z4ne56Twr_5-mBP9OxgFeHMA8lx-3buYT0xRQkQgzBBtiGS_ALFyxtM</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Li, Ying-Bo</creator><creator>Wu, Qun</creator><creator>Liu, Jie</creator><creator>Fan, Yong-Zhi</creator><creator>Yu, Kai-Feng</creator><creator>Cai, Yi</creator><general>D.A. Spandidos</general><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><scope>5PM</scope></search><sort><creationdate>20170901</creationdate><title>miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2</title><author>Li, Ying-Bo ; Wu, Qun ; Liu, Jie ; Fan, Yong-Zhi ; Yu, Kai-Feng ; Cai, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-5fec903b8be8da525f3496710db559d67b69c8754a57286fbc12f5cadb6d8bf83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Blood Coagulation</topic><topic>Care and treatment</topic><topic>Cell Line</topic><topic>Cellular proteins</topic><topic>coagulation</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Type 2 - blood</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetic neuropathies</topic><topic>Diabetic Neuropathies - blood</topic><topic>Diabetic Neuropathies - genetics</topic><topic>Diabetic neuropathy</topic><topic>diabetic peripheral neuropathy</topic><topic>Disease</topic><topic>Disease Progression</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Fibrinogen</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Male</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - blood</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miR-199a-3p</topic><topic>miRNA</topic><topic>Pathogenesis</topic><topic>Peripheral blood</topic><topic>Plasma</topic><topic>Polymerase chain reaction</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Reverse transcription</topic><topic>Rodents</topic><topic>Serine</topic><topic>Serine proteinase</topic><topic>Serpin E2 - genetics</topic><topic>SerpinE2</topic><topic>Skin</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ying-Bo</creatorcontrib><creatorcontrib>Wu, Qun</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Fan, Yong-Zhi</creatorcontrib><creatorcontrib>Yu, Kai-Feng</creatorcontrib><creatorcontrib>Cai, Yi</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</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>Li, Ying-Bo</au><au>Wu, Qun</au><au>Liu, Jie</au><au>Fan, Yong-Zhi</au><au>Yu, Kai-Feng</au><au>Cai, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>16</volume><issue>3</issue><spage>2417</spage><epage>2424</epage><pages>2417-2424</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>The present study aimed to investigate the expression status of miRNA-199a-3p in patients with diabetic neuropathy (DN) and the mechanism by which this miRNA is involved in the genesis of DN. The expression of miRNA-199a-3p in plasma of peripheral blood was compared between patients with diabetes and a family history of diabetes and control volunteers by reverse transcription-quantitative polymerase chain reaction (RT-qPCR); in 60 diabetes patients, 45 (75%) demosntrated upregulated miR-199a-3p expression compared with control volunteer plasma. RT-qPCR was also used to detect miRNA-199a-3p expression in paired lower limb skin tissues from 30 patients with DN and 20 control volunteers; miR-199a-3p expression in patients with DN was significantly higher than in the control group. Next miR-199a-3p expression levels were evaluated with respect to the clinic-pathological parameters of diabetes; increased expression of miR-199a-3p was significantly associated with increased disease duration (P=0.041), glycated hemoglobin (HbA1C) levels (P=0.033), and fibrinogen levels (P=0.003). Finally, the effects on downstream mRNA expression levels were investigated as a result of manipulating miR-199a-3p levels. miR-199a-3p overexpression inhibited the expression of the extracellular serine protease inhibitor E2 (SerpinE2). Therefore, it may be hypothesized that miR-199a-3p can induce DN via promoting coagulation in skin peripheral circulation, through the downregulation of SerpinE2. The present findings suggested that miR-199a-3p may have potential as a novel therapeutic target for the treatment of patients with DN.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28677735</pmid><doi>10.3892/mmr.2017.6874</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular medicine reports, 2017-09, Vol.16 (3), p.2417-2424 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult Aged Blood Coagulation Care and treatment Cell Line Cellular proteins coagulation Development and progression Diabetes Diabetes mellitus Diabetes Mellitus, Type 2 - blood Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - genetics Diabetic neuropathies Diabetic Neuropathies - blood Diabetic Neuropathies - genetics Diabetic neuropathy diabetic peripheral neuropathy Disease Disease Progression Down-Regulation Female Fibrinogen Gene expression Genetic aspects Health aspects Hemoglobin Humans Male MicroRNA MicroRNAs MicroRNAs - blood MicroRNAs - genetics Middle Aged miR-199a-3p miRNA Pathogenesis Peripheral blood Plasma Polymerase chain reaction Protein expression Proteins Reverse transcription Rodents Serine Serine proteinase Serpin E2 - genetics SerpinE2 Skin Up-Regulation |
| title | miR-199a-3p is involved in the pathogenesis and progression of diabetic neuropathy through downregulation of SerpinE2 |
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