Dysregulation of PTEN caused by the underexpression of microRNA‑130b is associated with the severity of lupus nephritis
There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collec...
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| Veröffentlicht in: | Molecular medicine reports 2018-06, Vol.17 (6), p.7966-7972 |
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| description | There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collected and the expression level of miR‑130b was determined. The online miRNA database was then searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene. Linear analysis and a luciferase assay were performed to understand the regulatory association between miR‑130b and phosphatase and tensin homolog (PTEN). In addition, reverse transcription‑polymerase chain reaction and western blot analyses were performed to examine the mRNA and protein expression levels of PTEN among individuals with lupus nephritis (n=28) and those without lupus nephritis (n=31), and in mesangial cells treated with scramble control, miR‑130b mimics, PTEN small interfering (si)RNA and miR‑130b inhibitors. In addition mesangial cells were treated with scramble control, miR‑130b mimics, PTEN siRNA and miR‑130b inhibitors to investigate the affect of miR‑130b and PTEN on the viability and apoptosis of mesangial cells. The results demonstrated that miR‑130b was downregulated in the hormone‑resistant group of lupus nephritis patients. PTEN was a virtual target of miR‑130b. There was a negative regulatory association between miR‑130b and PTEN. The mRNA and protein expression levels of PTEN were increased in the hormone‑resistant group. miR‑130b decreased the expression of PTEN. miR‑130b negatively interfered with the viability of mesangial cells and PTEN positively interfered with the viability of mesangial cells. miR‑130b accelerated apoptosis and PTEN inhibited apoptosis. Taken together, the results showed that miR‑130b was upregulated in the lupus nephritis group. PTEN was a virtual target of miR‑130b, and there was a negative regulatory association between miR‑130b and PTEN. miR‑130b and PTEN interfered with the viability and apoptosis of the mesangial cells. |
| doi_str_mv | 10.3892/mmr.2018.8839 |
| format | Article |
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It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collected and the expression level of miR‑130b was determined. The online miRNA database was then searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene. Linear analysis and a luciferase assay were performed to understand the regulatory association between miR‑130b and phosphatase and tensin homolog (PTEN). In addition, reverse transcription‑polymerase chain reaction and western blot analyses were performed to examine the mRNA and protein expression levels of PTEN among individuals with lupus nephritis (n=28) and those without lupus nephritis (n=31), and in mesangial cells treated with scramble control, miR‑130b mimics, PTEN small interfering (si)RNA and miR‑130b inhibitors. In addition mesangial cells were treated with scramble control, miR‑130b mimics, PTEN siRNA and miR‑130b inhibitors to investigate the affect of miR‑130b and PTEN on the viability and apoptosis of mesangial cells. The results demonstrated that miR‑130b was downregulated in the hormone‑resistant group of lupus nephritis patients. PTEN was a virtual target of miR‑130b. There was a negative regulatory association between miR‑130b and PTEN. The mRNA and protein expression levels of PTEN were increased in the hormone‑resistant group. miR‑130b decreased the expression of PTEN. miR‑130b negatively interfered with the viability of mesangial cells and PTEN positively interfered with the viability of mesangial cells. miR‑130b accelerated apoptosis and PTEN inhibited apoptosis. Taken together, the results showed that miR‑130b was upregulated in the lupus nephritis group. PTEN was a virtual target of miR‑130b, and there was a negative regulatory association between miR‑130b and PTEN. miR‑130b and PTEN interfered with the viability and apoptosis of the mesangial cells.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8839</identifier><identifier>PMID: 29620214</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>3' Untranslated Regions ; Adult ; Apoptosis ; Apoptosis - genetics ; Care and treatment ; Cell growth ; Cell Proliferation ; Cell Survival - genetics ; Complications and side effects ; Development and progression ; Gene expression ; Gene Expression Regulation ; Genetic aspects ; Health aspects ; Humans ; Kidney diseases ; Kinases ; Lupus ; Lupus nephritis ; Lupus Nephritis - diagnosis ; Lupus Nephritis - genetics ; Lupus Nephritis - metabolism ; Mesangial cells ; Mesangial Cells - metabolism ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; Nephritis ; Polymerase chain reaction ; PTEN Phosphohydrolase - genetics ; PTEN protein ; Reverse transcription ; RNA Interference ; RNA, Messenger - genetics ; Rodents ; Severity of Illness Index ; siRNA ; Studies ; Tensin</subject><ispartof>Molecular medicine reports, 2018-06, Vol.17 (6), p.7966-7972</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-8f99ec51c20dfeedca0f1bccf6710a7dd12a27ce7423e5b9e077928eeeb0610f3</citedby><cites>FETCH-LOGICAL-c427t-8f99ec51c20dfeedca0f1bccf6710a7dd12a27ce7423e5b9e077928eeeb0610f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29620214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Shupeng</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Li, Fang</creatorcontrib><title>Dysregulation of PTEN caused by the underexpression of microRNA‑130b is associated with the severity of lupus nephritis</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collected and the expression level of miR‑130b was determined. The online miRNA database was then searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene. Linear analysis and a luciferase assay were performed to understand the regulatory association between miR‑130b and phosphatase and tensin homolog (PTEN). In addition, reverse transcription‑polymerase chain reaction and western blot analyses were performed to examine the mRNA and protein expression levels of PTEN among individuals with lupus nephritis (n=28) and those without lupus nephritis (n=31), and in mesangial cells treated with scramble control, miR‑130b mimics, PTEN small interfering (si)RNA and miR‑130b inhibitors. In addition mesangial cells were treated with scramble control, miR‑130b mimics, PTEN siRNA and miR‑130b inhibitors to investigate the affect of miR‑130b and PTEN on the viability and apoptosis of mesangial cells. The results demonstrated that miR‑130b was downregulated in the hormone‑resistant group of lupus nephritis patients. PTEN was a virtual target of miR‑130b. There was a negative regulatory association between miR‑130b and PTEN. The mRNA and protein expression levels of PTEN were increased in the hormone‑resistant group. miR‑130b decreased the expression of PTEN. miR‑130b negatively interfered with the viability of mesangial cells and PTEN positively interfered with the viability of mesangial cells. miR‑130b accelerated apoptosis and PTEN inhibited apoptosis. Taken together, the results showed that miR‑130b was upregulated in the lupus nephritis group. PTEN was a virtual target of miR‑130b, and there was a negative regulatory association between miR‑130b and PTEN. miR‑130b and PTEN interfered with the viability and apoptosis of the mesangial cells.</description><subject>3' Untranslated Regions</subject><subject>Adult</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Cell Survival - genetics</subject><subject>Complications and side effects</subject><subject>Development and progression</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kidney diseases</subject><subject>Kinases</subject><subject>Lupus</subject><subject>Lupus nephritis</subject><subject>Lupus Nephritis - diagnosis</subject><subject>Lupus Nephritis - genetics</subject><subject>Lupus Nephritis - metabolism</subject><subject>Mesangial cells</subject><subject>Mesangial Cells - metabolism</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Nephritis</subject><subject>Polymerase chain reaction</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN protein</subject><subject>Reverse transcription</subject><subject>RNA Interference</subject><subject>RNA, Messenger - genetics</subject><subject>Rodents</subject><subject>Severity of Illness Index</subject><subject>siRNA</subject><subject>Studies</subject><subject>Tensin</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</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>eNptkc1u1TAQhS1ERUthyRZZYsMmt_5J4nh5VcqPVBWEytpynHGvqyQOdgxk11foK_IkOO0tCIS8GGv0naPROQi9oGTDG8lOhiFsGKHNpmm4fISOqJC04ISUj_d_JqU4RE9jvCakrlgln6BDJmtGGC2P0PJmiQGuUq9n50fsLf50eXaBjU4ROtwueN4BTmMHAX5MAWLcU4MzwX--2P68uaWctNhFrGP0xuk56767eXenjPANgpuXVdKnKUU8wrTLGxefoQOr-wjP9_MYfXl7dnn6vjj_-O7D6fa8MCUTc9FYKcFU1DDSWYDOaGJpa4ytBSVadB1lmgkDomQcqlYCEUKyBgBaUlNi-TF6fe87Bf81QZzV4KKBvtcj-BRVDoJRzhpeZvTVP-i1T2HM12WKN1UlOGF_qCvdg3Kj9XPQZjVV26qkQtSUrV6b_1D5dZCz8yNYl_d_CYp7QQ425k6smoIbdFgUJWqtWuWq1Vq1WqvO_Mv9sakdoPtNP3TLfwGkUqUl</recordid><startdate>20180601</startdate><enddate>20180601</enddate><creator>Wu, Shupeng</creator><creator>Wang, Jing</creator><creator>Li, Fang</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>20180601</creationdate><title>Dysregulation of PTEN caused by the underexpression of microRNA‑130b is associated with the severity of lupus nephritis</title><author>Wu, Shupeng ; Wang, Jing ; Li, Fang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-8f99ec51c20dfeedca0f1bccf6710a7dd12a27ce7423e5b9e077928eeeb0610f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>3' Untranslated Regions</topic><topic>Adult</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Care and treatment</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Cell Survival - genetics</topic><topic>Complications and side effects</topic><topic>Development and progression</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kidney diseases</topic><topic>Kinases</topic><topic>Lupus</topic><topic>Lupus nephritis</topic><topic>Lupus Nephritis - diagnosis</topic><topic>Lupus Nephritis - genetics</topic><topic>Lupus Nephritis - metabolism</topic><topic>Mesangial cells</topic><topic>Mesangial Cells - metabolism</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Nephritis</topic><topic>Polymerase chain reaction</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN protein</topic><topic>Reverse transcription</topic><topic>RNA Interference</topic><topic>RNA, Messenger - genetics</topic><topic>Rodents</topic><topic>Severity of Illness Index</topic><topic>siRNA</topic><topic>Studies</topic><topic>Tensin</topic><toplevel>online_resources</toplevel><creatorcontrib>Wu, Shupeng</creatorcontrib><creatorcontrib>Wang, Jing</creatorcontrib><creatorcontrib>Li, Fang</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><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Shupeng</au><au>Wang, Jing</au><au>Li, Fang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation of PTEN caused by the underexpression of microRNA‑130b is associated with the severity of lupus nephritis</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-06-01</date><risdate>2018</risdate><volume>17</volume><issue>6</issue><spage>7966</spage><epage>7972</epage><pages>7966-7972</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>There are several reports in the literature regarding microRNA (miR)‑130b. It has been reported that miR‑130b is involved in several diseases. The present study aimed to understand the association between the levels of miR‑130b and lupus nephritis in patients. A total of 61 blood samples were collected and the expression level of miR‑130b was determined. The online miRNA database was then searched using the 'seed sequence' located within the 3'‑untranslated region of the target gene. Linear analysis and a luciferase assay were performed to understand the regulatory association between miR‑130b and phosphatase and tensin homolog (PTEN). In addition, reverse transcription‑polymerase chain reaction and western blot analyses were performed to examine the mRNA and protein expression levels of PTEN among individuals with lupus nephritis (n=28) and those without lupus nephritis (n=31), and in mesangial cells treated with scramble control, miR‑130b mimics, PTEN small interfering (si)RNA and miR‑130b inhibitors. In addition mesangial cells were treated with scramble control, miR‑130b mimics, PTEN siRNA and miR‑130b inhibitors to investigate the affect of miR‑130b and PTEN on the viability and apoptosis of mesangial cells. The results demonstrated that miR‑130b was downregulated in the hormone‑resistant group of lupus nephritis patients. PTEN was a virtual target of miR‑130b. There was a negative regulatory association between miR‑130b and PTEN. The mRNA and protein expression levels of PTEN were increased in the hormone‑resistant group. miR‑130b decreased the expression of PTEN. miR‑130b negatively interfered with the viability of mesangial cells and PTEN positively interfered with the viability of mesangial cells. miR‑130b accelerated apoptosis and PTEN inhibited apoptosis. Taken together, the results showed that miR‑130b was upregulated in the lupus nephritis group. PTEN was a virtual target of miR‑130b, and there was a negative regulatory association between miR‑130b and PTEN. miR‑130b and PTEN interfered with the viability and apoptosis of the mesangial cells.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29620214</pmid><doi>10.3892/mmr.2018.8839</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | 3' Untranslated Regions Adult Apoptosis Apoptosis - genetics Care and treatment Cell growth Cell Proliferation Cell Survival - genetics Complications and side effects Development and progression Gene expression Gene Expression Regulation Genetic aspects Health aspects Humans Kidney diseases Kinases Lupus Lupus nephritis Lupus Nephritis - diagnosis Lupus Nephritis - genetics Lupus Nephritis - metabolism Mesangial cells Mesangial Cells - metabolism MicroRNA MicroRNAs MicroRNAs - genetics miRNA Nephritis Polymerase chain reaction PTEN Phosphohydrolase - genetics PTEN protein Reverse transcription RNA Interference RNA, Messenger - genetics Rodents Severity of Illness Index siRNA Studies Tensin |
| title | Dysregulation of PTEN caused by the underexpression of microRNA‑130b is associated with the severity of lupus nephritis |
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