miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways
Pulmonary arterial hypertension (PAH) is a clinical hemodynamic syndrome. It is characterized by elevated PA pressure and pulmonary vascular resistance. In the present study, the role of microRNA (miRNA/miR)‑371b‑5p in monocrotaline‑induced PAH and the underlying mechanisms were investigated. In a m...
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| Veröffentlicht in: | Molecular medicine reports 2018-12, Vol.18 (6), p.5489-5501 |
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| creator | Zhu, Guangfa Zhang, Wenmei Liu, Yan Wang, Shenghao |
| description | Pulmonary arterial hypertension (PAH) is a clinical hemodynamic syndrome. It is characterized by elevated PA pressure and pulmonary vascular resistance. In the present study, the role of microRNA (miRNA/miR)‑371b‑5p in monocrotaline‑induced PAH and the underlying mechanisms were investigated. In a monocrotaline‑induced PAH rat model, gene chip and reverse transcription‑quantitative polymerase chain reaction were employed to measure miRNA expression levels. The results revealed that miR‑371b‑5p was downregulated in PAH rats compared with the control group. In addition, in vitro results demonstrated that an miR‑371b‑5p inhibitor reduced miR‑371b‑5p expression levels, increased apoptosis and reduced proliferation of pulmonary arterial endothelial cells (PAECs) in rats with monocrotaline‑induced PAH. Furthermore, inhibition of miR‑371b‑5p induced phosphatase and tensin homolog (PTEN) protein expression and suppressed that of phosphoinositide 3‑kinase (PI3K) and phosphorylated (p)‑Akt in the PAECs. In addition, VO‑OHpic, a PTEN inhibitor, reduced the protein expression levels of PTEN in the PAECs and inhibited the effects of anti‑miR‑371b‑5p on cell apoptosis. In addition, LY294002, a PI3K inhibitor, reduced the PI3K and p‑Akt protein expression in the PAECs and reversed the effects of miR‑371b‑5p overexpression on the apoptosis of PAECs in rats with monocrotaline‑induced PAH. Collectively, the results of the present study indicate that, in this animal model of PAH, miR‑371b‑5p inhibits apoptosis of PAECs via PTEN/PI3K/Akt signaling pathways. |
| doi_str_mv | 10.3892/mmr.2018.9614 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6236307</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A563359053</galeid><sourcerecordid>A563359053</sourcerecordid><originalsourceid>FETCH-LOGICAL-c482t-69e9390660cb3c0bcd9c2ddd098c369f5aaf755007863fe5f29a931d180de5653</originalsourceid><addsrcrecordid>eNptks9u1DAQxiMEon_gyBVZ4tJLdm3P2okvSKuqQEUFFSpny7GdXZfEDnZStDdeoeINeRIcdalahHyYkec3nzXjryheEbyAWtBl38cFxaReCE5WT4pDUglSAsarp_ucClEdFEcpXWPMGWXieXEAGOqqJvyw-NW7L79_3kJFmhzYgJzfusaNCVlvwri1nVMd0rbrkBrCMIbkUmZQH3zQMYyqc97mTufNpK1Bw9Tlkoo7pOJo49y83Q025z654NGNU-jy6uzT8vIcPi7X30aU3MbPKhs0qHH7Q-3Si-JZq7pkX-7jcfH13dnV6Yfy4vP789P1RalXNR1LLqwAgTnHugGNG22EpsYYLGoNXLRMqbZiDOOq5tBa1lKhBBBDamws4wyOi7d3usPU9NZo68eoOjlE1-cBZFBOPq54t5WbcCM5BQ64ygIne4EYvk82jbJ3ad6V8jZMSVJCBYMKVjSjb_5Br8MU8-AzBQCEgXhAbVRnpfNtyO_qWVSuGQdgAjPI1OI_VD7G9k4Hb1uX7x81lHcN-cdSira9n5FgObtIZhfJ2UVydlHmXz9czD391zbwB1yJx1E</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2133315392</pqid></control><display><type>article</type><title>miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB Free E-Journals</source><source>Alma/SFX Local Collection</source><creator>Zhu, Guangfa ; Zhang, Wenmei ; Liu, Yan ; Wang, Shenghao</creator><creatorcontrib>Zhu, Guangfa ; Zhang, Wenmei ; Liu, Yan ; Wang, Shenghao</creatorcontrib><description>Pulmonary arterial hypertension (PAH) is a clinical hemodynamic syndrome. It is characterized by elevated PA pressure and pulmonary vascular resistance. In the present study, the role of microRNA (miRNA/miR)‑371b‑5p in monocrotaline‑induced PAH and the underlying mechanisms were investigated. In a monocrotaline‑induced PAH rat model, gene chip and reverse transcription‑quantitative polymerase chain reaction were employed to measure miRNA expression levels. The results revealed that miR‑371b‑5p was downregulated in PAH rats compared with the control group. In addition, in vitro results demonstrated that an miR‑371b‑5p inhibitor reduced miR‑371b‑5p expression levels, increased apoptosis and reduced proliferation of pulmonary arterial endothelial cells (PAECs) in rats with monocrotaline‑induced PAH. Furthermore, inhibition of miR‑371b‑5p induced phosphatase and tensin homolog (PTEN) protein expression and suppressed that of phosphoinositide 3‑kinase (PI3K) and phosphorylated (p)‑Akt in the PAECs. In addition, VO‑OHpic, a PTEN inhibitor, reduced the protein expression levels of PTEN in the PAECs and inhibited the effects of anti‑miR‑371b‑5p on cell apoptosis. In addition, LY294002, a PI3K inhibitor, reduced the PI3K and p‑Akt protein expression in the PAECs and reversed the effects of miR‑371b‑5p overexpression on the apoptosis of PAECs in rats with monocrotaline‑induced PAH. Collectively, the results of the present study indicate that, in this animal model of PAH, miR‑371b‑5p inhibits apoptosis of PAECs via PTEN/PI3K/Akt signaling pathways.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.9614</identifier><identifier>PMID: 30387816</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Analysis ; Animals ; Apoptosis ; Apoptosis - genetics ; Cell growth ; Cell Proliferation ; Disease Models, Animal ; Endothelial cells ; Endothelial Cells - metabolism ; Gene Expression Profiling ; Genes, Reporter ; Genetic transcription ; Health aspects ; Humans ; Hypertension ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - metabolism ; Kinases ; Male ; MicroRNA ; MicroRNAs - genetics ; miRNA ; Models, Biological ; Monocrotaline ; Monocrotaline - adverse effects ; Mortality ; Nitric Oxide Synthase Type III - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Polymerase chain reaction ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - metabolism ; PTEN protein ; Pulmonary hypertension ; Rats ; Reverse transcription ; Rodents ; Signal Transduction ; Tensin ; Transcription Factor AP-1 - metabolism</subject><ispartof>Molecular medicine reports, 2018-12, Vol.18 (6), p.5489-5501</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Zhu et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-69e9390660cb3c0bcd9c2ddd098c369f5aaf755007863fe5f29a931d180de5653</citedby><cites>FETCH-LOGICAL-c482t-69e9390660cb3c0bcd9c2ddd098c369f5aaf755007863fe5f29a931d180de5653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30387816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Guangfa</creatorcontrib><creatorcontrib>Zhang, Wenmei</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Wang, Shenghao</creatorcontrib><title>miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Pulmonary arterial hypertension (PAH) is a clinical hemodynamic syndrome. It is characterized by elevated PA pressure and pulmonary vascular resistance. In the present study, the role of microRNA (miRNA/miR)‑371b‑5p in monocrotaline‑induced PAH and the underlying mechanisms were investigated. In a monocrotaline‑induced PAH rat model, gene chip and reverse transcription‑quantitative polymerase chain reaction were employed to measure miRNA expression levels. The results revealed that miR‑371b‑5p was downregulated in PAH rats compared with the control group. In addition, in vitro results demonstrated that an miR‑371b‑5p inhibitor reduced miR‑371b‑5p expression levels, increased apoptosis and reduced proliferation of pulmonary arterial endothelial cells (PAECs) in rats with monocrotaline‑induced PAH. Furthermore, inhibition of miR‑371b‑5p induced phosphatase and tensin homolog (PTEN) protein expression and suppressed that of phosphoinositide 3‑kinase (PI3K) and phosphorylated (p)‑Akt in the PAECs. In addition, VO‑OHpic, a PTEN inhibitor, reduced the protein expression levels of PTEN in the PAECs and inhibited the effects of anti‑miR‑371b‑5p on cell apoptosis. In addition, LY294002, a PI3K inhibitor, reduced the PI3K and p‑Akt protein expression in the PAECs and reversed the effects of miR‑371b‑5p overexpression on the apoptosis of PAECs in rats with monocrotaline‑induced PAH. Collectively, the results of the present study indicate that, in this animal model of PAH, miR‑371b‑5p inhibits apoptosis of PAECs via PTEN/PI3K/Akt signaling pathways.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Cell growth</subject><subject>Cell Proliferation</subject><subject>Disease Models, Animal</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Gene Expression Profiling</subject><subject>Genes, Reporter</subject><subject>Genetic transcription</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Models, Biological</subject><subject>Monocrotaline</subject><subject>Monocrotaline - adverse effects</subject><subject>Mortality</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Polymerase chain reaction</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>PTEN protein</subject><subject>Pulmonary hypertension</subject><subject>Rats</subject><subject>Reverse transcription</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Tensin</subject><subject>Transcription Factor AP-1 - metabolism</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>BENPR</sourceid><recordid>eNptks9u1DAQxiMEon_gyBVZ4tJLdm3P2okvSKuqQEUFFSpny7GdXZfEDnZStDdeoeINeRIcdalahHyYkec3nzXjryheEbyAWtBl38cFxaReCE5WT4pDUglSAsarp_ucClEdFEcpXWPMGWXieXEAGOqqJvyw-NW7L79_3kJFmhzYgJzfusaNCVlvwri1nVMd0rbrkBrCMIbkUmZQH3zQMYyqc97mTufNpK1Bw9Tlkoo7pOJo49y83Q025z654NGNU-jy6uzT8vIcPi7X30aU3MbPKhs0qHH7Q-3Si-JZq7pkX-7jcfH13dnV6Yfy4vP789P1RalXNR1LLqwAgTnHugGNG22EpsYYLGoNXLRMqbZiDOOq5tBa1lKhBBBDamws4wyOi7d3usPU9NZo68eoOjlE1-cBZFBOPq54t5WbcCM5BQ64ygIne4EYvk82jbJ3ad6V8jZMSVJCBYMKVjSjb_5Br8MU8-AzBQCEgXhAbVRnpfNtyO_qWVSuGQdgAjPI1OI_VD7G9k4Hb1uX7x81lHcN-cdSira9n5FgObtIZhfJ2UVydlHmXz9czD391zbwB1yJx1E</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Zhu, Guangfa</creator><creator>Zhang, Wenmei</creator><creator>Liu, Yan</creator><creator>Wang, Shenghao</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Zhang, Wenmei ; Liu, Yan ; Wang, Shenghao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-69e9390660cb3c0bcd9c2ddd098c369f5aaf755007863fe5f29a931d180de5653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Cell growth</topic><topic>Cell Proliferation</topic><topic>Disease Models, Animal</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Gene Expression Profiling</topic><topic>Genes, Reporter</topic><topic>Genetic transcription</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>MicroRNA</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Models, Biological</topic><topic>Monocrotaline</topic><topic>Monocrotaline - adverse effects</topic><topic>Mortality</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Polymerase chain reaction</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>PTEN protein</topic><topic>Pulmonary hypertension</topic><topic>Rats</topic><topic>Reverse transcription</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Tensin</topic><topic>Transcription Factor AP-1 - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Guangfa</creatorcontrib><creatorcontrib>Zhang, Wenmei</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Wang, Shenghao</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)</collection><collection>ProQuest Central</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</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>Biological Sciences</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>Zhu, Guangfa</au><au>Zhang, Wenmei</au><au>Liu, Yan</au><au>Wang, Shenghao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>18</volume><issue>6</issue><spage>5489</spage><epage>5501</epage><pages>5489-5501</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Pulmonary arterial hypertension (PAH) is a clinical hemodynamic syndrome. It is characterized by elevated PA pressure and pulmonary vascular resistance. In the present study, the role of microRNA (miRNA/miR)‑371b‑5p in monocrotaline‑induced PAH and the underlying mechanisms were investigated. In a monocrotaline‑induced PAH rat model, gene chip and reverse transcription‑quantitative polymerase chain reaction were employed to measure miRNA expression levels. The results revealed that miR‑371b‑5p was downregulated in PAH rats compared with the control group. In addition, in vitro results demonstrated that an miR‑371b‑5p inhibitor reduced miR‑371b‑5p expression levels, increased apoptosis and reduced proliferation of pulmonary arterial endothelial cells (PAECs) in rats with monocrotaline‑induced PAH. Furthermore, inhibition of miR‑371b‑5p induced phosphatase and tensin homolog (PTEN) protein expression and suppressed that of phosphoinositide 3‑kinase (PI3K) and phosphorylated (p)‑Akt in the PAECs. In addition, VO‑OHpic, a PTEN inhibitor, reduced the protein expression levels of PTEN in the PAECs and inhibited the effects of anti‑miR‑371b‑5p on cell apoptosis. In addition, LY294002, a PI3K inhibitor, reduced the PI3K and p‑Akt protein expression in the PAECs and reversed the effects of miR‑371b‑5p overexpression on the apoptosis of PAECs in rats with monocrotaline‑induced PAH. Collectively, the results of the present study indicate that, in this animal model of PAH, miR‑371b‑5p inhibits apoptosis of PAECs via PTEN/PI3K/Akt signaling pathways.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30387816</pmid><doi>10.3892/mmr.2018.9614</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Analysis Animals Apoptosis Apoptosis - genetics Cell growth Cell Proliferation Disease Models, Animal Endothelial cells Endothelial Cells - metabolism Gene Expression Profiling Genes, Reporter Genetic transcription Health aspects Humans Hypertension Hypertension, Pulmonary - etiology Hypertension, Pulmonary - metabolism Kinases Male MicroRNA MicroRNAs - genetics miRNA Models, Biological Monocrotaline Monocrotaline - adverse effects Mortality Nitric Oxide Synthase Type III - metabolism Phosphatidylinositol 3-Kinases - metabolism Polymerase chain reaction Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - metabolism PTEN protein Pulmonary hypertension Rats Reverse transcription Rodents Signal Transduction Tensin Transcription Factor AP-1 - metabolism |
| title | miR‑371b‑5p inhibits endothelial cell apoptosis in monocrotaline‑induced pulmonary arterial hypertension via PTEN/PI3K/Akt signaling pathways |
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