Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction
Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients...
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Veröffentlicht in: | Internal Medicine 2022/01/15, Vol.61(2), pp.151-158 |
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creator | Park, Jeong Rang Ahn, Jong Hwa Jung, Myeong Hee Kim, Jin Hyun Kang, Min Gyu Kim, Kye Hwan Jang, Jeong Yoon Park, Hyun Woong Koh, Jin-Sin Hwang, Seok-Jae Park, Yongwhi Jeong, Young-Hoon Kwak, Choong Hwan Hwang, Jin-Yong |
description | Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-β and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling. |
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fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8851187</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2624705816</sourcerecordid><originalsourceid>FETCH-LOGICAL-c609t-9158fe457c91cc747603ae65bb7157b8d41fcfb93c8c3029cd18803d7c26ebb73</originalsourceid><addsrcrecordid>eNplkU1v1DAQhi0EokvhLyBLXLik-COO7QvSqmqh0lIQLWfLcSa7XiVOayeL9t_jaJcVLZexNPPMO-N5EcKUXDBa6U8-jBCD7XpovPMBLqTQZcHoC7SgvNSFZFy8RAuiqSpYDmfoTUpbQriSmr1GZ7xkpaKMLtDjHcSpx713cfh5uyyoEngFO-gStqHB3_aDs7HxtsM3YTvFPfYB_7CjhzAm_NuPG7x00wj47r5IsO5zGl91sMvEEJ52tza6OfsWvWptl-Dd8T1Hv66v7i-_FqvvX24ul6vCVUSPhaZCtVAK6TR1TpayItxCJepaUiFr1ZS0dW2tuVOOE6ZdQ5UivJGOVZAhfo4-H3QfpjrfyeXVou3MQ_S9jXszWG-eVoLfmPWwM0oJStUs8PEoEIfHCdJoep8cdJ0NMEzJMCFIxXlZsox-eIZuh2k2KFMVKyURilaZUgcq3zqlCO1pGUrM7Kt57quZfc2l3Pr-38-cGv8amYHbA7BNo13DCbBx9K6D_5UratgcjhNOoNvYaCDwP8OZwkE</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2624705816</pqid></control><display><type>article</type><title>Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction</title><source>MEDLINE</source><source>J-STAGE (Japan Science & Technology Information Aggregator, Electronic) Freely Available Titles - Japanese</source><source>PubMed Central</source><source>PubMed Central Open Access</source><creator>Park, Jeong Rang ; Ahn, Jong Hwa ; Jung, Myeong Hee ; Kim, Jin Hyun ; Kang, Min Gyu ; Kim, Kye Hwan ; Jang, Jeong Yoon ; Park, Hyun Woong ; Koh, Jin-Sin ; Hwang, Seok-Jae ; Park, Yongwhi ; Jeong, Young-Hoon ; Kwak, Choong Hwan ; Hwang, Jin-Yong</creator><creatorcontrib>Park, Jeong Rang ; Ahn, Jong Hwa ; Jung, Myeong Hee ; Kim, Jin Hyun ; Kang, Min Gyu ; Kim, Kye Hwan ; Jang, Jeong Yoon ; Park, Hyun Woong ; Koh, Jin-Sin ; Hwang, Seok-Jae ; Park, Yongwhi ; Jeong, Young-Hoon ; Kwak, Choong Hwan ; Hwang, Jin-Yong</creatorcontrib><description>Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-β and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling.</description><identifier>ISSN: 0918-2918</identifier><identifier>EISSN: 1349-7235</identifier><identifier>DOI: 10.2169/internalmedicine.7594-21</identifier><identifier>PMID: 34248121</identifier><language>eng</language><publisher>Japan: The Japanese Society of Internal Medicine</publisher><subject>Aged ; Angiogenesis ; Biomarkers ; Brain natriuretic peptide ; Calcium-binding protein ; Creatine Kinase, MB Form ; DNA microarrays ; Echocardiography ; Female ; Fibrosis ; Heart attacks ; human microRNA ; Humans ; Internal medicine ; MicroRNAs ; MicroRNAs - genetics ; Middle Aged ; miR-185 ; miRNA ; Myocardial infarction ; Original ; Patients ; Polymerase chain reaction ; Reverse transcription ; ST Elevation Myocardial Infarction - genetics ; Transforming growth factor-b ; Troponin ; Troponin I</subject><ispartof>Internal Medicine, 2022/01/15, Vol.61(2), pp.151-158</ispartof><rights>2022 by The Japanese Society of Internal Medicine</rights><rights>Copyright Japan Science and Technology Agency 2022</rights><rights>Copyright © 2022 by The Japanese Society of Internal Medicine</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c609t-9158fe457c91cc747603ae65bb7157b8d41fcfb93c8c3029cd18803d7c26ebb73</citedby><cites>FETCH-LOGICAL-c609t-9158fe457c91cc747603ae65bb7157b8d41fcfb93c8c3029cd18803d7c26ebb73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8851187/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8851187/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1877,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34248121$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Park, Jeong Rang</creatorcontrib><creatorcontrib>Ahn, Jong Hwa</creatorcontrib><creatorcontrib>Jung, Myeong Hee</creatorcontrib><creatorcontrib>Kim, Jin Hyun</creatorcontrib><creatorcontrib>Kang, Min Gyu</creatorcontrib><creatorcontrib>Kim, Kye Hwan</creatorcontrib><creatorcontrib>Jang, Jeong Yoon</creatorcontrib><creatorcontrib>Park, Hyun Woong</creatorcontrib><creatorcontrib>Koh, Jin-Sin</creatorcontrib><creatorcontrib>Hwang, Seok-Jae</creatorcontrib><creatorcontrib>Park, Yongwhi</creatorcontrib><creatorcontrib>Jeong, Young-Hoon</creatorcontrib><creatorcontrib>Kwak, Choong Hwan</creatorcontrib><creatorcontrib>Hwang, Jin-Yong</creatorcontrib><title>Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction</title><title>Internal Medicine</title><addtitle>Intern. Med.</addtitle><description>Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-β and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling.</description><subject>Aged</subject><subject>Angiogenesis</subject><subject>Biomarkers</subject><subject>Brain natriuretic peptide</subject><subject>Calcium-binding protein</subject><subject>Creatine Kinase, MB Form</subject><subject>DNA microarrays</subject><subject>Echocardiography</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Heart attacks</subject><subject>human microRNA</subject><subject>Humans</subject><subject>Internal medicine</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Middle Aged</subject><subject>miR-185</subject><subject>miRNA</subject><subject>Myocardial infarction</subject><subject>Original</subject><subject>Patients</subject><subject>Polymerase chain reaction</subject><subject>Reverse transcription</subject><subject>ST Elevation Myocardial Infarction - genetics</subject><subject>Transforming growth factor-b</subject><subject>Troponin</subject><subject>Troponin I</subject><issn>0918-2918</issn><issn>1349-7235</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNplkU1v1DAQhi0EokvhLyBLXLik-COO7QvSqmqh0lIQLWfLcSa7XiVOayeL9t_jaJcVLZexNPPMO-N5EcKUXDBa6U8-jBCD7XpovPMBLqTQZcHoC7SgvNSFZFy8RAuiqSpYDmfoTUpbQriSmr1GZ7xkpaKMLtDjHcSpx713cfh5uyyoEngFO-gStqHB3_aDs7HxtsM3YTvFPfYB_7CjhzAm_NuPG7x00wj47r5IsO5zGl91sMvEEJ52tza6OfsWvWptl-Dd8T1Hv66v7i-_FqvvX24ul6vCVUSPhaZCtVAK6TR1TpayItxCJepaUiFr1ZS0dW2tuVOOE6ZdQ5UivJGOVZAhfo4-H3QfpjrfyeXVou3MQ_S9jXszWG-eVoLfmPWwM0oJStUs8PEoEIfHCdJoep8cdJ0NMEzJMCFIxXlZsox-eIZuh2k2KFMVKyURilaZUgcq3zqlCO1pGUrM7Kt57quZfc2l3Pr-38-cGv8amYHbA7BNo13DCbBx9K6D_5UratgcjhNOoNvYaCDwP8OZwkE</recordid><startdate>20220115</startdate><enddate>20220115</enddate><creator>Park, Jeong Rang</creator><creator>Ahn, Jong Hwa</creator><creator>Jung, Myeong Hee</creator><creator>Kim, Jin Hyun</creator><creator>Kang, Min Gyu</creator><creator>Kim, Kye Hwan</creator><creator>Jang, Jeong Yoon</creator><creator>Park, Hyun Woong</creator><creator>Koh, Jin-Sin</creator><creator>Hwang, Seok-Jae</creator><creator>Park, Yongwhi</creator><creator>Jeong, Young-Hoon</creator><creator>Kwak, Choong Hwan</creator><creator>Hwang, Jin-Yong</creator><general>The Japanese Society of Internal Medicine</general><general>Japan Science and Technology Agency</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>7T5</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20220115</creationdate><title>Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction</title><author>Park, Jeong Rang ; Ahn, Jong Hwa ; Jung, Myeong Hee ; Kim, Jin Hyun ; Kang, Min Gyu ; Kim, Kye Hwan ; Jang, Jeong Yoon ; Park, Hyun Woong ; Koh, Jin-Sin ; Hwang, Seok-Jae ; Park, Yongwhi ; Jeong, Young-Hoon ; Kwak, Choong Hwan ; Hwang, Jin-Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c609t-9158fe457c91cc747603ae65bb7157b8d41fcfb93c8c3029cd18803d7c26ebb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Aged</topic><topic>Angiogenesis</topic><topic>Biomarkers</topic><topic>Brain natriuretic peptide</topic><topic>Calcium-binding protein</topic><topic>Creatine Kinase, MB Form</topic><topic>DNA microarrays</topic><topic>Echocardiography</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Heart attacks</topic><topic>human microRNA</topic><topic>Humans</topic><topic>Internal medicine</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>Middle Aged</topic><topic>miR-185</topic><topic>miRNA</topic><topic>Myocardial infarction</topic><topic>Original</topic><topic>Patients</topic><topic>Polymerase chain reaction</topic><topic>Reverse transcription</topic><topic>ST Elevation Myocardial Infarction - genetics</topic><topic>Transforming growth factor-b</topic><topic>Troponin</topic><topic>Troponin I</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Jeong Rang</creatorcontrib><creatorcontrib>Ahn, Jong Hwa</creatorcontrib><creatorcontrib>Jung, Myeong Hee</creatorcontrib><creatorcontrib>Kim, Jin Hyun</creatorcontrib><creatorcontrib>Kang, Min Gyu</creatorcontrib><creatorcontrib>Kim, Kye Hwan</creatorcontrib><creatorcontrib>Jang, Jeong Yoon</creatorcontrib><creatorcontrib>Park, Hyun Woong</creatorcontrib><creatorcontrib>Koh, Jin-Sin</creatorcontrib><creatorcontrib>Hwang, Seok-Jae</creatorcontrib><creatorcontrib>Park, Yongwhi</creatorcontrib><creatorcontrib>Jeong, Young-Hoon</creatorcontrib><creatorcontrib>Kwak, Choong Hwan</creatorcontrib><creatorcontrib>Hwang, Jin-Yong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Internal Medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Jeong Rang</au><au>Ahn, Jong Hwa</au><au>Jung, Myeong Hee</au><au>Kim, Jin Hyun</au><au>Kang, Min Gyu</au><au>Kim, Kye Hwan</au><au>Jang, Jeong Yoon</au><au>Park, Hyun Woong</au><au>Koh, Jin-Sin</au><au>Hwang, Seok-Jae</au><au>Park, Yongwhi</au><au>Jeong, Young-Hoon</au><au>Kwak, Choong Hwan</au><au>Hwang, Jin-Yong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction</atitle><jtitle>Internal Medicine</jtitle><addtitle>Intern. Med.</addtitle><date>2022-01-15</date><risdate>2022</risdate><volume>61</volume><issue>2</issue><spage>151</spage><epage>158</epage><pages>151-158</pages><artnum>7594-21</artnum><issn>0918-2918</issn><eissn>1349-7235</eissn><abstract>Objective Human microRNA-185 (miR-185) has been reported to act as a regulator of fibrosis and angiogenesis in cancer. However, miR-185 has not been investigated in patients with ST-segment elevation myocardial infarction (STEMI). We hypothesized that the changes in miR-185 levels in STEMI patients are related to the processes of myocardial healing and remodeling. Methods Between January 2011 and December 2013, 145 patients with STEMI (65.9±11.6 years old; 41 women) were enrolled. Initial and discharge serum samples collected from 20 patients with STEMI and mixed sera from 8 healthy controls were analyzed by a microarray. A quantitative reverse transcription polymerase chain reaction (RT-qPCR) analysis of miR-185 was performed in all 145 patients. The correlation between the miR-185 levels and the clinical, laboratory, angiographic, and echocardiographic parameters was analyzed. Results The microarray analysis revealed a biphasic pattern in miR-185 levels, with an initial decrease followed by an increase at discharge. The miR-185 levels at discharge were significantly correlated with the troponin-I, CK-MB, and area under the curve of CK-MB levels. There was a positive correlation between the transforming growth factor-β and miR-185 levels at discharge (ρ=0.242, p=0.026). A high wall motion score index and a low ejection fraction, as measured by echocardiography, and high B-type natriuretic peptide level at one month after STEMI were related to high miR-185 levels. Conclusion Our results showed that elevated miR-185 levels at the late stage of STEMI were related to a large amount of myocardial injury and adverse remodeling.</abstract><cop>Japan</cop><pub>The Japanese Society of Internal Medicine</pub><pmid>34248121</pmid><doi>10.2169/internalmedicine.7594-21</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Angiogenesis Biomarkers Brain natriuretic peptide Calcium-binding protein Creatine Kinase, MB Form DNA microarrays Echocardiography Female Fibrosis Heart attacks human microRNA Humans Internal medicine MicroRNAs MicroRNAs - genetics Middle Aged miR-185 miRNA Myocardial infarction Original Patients Polymerase chain reaction Reverse transcription ST Elevation Myocardial Infarction - genetics Transforming growth factor-b Troponin Troponin I |
title | Serum microRNA-185 Levels and Myocardial Injury in Patients with Acute ST-segment Elevation Myocardial Infarction |
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