Pre-miRNA Hsa-Let-7a-2: a Novel Intracellular Partner of Angiotensin II Type 2 Receptor Negatively Regulating its Signals
G protein-coupled receptors (GPCRs) are the largest family of druggable targets, and their biological functions depend on different ligands and intracellular interactomes. Some microRNAs (miRNAs) bind as ligands to RNA-sensitive toll-like receptor 7 to regulate the inflammatory response, thereby con...
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| Veröffentlicht in: | International journal of biological sciences 2022-01, Vol.18 (8), p.3237-3250 |
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| creator | Liu, Xiaoyan Chen, Zhenzhen Li, Shuangyue Jin, Ling Cui, Xiao Cui, Changting Deng, Yue Gao, Qiannan Fan, Luyun Niu, Yaping Wang, Wenjie Cui, Chunmei Zhong, Jiuchang Cui, Qinghua Geng, Bin Cai, Jun |
| description | G protein-coupled receptors (GPCRs) are the largest family of druggable targets, and their biological functions depend on different ligands and intracellular interactomes. Some microRNAs (miRNAs) bind as ligands to RNA-sensitive toll-like receptor 7 to regulate the inflammatory response, thereby contributing to the pathogenesis of cancer or neurodegeneration. It is unknown whether miRNAs bind to angiotensin II (Ang II) type 2 receptor (AGTR2), a critical protective GPCR in cardiovascular diseases, as ligands or intracellular interactomes. Here, screening for miRNAs that bind to AGTR2, we identified and confirmed that the pre-miRNA hsa-let-7a-2 non-competitively binds to the intracellular third loop of AGTR2. Functionally, intracellular hsa-let-7a-2 overexpression suppressed the Ang II-induced AGTR2 effects such as cAMP lowering, RhoA inhibition, and activation of Src homology 2 domain-containing protein-tyrosine phosphatase 1, whereas hsa-let-7a-2 knockdown enhanced these effects. Consistently, overexpressed hsa-let-7a-2 restrained the AGTR2-induced antiproliferation, antimigration, and proapoptosis of cells, and vasodilation of mesenteric arteries. Our findings demonstrated that hsa-let-7a-2 is a novel intracellular partner of AGTR2 that negatively regulates AGTR2-activated signals. |
| doi_str_mv | 10.7150/ijbs.70455 |
| format | Article |
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Some microRNAs (miRNAs) bind as ligands to RNA-sensitive toll-like receptor 7 to regulate the inflammatory response, thereby contributing to the pathogenesis of cancer or neurodegeneration. It is unknown whether miRNAs bind to angiotensin II (Ang II) type 2 receptor (AGTR2), a critical protective GPCR in cardiovascular diseases, as ligands or intracellular interactomes. Here, screening for miRNAs that bind to AGTR2, we identified and confirmed that the pre-miRNA hsa-let-7a-2 non-competitively binds to the intracellular third loop of AGTR2. Functionally, intracellular hsa-let-7a-2 overexpression suppressed the Ang II-induced AGTR2 effects such as cAMP lowering, RhoA inhibition, and activation of Src homology 2 domain-containing protein-tyrosine phosphatase 1, whereas hsa-let-7a-2 knockdown enhanced these effects. Consistently, overexpressed hsa-let-7a-2 restrained the AGTR2-induced antiproliferation, antimigration, and proapoptosis of cells, and vasodilation of mesenteric arteries. Our findings demonstrated that hsa-let-7a-2 is a novel intracellular partner of AGTR2 that negatively regulates AGTR2-activated signals.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.70455</identifier><identifier>PMID: 35637969</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Angiotensin ; Angiotensin II ; Arteries ; Cardiovascular diseases ; Competition ; Coronaviruses ; COVID-19 ; G protein-coupled receptors ; Homology ; Hypertension ; Inflammation ; Inflammatory response ; Intracellular ; Kinetics ; Ligands ; MicroRNAs ; MicroRNAs - metabolism ; miRNA ; Neurodegeneration ; Pathogenesis ; Peptides ; Phosphorylation ; Plasmids ; Protein-tyrosine-phosphatase ; Proteins ; Receptor, Angiotensin, Type 2 - genetics ; Receptors ; Research Paper ; RhoA protein ; Toll-like receptors ; Tyrosine ; Vasodilation</subject><ispartof>International journal of biological sciences, 2022-01, Vol.18 (8), p.3237-3250</ispartof><rights>The author(s).</rights><rights>2022. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-cb89ed554f909bc62aa548840c995fe73c0ddd4a7f2450593e8fbe7799f828013</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9134915/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9134915/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35637969$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Xiaoyan</creatorcontrib><creatorcontrib>Chen, Zhenzhen</creatorcontrib><creatorcontrib>Li, Shuangyue</creatorcontrib><creatorcontrib>Jin, Ling</creatorcontrib><creatorcontrib>Cui, Xiao</creatorcontrib><creatorcontrib>Cui, Changting</creatorcontrib><creatorcontrib>Deng, Yue</creatorcontrib><creatorcontrib>Gao, Qiannan</creatorcontrib><creatorcontrib>Fan, Luyun</creatorcontrib><creatorcontrib>Niu, Yaping</creatorcontrib><creatorcontrib>Wang, Wenjie</creatorcontrib><creatorcontrib>Cui, Chunmei</creatorcontrib><creatorcontrib>Zhong, Jiuchang</creatorcontrib><creatorcontrib>Cui, Qinghua</creatorcontrib><creatorcontrib>Geng, Bin</creatorcontrib><creatorcontrib>Cai, Jun</creatorcontrib><title>Pre-miRNA Hsa-Let-7a-2: a Novel Intracellular Partner of Angiotensin II Type 2 Receptor Negatively Regulating its Signals</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>G protein-coupled receptors (GPCRs) are the largest family of druggable targets, and their biological functions depend on different ligands and intracellular interactomes. Some microRNAs (miRNAs) bind as ligands to RNA-sensitive toll-like receptor 7 to regulate the inflammatory response, thereby contributing to the pathogenesis of cancer or neurodegeneration. It is unknown whether miRNAs bind to angiotensin II (Ang II) type 2 receptor (AGTR2), a critical protective GPCR in cardiovascular diseases, as ligands or intracellular interactomes. Here, screening for miRNAs that bind to AGTR2, we identified and confirmed that the pre-miRNA hsa-let-7a-2 non-competitively binds to the intracellular third loop of AGTR2. Functionally, intracellular hsa-let-7a-2 overexpression suppressed the Ang II-induced AGTR2 effects such as cAMP lowering, RhoA inhibition, and activation of Src homology 2 domain-containing protein-tyrosine phosphatase 1, whereas hsa-let-7a-2 knockdown enhanced these effects. Consistently, overexpressed hsa-let-7a-2 restrained the AGTR2-induced antiproliferation, antimigration, and proapoptosis of cells, and vasodilation of mesenteric arteries. Our findings demonstrated that hsa-let-7a-2 is a novel intracellular partner of AGTR2 that negatively regulates AGTR2-activated signals.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Arteries</subject><subject>Cardiovascular diseases</subject><subject>Competition</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>G protein-coupled receptors</subject><subject>Homology</subject><subject>Hypertension</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Intracellular</subject><subject>Kinetics</subject><subject>Ligands</subject><subject>MicroRNAs</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neurodegeneration</subject><subject>Pathogenesis</subject><subject>Peptides</subject><subject>Phosphorylation</subject><subject>Plasmids</subject><subject>Protein-tyrosine-phosphatase</subject><subject>Proteins</subject><subject>Receptor, Angiotensin, Type 2 - genetics</subject><subject>Receptors</subject><subject>Research Paper</subject><subject>RhoA protein</subject><subject>Toll-like receptors</subject><subject>Tyrosine</subject><subject>Vasodilation</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</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><recordid>eNpVUU1rGzEQFaEln73kBxRBb4V1tfpYST0UTGgag3GD456FVju7kVmvXEkO-N9nnbghPb1h5s2beTyErksykaUg3_y6ThNJuBAn6LzkXBeUKvXhXX2GLlJaE8IqocgpOmOiYlJX-hzt7yMUG79cTPFdssUcciFtQb9jixfhCXo8G3K0Dvp-19uI723MA0QcWjwdOh8yDMkPeDbDq_0WMMVLcLDNIeIFdDb7UWE_9rpxOfuhwz4n_OC7wfbpCn1sR4BPR7xEf25_rm7uivnvX7Ob6bxwTLJcuFppaITgrSa6dhW1VnClOHFaixYkc6RpGm5lS7kgQjNQbQ1Sat0qqkjJLtGPV93trt5A4-BgqDfb6Dc27k2w3vw_Gfyj6cKT0SXjuhSjwJejQAx_d5CyWYddPFgwtKpEyamSdGR9fWW5GFKK0L5dKIk5xGQOMZmXmEby5_c_vVH_5cKeARFHjoQ</recordid><startdate>20220101</startdate><enddate>20220101</enddate><creator>Liu, Xiaoyan</creator><creator>Chen, Zhenzhen</creator><creator>Li, Shuangyue</creator><creator>Jin, Ling</creator><creator>Cui, Xiao</creator><creator>Cui, Changting</creator><creator>Deng, Yue</creator><creator>Gao, Qiannan</creator><creator>Fan, Luyun</creator><creator>Niu, Yaping</creator><creator>Wang, Wenjie</creator><creator>Cui, Chunmei</creator><creator>Zhong, Jiuchang</creator><creator>Cui, Qinghua</creator><creator>Geng, Bin</creator><creator>Cai, Jun</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>COVID</scope><scope>DWQXO</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20220101</creationdate><title>Pre-miRNA Hsa-Let-7a-2: a Novel Intracellular Partner of Angiotensin II Type 2 Receptor Negatively Regulating its Signals</title><author>Liu, Xiaoyan ; 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Some microRNAs (miRNAs) bind as ligands to RNA-sensitive toll-like receptor 7 to regulate the inflammatory response, thereby contributing to the pathogenesis of cancer or neurodegeneration. It is unknown whether miRNAs bind to angiotensin II (Ang II) type 2 receptor (AGTR2), a critical protective GPCR in cardiovascular diseases, as ligands or intracellular interactomes. Here, screening for miRNAs that bind to AGTR2, we identified and confirmed that the pre-miRNA hsa-let-7a-2 non-competitively binds to the intracellular third loop of AGTR2. Functionally, intracellular hsa-let-7a-2 overexpression suppressed the Ang II-induced AGTR2 effects such as cAMP lowering, RhoA inhibition, and activation of Src homology 2 domain-containing protein-tyrosine phosphatase 1, whereas hsa-let-7a-2 knockdown enhanced these effects. Consistently, overexpressed hsa-let-7a-2 restrained the AGTR2-induced antiproliferation, antimigration, and proapoptosis of cells, and vasodilation of mesenteric arteries. Our findings demonstrated that hsa-let-7a-2 is a novel intracellular partner of AGTR2 that negatively regulates AGTR2-activated signals.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>35637969</pmid><doi>10.7150/ijbs.70455</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin Angiotensin II Arteries Cardiovascular diseases Competition Coronaviruses COVID-19 G protein-coupled receptors Homology Hypertension Inflammation Inflammatory response Intracellular Kinetics Ligands MicroRNAs MicroRNAs - metabolism miRNA Neurodegeneration Pathogenesis Peptides Phosphorylation Plasmids Protein-tyrosine-phosphatase Proteins Receptor, Angiotensin, Type 2 - genetics Receptors Research Paper RhoA protein Toll-like receptors Tyrosine Vasodilation |
| title | Pre-miRNA Hsa-Let-7a-2: a Novel Intracellular Partner of Angiotensin II Type 2 Receptor Negatively Regulating its Signals |
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