Lin28B Regulates Angiotensin II-Mediated Let-7c/miR-99a MicroRNA Formation Consequently Affecting Macrophage Polarization and Allergic Inflammation
Angiotensin-II (Ang-II) receptor plays a role in allergic airway inflammation; however, the underlying mechanism and role of macrophages need better understanding. In the present study, angiotensin-II infusion (1 μg/kg/min) in ovalbumin-induced airway inflammation mice model significantly decreased...
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| Veröffentlicht in: | Inflammation 2020-10, Vol.43 (5), p.1846-1861 |
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| description | Angiotensin-II (Ang-II) receptor plays a role in allergic airway inflammation; however, the underlying mechanism and role of macrophages need better understanding. In the present study, angiotensin-II infusion (1 μg/kg/min) in ovalbumin-induced airway inflammation mice model significantly decreased immune cell infiltration, goblet cell hyperplasia, and eosinophil numbers in lungs. Ang-II infusion increased M1 and decreased M2 macrophage population in bronchoalveolar lavage fluid and respective macrophage markers in lung macrophages. Similarly,
in vitro
Ang-II treatment in murine bone marrow-derived macrophages (BMDMs) induced M1 and reduced M2 macrophage phenotype with enhanced bactericidal activity. Mechanistically, Ang-II inhibits Let-7c and miR-99a expression in BMDMs and
in vivo
as well. Lentiviral overexpression of Let-7c and miR-99a miRNAs in BMDMs abrogated Ang-II-induced M1 phenotype activation and promoted M2 phenotype, which is governed by targeting TNFα by miR-99a. In lung macrophages, ovalbumin-induced TNFα inhibition was rescued after Ang-II treatment. In BMDMs, knockdown of TNFα abrogated Ang-II-induced M2 to M1 macrophage phenotype switch and associated bactericidal activity. Ang-II affects mature miRNA formation by enhancing Lin28B levels in macrophages
in vivo
and
in vitro
. Furthermore, Lin28B knockdown prevented Ang-II-mediated inhibition of mature Let-7c/miR-99a miRNA formation, M2 to M1 macrophage phenotype switch, and increased bactericidal activity. Therefore, present study suggests a role of Lin28B in Ang-II-induced Let-7c/miR-99a miRNA formation that consequently affects TNFα production, M1 phenotype activation, and allergic airway inflammation.
Graphical Abstract
Ovalbumin inhibits LIN28B expression thereby fails to inhibit premature to mature Let-7c/miR-99a miRNA formation. Mature miR-99a miRNA that inhibits TNFα consequently promotes M2 polarization and allergic airway inflammation.
While Ang-II induces Lin28B, which inhibits Let-7c/miR-99a miRNA processing and mature miRNA formation, this results in increased TNFα levels that lead to M1 polarization and allergic airway inflammation inhibition. |
| doi_str_mv | 10.1007/s10753-020-01258-1 |
| format | Article |
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in vitro
Ang-II treatment in murine bone marrow-derived macrophages (BMDMs) induced M1 and reduced M2 macrophage phenotype with enhanced bactericidal activity. Mechanistically, Ang-II inhibits Let-7c and miR-99a expression in BMDMs and
in vivo
as well. Lentiviral overexpression of Let-7c and miR-99a miRNAs in BMDMs abrogated Ang-II-induced M1 phenotype activation and promoted M2 phenotype, which is governed by targeting TNFα by miR-99a. In lung macrophages, ovalbumin-induced TNFα inhibition was rescued after Ang-II treatment. In BMDMs, knockdown of TNFα abrogated Ang-II-induced M2 to M1 macrophage phenotype switch and associated bactericidal activity. Ang-II affects mature miRNA formation by enhancing Lin28B levels in macrophages
in vivo
and
in vitro
. Furthermore, Lin28B knockdown prevented Ang-II-mediated inhibition of mature Let-7c/miR-99a miRNA formation, M2 to M1 macrophage phenotype switch, and increased bactericidal activity. Therefore, present study suggests a role of Lin28B in Ang-II-induced Let-7c/miR-99a miRNA formation that consequently affects TNFα production, M1 phenotype activation, and allergic airway inflammation.
Graphical Abstract
Ovalbumin inhibits LIN28B expression thereby fails to inhibit premature to mature Let-7c/miR-99a miRNA formation. Mature miR-99a miRNA that inhibits TNFα consequently promotes M2 polarization and allergic airway inflammation.
While Ang-II induces Lin28B, which inhibits Let-7c/miR-99a miRNA processing and mature miRNA formation, this results in increased TNFα levels that lead to M1 polarization and allergic airway inflammation inhibition.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-020-01258-1</identifier><identifier>PMID: 32458348</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Alveoli ; Angiotensin ; Angiotensin II ; Bactericidal activity ; Biomedical and Life Sciences ; Biomedicine ; Bone marrow ; Bronchus ; Genotype & phenotype ; Hyperplasia ; Hypersensitivity ; Immunology ; Inflammation ; Internal Medicine ; Leukocytes (eosinophilic) ; Macrophages ; MicroRNAs ; miRNA ; Original Article ; Ovalbumin ; Pathology ; Pharmacology/Toxicology ; Phenotypes ; Respiratory tract ; Respiratory tract diseases ; Rheumatology ; Tumor necrosis factor-α</subject><ispartof>Inflammation, 2020-10, Vol.43 (5), p.1846-1861</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-b5c18abc29748d65f4b9b626252554956fd0afaf1e685c23d177e38f0a74086c3</citedby><cites>FETCH-LOGICAL-c375t-b5c18abc29748d65f4b9b626252554956fd0afaf1e685c23d177e38f0a74086c3</cites><orcidid>0000-0001-7574-482X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-020-01258-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-020-01258-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32458348$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jaiswal, Anant</creatorcontrib><creatorcontrib>Maurya, Mohita</creatorcontrib><creatorcontrib>Maurya, Preeti</creatorcontrib><creatorcontrib>Barthwal, Manoj Kumar</creatorcontrib><title>Lin28B Regulates Angiotensin II-Mediated Let-7c/miR-99a MicroRNA Formation Consequently Affecting Macrophage Polarization and Allergic Inflammation</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Angiotensin-II (Ang-II) receptor plays a role in allergic airway inflammation; however, the underlying mechanism and role of macrophages need better understanding. In the present study, angiotensin-II infusion (1 μg/kg/min) in ovalbumin-induced airway inflammation mice model significantly decreased immune cell infiltration, goblet cell hyperplasia, and eosinophil numbers in lungs. Ang-II infusion increased M1 and decreased M2 macrophage population in bronchoalveolar lavage fluid and respective macrophage markers in lung macrophages. Similarly,
in vitro
Ang-II treatment in murine bone marrow-derived macrophages (BMDMs) induced M1 and reduced M2 macrophage phenotype with enhanced bactericidal activity. Mechanistically, Ang-II inhibits Let-7c and miR-99a expression in BMDMs and
in vivo
as well. Lentiviral overexpression of Let-7c and miR-99a miRNAs in BMDMs abrogated Ang-II-induced M1 phenotype activation and promoted M2 phenotype, which is governed by targeting TNFα by miR-99a. In lung macrophages, ovalbumin-induced TNFα inhibition was rescued after Ang-II treatment. In BMDMs, knockdown of TNFα abrogated Ang-II-induced M2 to M1 macrophage phenotype switch and associated bactericidal activity. Ang-II affects mature miRNA formation by enhancing Lin28B levels in macrophages
in vivo
and
in vitro
. Furthermore, Lin28B knockdown prevented Ang-II-mediated inhibition of mature Let-7c/miR-99a miRNA formation, M2 to M1 macrophage phenotype switch, and increased bactericidal activity. Therefore, present study suggests a role of Lin28B in Ang-II-induced Let-7c/miR-99a miRNA formation that consequently affects TNFα production, M1 phenotype activation, and allergic airway inflammation.
Graphical Abstract
Ovalbumin inhibits LIN28B expression thereby fails to inhibit premature to mature Let-7c/miR-99a miRNA formation. Mature miR-99a miRNA that inhibits TNFα consequently promotes M2 polarization and allergic airway inflammation.
While Ang-II induces Lin28B, which inhibits Let-7c/miR-99a miRNA processing and mature miRNA formation, this results in increased TNFα levels that lead to M1 polarization and allergic airway inflammation inhibition.</description><subject>Alveoli</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Bactericidal activity</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bone marrow</subject><subject>Bronchus</subject><subject>Genotype & phenotype</subject><subject>Hyperplasia</subject><subject>Hypersensitivity</subject><subject>Immunology</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Leukocytes (eosinophilic)</subject><subject>Macrophages</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>Original Article</subject><subject>Ovalbumin</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Phenotypes</subject><subject>Respiratory tract</subject><subject>Respiratory tract diseases</subject><subject>Rheumatology</subject><subject>Tumor necrosis factor-α</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kc1u1DAURi1ERYfCC7BAlth0Y-qfOLaXYdTCSDOARrC2HMcOrhJnsJNFeY2-MIYUkLpgZck-9_O99wDwiuC3BGNxlQkWnCFMMcKEconIE7AhXDBEuaifgg1mNUZMKXEOnud8izGWSrJn4JzRiktWyQ2434dI5Tt4dP0ymNll2MQ-TLOLOUS426GD60K57-DezUjYqzEckVIGHoJN0_FjA2-mNJo5TBFup5jd98XFebiDjffOziH28GAKefpmegc_T4NJ4ceKm9jBZhhc6oOFu-gHM65BL8CZN0N2Lx_OC_D15vrL9gPaf3q_2zZ7ZJngM2q5JdK0lipRya7mvmpVW9Oacsp5pXjtO2y88cTVklvKOiKEY9JjIyosa8suwOWae0pTaTvPegzZumEw0U1L1rTCghFeU1XQN4_Q22lJsXRXqArzsuSKFYquVBk45-S8PqUwmnSnCda_lOlVmS7K9G9lmpSi1w_RSzu67m_JH0cFYCuQy1PsXfr3939ifwJMQKEa</recordid><startdate>20201001</startdate><enddate>20201001</enddate><creator>Jaiswal, Anant</creator><creator>Maurya, Mohita</creator><creator>Maurya, Preeti</creator><creator>Barthwal, Manoj Kumar</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7574-482X</orcidid></search><sort><creationdate>20201001</creationdate><title>Lin28B Regulates Angiotensin II-Mediated Let-7c/miR-99a MicroRNA Formation Consequently Affecting Macrophage Polarization and Allergic Inflammation</title><author>Jaiswal, Anant ; Maurya, Mohita ; Maurya, Preeti ; Barthwal, Manoj Kumar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-b5c18abc29748d65f4b9b626252554956fd0afaf1e685c23d177e38f0a74086c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alveoli</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Bactericidal activity</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bone marrow</topic><topic>Bronchus</topic><topic>Genotype & phenotype</topic><topic>Hyperplasia</topic><topic>Hypersensitivity</topic><topic>Immunology</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Leukocytes (eosinophilic)</topic><topic>Macrophages</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>Original Article</topic><topic>Ovalbumin</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Phenotypes</topic><topic>Respiratory tract</topic><topic>Respiratory tract diseases</topic><topic>Rheumatology</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jaiswal, Anant</creatorcontrib><creatorcontrib>Maurya, Mohita</creatorcontrib><creatorcontrib>Maurya, Preeti</creatorcontrib><creatorcontrib>Barthwal, Manoj Kumar</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</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>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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jaiswal, Anant</au><au>Maurya, Mohita</au><au>Maurya, Preeti</au><au>Barthwal, Manoj Kumar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lin28B Regulates Angiotensin II-Mediated Let-7c/miR-99a MicroRNA Formation Consequently Affecting Macrophage Polarization and Allergic Inflammation</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2020-10-01</date><risdate>2020</risdate><volume>43</volume><issue>5</issue><spage>1846</spage><epage>1861</epage><pages>1846-1861</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Angiotensin-II (Ang-II) receptor plays a role in allergic airway inflammation; however, the underlying mechanism and role of macrophages need better understanding. In the present study, angiotensin-II infusion (1 μg/kg/min) in ovalbumin-induced airway inflammation mice model significantly decreased immune cell infiltration, goblet cell hyperplasia, and eosinophil numbers in lungs. Ang-II infusion increased M1 and decreased M2 macrophage population in bronchoalveolar lavage fluid and respective macrophage markers in lung macrophages. Similarly,
in vitro
Ang-II treatment in murine bone marrow-derived macrophages (BMDMs) induced M1 and reduced M2 macrophage phenotype with enhanced bactericidal activity. Mechanistically, Ang-II inhibits Let-7c and miR-99a expression in BMDMs and
in vivo
as well. Lentiviral overexpression of Let-7c and miR-99a miRNAs in BMDMs abrogated Ang-II-induced M1 phenotype activation and promoted M2 phenotype, which is governed by targeting TNFα by miR-99a. In lung macrophages, ovalbumin-induced TNFα inhibition was rescued after Ang-II treatment. In BMDMs, knockdown of TNFα abrogated Ang-II-induced M2 to M1 macrophage phenotype switch and associated bactericidal activity. Ang-II affects mature miRNA formation by enhancing Lin28B levels in macrophages
in vivo
and
in vitro
. Furthermore, Lin28B knockdown prevented Ang-II-mediated inhibition of mature Let-7c/miR-99a miRNA formation, M2 to M1 macrophage phenotype switch, and increased bactericidal activity. Therefore, present study suggests a role of Lin28B in Ang-II-induced Let-7c/miR-99a miRNA formation that consequently affects TNFα production, M1 phenotype activation, and allergic airway inflammation.
Graphical Abstract
Ovalbumin inhibits LIN28B expression thereby fails to inhibit premature to mature Let-7c/miR-99a miRNA formation. Mature miR-99a miRNA that inhibits TNFα consequently promotes M2 polarization and allergic airway inflammation.
While Ang-II induces Lin28B, which inhibits Let-7c/miR-99a miRNA processing and mature miRNA formation, this results in increased TNFα levels that lead to M1 polarization and allergic airway inflammation inhibition.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32458348</pmid><doi>10.1007/s10753-020-01258-1</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-7574-482X</orcidid></addata></record> |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Alveoli Angiotensin Angiotensin II Bactericidal activity Biomedical and Life Sciences Biomedicine Bone marrow Bronchus Genotype & phenotype Hyperplasia Hypersensitivity Immunology Inflammation Internal Medicine Leukocytes (eosinophilic) Macrophages MicroRNAs miRNA Original Article Ovalbumin Pathology Pharmacology/Toxicology Phenotypes Respiratory tract Respiratory tract diseases Rheumatology Tumor necrosis factor-α |
| title | Lin28B Regulates Angiotensin II-Mediated Let-7c/miR-99a MicroRNA Formation Consequently Affecting Macrophage Polarization and Allergic Inflammation |
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