Co‐expression of glycosylated aquaporin‐1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis‐prone mice
Increased stiffness characterizes the early change in the arterial wall with subclinical atherosclerosis. Proteins inducing arterial stiffness in diabetes and hypercholesterolaemia are largely unknown. This study aimed at determining the pattern of protein expression in stiffening aorta of diabetic...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2020-03, Vol.24 (5), p.2857-2865 |
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| creator | Madonna, Rosalinda Doria, Vanessa Görbe, Anikó Cocco, Nino Ferdinandy, Péter Geng, Yong‐Jian Pierdomenico, Sante Donato De Caterina, Raffaele |
| description | Increased stiffness characterizes the early change in the arterial wall with subclinical atherosclerosis. Proteins inducing arterial stiffness in diabetes and hypercholesterolaemia are largely unknown. This study aimed at determining the pattern of protein expression in stiffening aorta of diabetic and hypercholesterolaemic mice. Male Ins2+/Akita mice were crossbred with ApoE−/− (Ins2+/Akita: ApoE−/−) mice. Relative aortic distension (relD) values were determined by ultrasound analysis and arterial stiffness modulators by immunoblotting. Compared with age‐ and sex‐matched C57/BL6 control mice, the aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed increased aortic stiffness. The aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed greater expression of VCAM‐1, collagen type III, NADPH oxidase and iNOS, as well as reduced elastin, with increased collagen type III‐to‐elastin ratio. The aorta of Ins2+/Akita and Ins2+/Akita:ApoE−/− mice showed higher expression of eNOS and cytoskeletal remodelling proteins, such as F‐actin and α‐smooth muscle actin, in addition to increased glycosylated aquaporin (AQP)‐1 and transcription factor NFAT5, which control the expression of genes activated by high glucose‐induced hyperosmotic stress. Diabetic and hypercholesterolaemic mice have increased aortic stiffness. The association of AQP1 and NFAT5 co‐expression with aortic stiffness in diabetes and hypercholesterolaemia may represent a novel molecular pathway or therapeutic target. |
| doi_str_mv | 10.1111/jcmm.14843 |
| format | Article |
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Proteins inducing arterial stiffness in diabetes and hypercholesterolaemia are largely unknown. This study aimed at determining the pattern of protein expression in stiffening aorta of diabetic and hypercholesterolaemic mice. Male Ins2+/Akita mice were crossbred with ApoE−/− (Ins2+/Akita: ApoE−/−) mice. Relative aortic distension (relD) values were determined by ultrasound analysis and arterial stiffness modulators by immunoblotting. Compared with age‐ and sex‐matched C57/BL6 control mice, the aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed increased aortic stiffness. The aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed greater expression of VCAM‐1, collagen type III, NADPH oxidase and iNOS, as well as reduced elastin, with increased collagen type III‐to‐elastin ratio. The aorta of Ins2+/Akita and Ins2+/Akita:ApoE−/− mice showed higher expression of eNOS and cytoskeletal remodelling proteins, such as F‐actin and α‐smooth muscle actin, in addition to increased glycosylated aquaporin (AQP)‐1 and transcription factor NFAT5, which control the expression of genes activated by high glucose‐induced hyperosmotic stress. Diabetic and hypercholesterolaemic mice have increased aortic stiffness. The association of AQP1 and NFAT5 co‐expression with aortic stiffness in diabetes and hypercholesterolaemia may represent a novel molecular pathway or therapeutic target.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.14843</identifier><identifier>PMID: 31970899</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Actin ; Animals ; Aorta ; Apolipoprotein E ; Aquaporin 1 ; Aquaporin 1 - metabolism ; Aquaporins ; arterial stiffening ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - metabolism ; Atherosclerosis - physiopathology ; Biomechanics ; Cell adhesion & migration ; Cholesterol ; Collagen (type III) ; Collagen Type III - metabolism ; cytoskeletal remodelling ; Cytoskeleton ; Cytoskeleton - metabolism ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - physiopathology ; Distension ; Elastin ; Elastin - metabolism ; Gene expression ; Glycosylation ; hypercholesterolaemia ; hyperosmolarity ; Immunoblotting ; Immunomodulation ; Laboratory animals ; Male ; Mice, Inbred C57BL ; Muscle, Smooth - metabolism ; Mutation ; NAD(P)H oxidase ; NADPH Oxidases - metabolism ; Nitric Oxide Synthase - metabolism ; Nitric-oxide synthase ; Original ; Phenotype ; Protein expression ; Protein Isoforms - metabolism ; Proteins ; R&D ; Research & development ; Smooth muscle ; subclinical atherosclerosis ; Therapeutic applications ; Transcription factors ; Transcription Factors - metabolism ; Ultrasonic imaging ; Ultrasound ; Vascular Cell Adhesion Molecule-1 - metabolism ; Vascular Stiffness</subject><ispartof>Journal of cellular and molecular medicine, 2020-03, Vol.24 (5), p.2857-2865</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4483-be0ac428a204c34513c50d6559149c5a76ba2b3104cd94c068de150d0b2859b83</citedby><cites>FETCH-LOGICAL-c4483-be0ac428a204c34513c50d6559149c5a76ba2b3104cd94c068de150d0b2859b83</cites><orcidid>0000-0001-6455-2777</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077545/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7077545/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31970899$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Madonna, Rosalinda</creatorcontrib><creatorcontrib>Doria, Vanessa</creatorcontrib><creatorcontrib>Görbe, Anikó</creatorcontrib><creatorcontrib>Cocco, Nino</creatorcontrib><creatorcontrib>Ferdinandy, Péter</creatorcontrib><creatorcontrib>Geng, Yong‐Jian</creatorcontrib><creatorcontrib>Pierdomenico, Sante Donato</creatorcontrib><creatorcontrib>De Caterina, Raffaele</creatorcontrib><title>Co‐expression of glycosylated aquaporin‐1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis‐prone mice</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Increased stiffness characterizes the early change in the arterial wall with subclinical atherosclerosis. Proteins inducing arterial stiffness in diabetes and hypercholesterolaemia are largely unknown. This study aimed at determining the pattern of protein expression in stiffening aorta of diabetic and hypercholesterolaemic mice. Male Ins2+/Akita mice were crossbred with ApoE−/− (Ins2+/Akita: ApoE−/−) mice. Relative aortic distension (relD) values were determined by ultrasound analysis and arterial stiffness modulators by immunoblotting. Compared with age‐ and sex‐matched C57/BL6 control mice, the aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed increased aortic stiffness. The aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed greater expression of VCAM‐1, collagen type III, NADPH oxidase and iNOS, as well as reduced elastin, with increased collagen type III‐to‐elastin ratio. The aorta of Ins2+/Akita and Ins2+/Akita:ApoE−/− mice showed higher expression of eNOS and cytoskeletal remodelling proteins, such as F‐actin and α‐smooth muscle actin, in addition to increased glycosylated aquaporin (AQP)‐1 and transcription factor NFAT5, which control the expression of genes activated by high glucose‐induced hyperosmotic stress. Diabetic and hypercholesterolaemic mice have increased aortic stiffness. The association of AQP1 and NFAT5 co‐expression with aortic stiffness in diabetes and hypercholesterolaemia may represent a novel molecular pathway or therapeutic target.</description><subject>Actin</subject><subject>Animals</subject><subject>Aorta</subject><subject>Apolipoprotein E</subject><subject>Aquaporin 1</subject><subject>Aquaporin 1 - metabolism</subject><subject>Aquaporins</subject><subject>arterial stiffening</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - physiopathology</subject><subject>Biomechanics</subject><subject>Cell adhesion & migration</subject><subject>Cholesterol</subject><subject>Collagen (type III)</subject><subject>Collagen Type III - metabolism</subject><subject>cytoskeletal remodelling</subject><subject>Cytoskeleton</subject><subject>Cytoskeleton - metabolism</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Distension</subject><subject>Elastin</subject><subject>Elastin - metabolism</subject><subject>Gene expression</subject><subject>Glycosylation</subject><subject>hypercholesterolaemia</subject><subject>hyperosmolarity</subject><subject>Immunoblotting</subject><subject>Immunomodulation</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Muscle, Smooth - metabolism</subject><subject>Mutation</subject><subject>NAD(P)H oxidase</subject><subject>NADPH Oxidases - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Original</subject><subject>Phenotype</subject><subject>Protein expression</subject><subject>Protein Isoforms - metabolism</subject><subject>Proteins</subject><subject>R&D</subject><subject>Research & development</subject><subject>Smooth muscle</subject><subject>subclinical atherosclerosis</subject><subject>Therapeutic applications</subject><subject>Transcription factors</subject><subject>Transcription Factors - metabolism</subject><subject>Ultrasonic imaging</subject><subject>Ultrasound</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>Vascular Stiffness</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1uFSEUgCdGY2t14wMYEjfG5FYYYICNSXPT-pNWN3VNzjBMy80MTIFR766P4NbX80lkvNdGXcgCCOfLd87hVNVTgo9JWa82ZhyPCZOM3qsOCZf1iinK7u_vRFJ5UD1KaYMxbQhVD6sDSpTAUqnD6vs6_Lj9Zr9O0abkgkehR1fD1oS0HSDbDsHNDFOIzheMIPAdyhF8MtFNeeF7MDlE9OHs5JIjE3yOrp2zTSgHBCFmZ1DKru998SPnUeegtcvrooJ8bWNIZlh2l0qKKQZv0eiMfVw96GFI9sn-PKo-nZ1ert-uzj--ebc-OV8ZxiRdtRaDYbWEGjNDGSfUcNw1nCvClOEgmhbqlpIS7RQzuJGdJYXAbS25aiU9ql7vvNPcjrYztrQAg56iGyFudQCn_454d62vwmctsBCc8SJ4sRfEcDPblPXokrHDAN6GOemaMlZTzPiS6_k_6CbM0Zf2CiVEI7ggi_DljjLlV1K0_V0xBOtl4nqZuP418QI_-7P8O_T3iAtAdsAXN9jtf1T6_friYif9CdrBvN0</recordid><startdate>202003</startdate><enddate>202003</enddate><creator>Madonna, Rosalinda</creator><creator>Doria, Vanessa</creator><creator>Görbe, Anikó</creator><creator>Cocco, Nino</creator><creator>Ferdinandy, Péter</creator><creator>Geng, Yong‐Jian</creator><creator>Pierdomenico, Sante Donato</creator><creator>De Caterina, Raffaele</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-6455-2777</orcidid></search><sort><creationdate>202003</creationdate><title>Co‐expression of glycosylated aquaporin‐1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis‐prone mice</title><author>Madonna, Rosalinda ; Doria, Vanessa ; Görbe, Anikó ; Cocco, Nino ; Ferdinandy, Péter ; Geng, Yong‐Jian ; Pierdomenico, Sante Donato ; De Caterina, Raffaele</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-be0ac428a204c34513c50d6559149c5a76ba2b3104cd94c068de150d0b2859b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Actin</topic><topic>Animals</topic><topic>Aorta</topic><topic>Apolipoprotein E</topic><topic>Aquaporin 1</topic><topic>Aquaporin 1 - metabolism</topic><topic>Aquaporins</topic><topic>arterial stiffening</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - physiopathology</topic><topic>Biomechanics</topic><topic>Cell adhesion & migration</topic><topic>Cholesterol</topic><topic>Collagen (type III)</topic><topic>Collagen Type III - metabolism</topic><topic>cytoskeletal remodelling</topic><topic>Cytoskeleton</topic><topic>Cytoskeleton - metabolism</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Distension</topic><topic>Elastin</topic><topic>Elastin - metabolism</topic><topic>Gene expression</topic><topic>Glycosylation</topic><topic>hypercholesterolaemia</topic><topic>hyperosmolarity</topic><topic>Immunoblotting</topic><topic>Immunomodulation</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Muscle, Smooth - metabolism</topic><topic>Mutation</topic><topic>NAD(P)H oxidase</topic><topic>NADPH Oxidases - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Original</topic><topic>Phenotype</topic><topic>Protein expression</topic><topic>Protein Isoforms - metabolism</topic><topic>Proteins</topic><topic>R&D</topic><topic>Research & development</topic><topic>Smooth muscle</topic><topic>subclinical atherosclerosis</topic><topic>Therapeutic applications</topic><topic>Transcription factors</topic><topic>Transcription Factors - metabolism</topic><topic>Ultrasonic imaging</topic><topic>Ultrasound</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>Vascular Stiffness</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Madonna, Rosalinda</creatorcontrib><creatorcontrib>Doria, Vanessa</creatorcontrib><creatorcontrib>Görbe, Anikó</creatorcontrib><creatorcontrib>Cocco, Nino</creatorcontrib><creatorcontrib>Ferdinandy, Péter</creatorcontrib><creatorcontrib>Geng, Yong‐Jian</creatorcontrib><creatorcontrib>Pierdomenico, Sante Donato</creatorcontrib><creatorcontrib>De Caterina, Raffaele</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content 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>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Madonna, Rosalinda</au><au>Doria, Vanessa</au><au>Görbe, Anikó</au><au>Cocco, Nino</au><au>Ferdinandy, Péter</au><au>Geng, Yong‐Jian</au><au>Pierdomenico, Sante Donato</au><au>De Caterina, Raffaele</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Co‐expression of glycosylated aquaporin‐1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis‐prone mice</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-03</date><risdate>2020</risdate><volume>24</volume><issue>5</issue><spage>2857</spage><epage>2865</epage><pages>2857-2865</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Increased stiffness characterizes the early change in the arterial wall with subclinical atherosclerosis. Proteins inducing arterial stiffness in diabetes and hypercholesterolaemia are largely unknown. This study aimed at determining the pattern of protein expression in stiffening aorta of diabetic and hypercholesterolaemic mice. Male Ins2+/Akita mice were crossbred with ApoE−/− (Ins2+/Akita: ApoE−/−) mice. Relative aortic distension (relD) values were determined by ultrasound analysis and arterial stiffness modulators by immunoblotting. Compared with age‐ and sex‐matched C57/BL6 control mice, the aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed increased aortic stiffness. The aortas of Ins2+/Akita, ApoE−/− and Ins2+/Akita:ApoE−/− mice showed greater expression of VCAM‐1, collagen type III, NADPH oxidase and iNOS, as well as reduced elastin, with increased collagen type III‐to‐elastin ratio. The aorta of Ins2+/Akita and Ins2+/Akita:ApoE−/− mice showed higher expression of eNOS and cytoskeletal remodelling proteins, such as F‐actin and α‐smooth muscle actin, in addition to increased glycosylated aquaporin (AQP)‐1 and transcription factor NFAT5, which control the expression of genes activated by high glucose‐induced hyperosmotic stress. Diabetic and hypercholesterolaemic mice have increased aortic stiffness. The association of AQP1 and NFAT5 co‐expression with aortic stiffness in diabetes and hypercholesterolaemia may represent a novel molecular pathway or therapeutic target.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31970899</pmid><doi>10.1111/jcmm.14843</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-6455-2777</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2020-03, Vol.24 (5), p.2857-2865 |
| issn | 1582-1838 1582-4934 |
| language | eng |
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| source | MEDLINE; Wiley-Blackwell Open Access Titles; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Actin Animals Aorta Apolipoprotein E Aquaporin 1 Aquaporin 1 - metabolism Aquaporins arterial stiffening Arteriosclerosis Atherosclerosis Atherosclerosis - metabolism Atherosclerosis - physiopathology Biomechanics Cell adhesion & migration Cholesterol Collagen (type III) Collagen Type III - metabolism cytoskeletal remodelling Cytoskeleton Cytoskeleton - metabolism Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - physiopathology Distension Elastin Elastin - metabolism Gene expression Glycosylation hypercholesterolaemia hyperosmolarity Immunoblotting Immunomodulation Laboratory animals Male Mice, Inbred C57BL Muscle, Smooth - metabolism Mutation NAD(P)H oxidase NADPH Oxidases - metabolism Nitric Oxide Synthase - metabolism Nitric-oxide synthase Original Phenotype Protein expression Protein Isoforms - metabolism Proteins R&D Research & development Smooth muscle subclinical atherosclerosis Therapeutic applications Transcription factors Transcription Factors - metabolism Ultrasonic imaging Ultrasound Vascular Cell Adhesion Molecule-1 - metabolism Vascular Stiffness |
| title | Co‐expression of glycosylated aquaporin‐1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis‐prone mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T19%3A21%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Co%E2%80%90expression%20of%20glycosylated%20aquaporin%E2%80%901%20and%20transcription%20factor%20NFAT5%20contributes%20to%20aortic%20stiffness%20in%20diabetic%20and%20atherosclerosis%E2%80%90prone%20mice&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Madonna,%20Rosalinda&rft.date=2020-03&rft.volume=24&rft.issue=5&rft.spage=2857&rft.epage=2865&rft.pages=2857-2865&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.14843&rft_dat=%3Cproquest_pubme%3E2344230458%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2377675715&rft_id=info:pmid/31970899&rfr_iscdi=true |