Characterization of the spontaneous degenerative mitral valve disease in FVB mice
The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models. We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J...
Gespeichert in:
| Veröffentlicht in: | PloS one 2021-09, Vol.16 (9), p.e0257022-e0257022 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0257022 |
|---|---|
| container_issue | 9 |
| container_start_page | e0257022 |
| container_title | PloS one |
| container_volume | 16 |
| creator | Ayme-Dietrich, Estelle Da Silva, Sylvia Bouabout, Ghina Alame Arnoux, Alizée Guyonnet, Jérôme Becker, Guillaume Monassier, Laurent |
| description | The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models.
We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system.
Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography.
Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium.
The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested. |
| doi_str_mv | 10.1371/journal.pone.0257022 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_2568584190</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A674089540</galeid><doaj_id>oai_doaj_org_article_52a824897d2b417f9971833ec6db8e9c</doaj_id><sourcerecordid>A674089540</sourcerecordid><originalsourceid>FETCH-LOGICAL-c726t-8452134f77dceacdbe80bc5b8770df0d3a3416abe9d4b3d8b5112b542f292d13</originalsourceid><addsrcrecordid>eNqNk11v0zAUhiMEYmPwDxBEQkLsosVfiZ0bpFIxVmnSBEy7tRz7pHGVxsVOKuDX49BsaqZdoFwkOec5r8-HT5K8xmiOKccfN673rWrmO9fCHJGMI0KeJKe4oGSWE0SfHn2fJC9C2CCUUZHnz5MTyhinnPPT5NuyVl7pDrz9ozrr2tRVaVdDGqJup1pwfUgNrKEFH_17SLe286pJ96qJP8YGUAFS26YXt5-jT8PL5FmlmgCvxvdZcnPx5WZ5Obu6_rpaLq5mmpO8mwmWEUxZxbnRoLQpQaBSZ6XgHJkKGaoow7kqoTCspEaUGcakzBipSEEMpmfJ24PsrnFBjs0IkmS5yATDBYrE6kAYpzZy5-1W-d_SKSv_GZxfS-U7qxuQGVGCMFFwQ0qGeVUUHAtKQeemFFDoqPVpPK0vtxAzbocmTESnntbWcu32MqZCSDYkc34QqB-EXS6u5GBDcSYZzfP9UNqH8TDvfvYQOrm1QUPTHMYx1FhQLlAuIvruAfp4J0ZqrWKxtq1czFEPonKRc4ZEkbGBmj9CxcdAnGu8ZZWN9knA-SQgMh386taqD0Gufnz_f_b6dsq-P2JrUE1XB9f0w_UMU5AdQO1dCB6q-85iJIclueuGHJZEjksSw94cD_M-6G4r6F_iCAr9</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2568584190</pqid></control><display><type>article</type><title>Characterization of the spontaneous degenerative mitral valve disease in FVB mice</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Public Library of Science (PLoS) Journals Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><creator>Ayme-Dietrich, Estelle ; Da Silva, Sylvia ; Bouabout, Ghina Alame ; Arnoux, Alizée ; Guyonnet, Jérôme ; Becker, Guillaume ; Monassier, Laurent</creator><contributor>Oury, Cécile</contributor><creatorcontrib>Ayme-Dietrich, Estelle ; Da Silva, Sylvia ; Bouabout, Ghina Alame ; Arnoux, Alizée ; Guyonnet, Jérôme ; Becker, Guillaume ; Monassier, Laurent ; Oury, Cécile</creatorcontrib><description>The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models.
We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system.
Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography.
Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium.
The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0257022</identifier><identifier>PMID: 34473777</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animal models ; Animal research ; Animals ; Atria ; Atrial Natriuretic Factor - blood ; Biology and Life Sciences ; Bleeding ; Bleeding Time ; Blood cells ; Blood levels ; Blood Pressure ; Body weight ; Cardiology and cardiovascular system ; Cardiovascular disease ; Coronary vessels ; Degeneration ; Disease Models, Animal ; Echocardiography ; Echocardiography - methods ; Female ; Fibrosis ; Gene expression ; Genetic aspects ; Glycosaminoglycans ; Heart Rate ; Heart valve diseases ; Heart valves ; Histology ; Human health and pathology ; Hydroxyindoleacetic Acid - urine ; Hypertrophy ; Inbreeding ; Laboratories ; Life Sciences ; Male ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Mitral valve ; Mitral Valve Insufficiency - blood ; Mitral Valve Insufficiency - diagnostic imaging ; Mitral Valve Insufficiency - physiopathology ; Mitral Valve Insufficiency - urine ; mRNA ; Myocardium ; Pathophysiology ; Platelet Count ; Pulmonary arteries ; Receptor mechanisms ; Rheumatic heart disease ; Serotonin ; Serotonin - blood ; Serotonin S2 receptors ; Thickening ; Transforming Growth Factor beta1 - blood ; Transforming growth factor-b1 ; Transforming growth factors ; Ventricle ; Ventricular Remodeling</subject><ispartof>PloS one, 2021-09, Vol.16 (9), p.e0257022-e0257022</ispartof><rights>COPYRIGHT 2021 Public Library of Science</rights><rights>2021 Ayme-Dietrich et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2021 Ayme-Dietrich et al 2021 Ayme-Dietrich et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c726t-8452134f77dceacdbe80bc5b8770df0d3a3416abe9d4b3d8b5112b542f292d13</citedby><cites>FETCH-LOGICAL-c726t-8452134f77dceacdbe80bc5b8770df0d3a3416abe9d4b3d8b5112b542f292d13</cites><orcidid>0000-0001-8341-4986 ; 0000-0002-0613-3803 ; 0000-0003-2710-0960 ; 0000-0002-1714-0267</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/PMC8412250/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8412250/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34473777$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03445366$$DView record in HAL$$Hfree_for_read</backlink></links><search><contributor>Oury, Cécile</contributor><creatorcontrib>Ayme-Dietrich, Estelle</creatorcontrib><creatorcontrib>Da Silva, Sylvia</creatorcontrib><creatorcontrib>Bouabout, Ghina Alame</creatorcontrib><creatorcontrib>Arnoux, Alizée</creatorcontrib><creatorcontrib>Guyonnet, Jérôme</creatorcontrib><creatorcontrib>Becker, Guillaume</creatorcontrib><creatorcontrib>Monassier, Laurent</creatorcontrib><title>Characterization of the spontaneous degenerative mitral valve disease in FVB mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models.
We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system.
Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography.
Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium.
The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.</description><subject>Analysis</subject><subject>Animal models</subject><subject>Animal research</subject><subject>Animals</subject><subject>Atria</subject><subject>Atrial Natriuretic Factor - blood</subject><subject>Biology and Life Sciences</subject><subject>Bleeding</subject><subject>Bleeding Time</subject><subject>Blood cells</subject><subject>Blood levels</subject><subject>Blood Pressure</subject><subject>Body weight</subject><subject>Cardiology and cardiovascular system</subject><subject>Cardiovascular disease</subject><subject>Coronary vessels</subject><subject>Degeneration</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Echocardiography - methods</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Glycosaminoglycans</subject><subject>Heart Rate</subject><subject>Heart valve diseases</subject><subject>Heart valves</subject><subject>Histology</subject><subject>Human health and pathology</subject><subject>Hydroxyindoleacetic Acid - urine</subject><subject>Hypertrophy</subject><subject>Inbreeding</subject><subject>Laboratories</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitral valve</subject><subject>Mitral Valve Insufficiency - blood</subject><subject>Mitral Valve Insufficiency - diagnostic imaging</subject><subject>Mitral Valve Insufficiency - physiopathology</subject><subject>Mitral Valve Insufficiency - urine</subject><subject>mRNA</subject><subject>Myocardium</subject><subject>Pathophysiology</subject><subject>Platelet Count</subject><subject>Pulmonary arteries</subject><subject>Receptor mechanisms</subject><subject>Rheumatic heart disease</subject><subject>Serotonin</subject><subject>Serotonin - blood</subject><subject>Serotonin S2 receptors</subject><subject>Thickening</subject><subject>Transforming Growth Factor beta1 - blood</subject><subject>Transforming growth factor-b1</subject><subject>Transforming growth factors</subject><subject>Ventricle</subject><subject>Ventricular Remodeling</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</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><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkLsosVfiZ0bpFIxVmnSBEy7tRz7pHGVxsVOKuDX49BsaqZdoFwkOec5r8-HT5K8xmiOKccfN673rWrmO9fCHJGMI0KeJKe4oGSWE0SfHn2fJC9C2CCUUZHnz5MTyhinnPPT5NuyVl7pDrz9ozrr2tRVaVdDGqJup1pwfUgNrKEFH_17SLe286pJ96qJP8YGUAFS26YXt5-jT8PL5FmlmgCvxvdZcnPx5WZ5Obu6_rpaLq5mmpO8mwmWEUxZxbnRoLQpQaBSZ6XgHJkKGaoow7kqoTCspEaUGcakzBipSEEMpmfJ24PsrnFBjs0IkmS5yATDBYrE6kAYpzZy5-1W-d_SKSv_GZxfS-U7qxuQGVGCMFFwQ0qGeVUUHAtKQeemFFDoqPVpPK0vtxAzbocmTESnntbWcu32MqZCSDYkc34QqB-EXS6u5GBDcSYZzfP9UNqH8TDvfvYQOrm1QUPTHMYx1FhQLlAuIvruAfp4J0ZqrWKxtq1czFEPonKRc4ZEkbGBmj9CxcdAnGu8ZZWN9knA-SQgMh386taqD0Gufnz_f_b6dsq-P2JrUE1XB9f0w_UMU5AdQO1dCB6q-85iJIclueuGHJZEjksSw94cD_M-6G4r6F_iCAr9</recordid><startdate>20210902</startdate><enddate>20210902</enddate><creator>Ayme-Dietrich, Estelle</creator><creator>Da Silva, Sylvia</creator><creator>Bouabout, Ghina Alame</creator><creator>Arnoux, Alizée</creator><creator>Guyonnet, Jérôme</creator><creator>Becker, Guillaume</creator><creator>Monassier, Laurent</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-8341-4986</orcidid><orcidid>https://orcid.org/0000-0002-0613-3803</orcidid><orcidid>https://orcid.org/0000-0003-2710-0960</orcidid><orcidid>https://orcid.org/0000-0002-1714-0267</orcidid></search><sort><creationdate>20210902</creationdate><title>Characterization of the spontaneous degenerative mitral valve disease in FVB mice</title><author>Ayme-Dietrich, Estelle ; Da Silva, Sylvia ; Bouabout, Ghina Alame ; Arnoux, Alizée ; Guyonnet, Jérôme ; Becker, Guillaume ; Monassier, Laurent</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c726t-8452134f77dceacdbe80bc5b8770df0d3a3416abe9d4b3d8b5112b542f292d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Analysis</topic><topic>Animal models</topic><topic>Animal research</topic><topic>Animals</topic><topic>Atria</topic><topic>Atrial Natriuretic Factor - blood</topic><topic>Biology and Life Sciences</topic><topic>Bleeding</topic><topic>Bleeding Time</topic><topic>Blood cells</topic><topic>Blood levels</topic><topic>Blood Pressure</topic><topic>Body weight</topic><topic>Cardiology and cardiovascular system</topic><topic>Cardiovascular disease</topic><topic>Coronary vessels</topic><topic>Degeneration</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Echocardiography - methods</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Glycosaminoglycans</topic><topic>Heart Rate</topic><topic>Heart valve diseases</topic><topic>Heart valves</topic><topic>Histology</topic><topic>Human health and pathology</topic><topic>Hydroxyindoleacetic Acid - urine</topic><topic>Hypertrophy</topic><topic>Inbreeding</topic><topic>Laboratories</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitral valve</topic><topic>Mitral Valve Insufficiency - blood</topic><topic>Mitral Valve Insufficiency - diagnostic imaging</topic><topic>Mitral Valve Insufficiency - physiopathology</topic><topic>Mitral Valve Insufficiency - urine</topic><topic>mRNA</topic><topic>Myocardium</topic><topic>Pathophysiology</topic><topic>Platelet Count</topic><topic>Pulmonary arteries</topic><topic>Receptor mechanisms</topic><topic>Rheumatic heart disease</topic><topic>Serotonin</topic><topic>Serotonin - blood</topic><topic>Serotonin S2 receptors</topic><topic>Thickening</topic><topic>Transforming Growth Factor beta1 - blood</topic><topic>Transforming growth factor-b1</topic><topic>Transforming growth factors</topic><topic>Ventricle</topic><topic>Ventricular Remodeling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ayme-Dietrich, Estelle</creatorcontrib><creatorcontrib>Da Silva, Sylvia</creatorcontrib><creatorcontrib>Bouabout, Ghina Alame</creatorcontrib><creatorcontrib>Arnoux, Alizée</creatorcontrib><creatorcontrib>Guyonnet, Jérôme</creatorcontrib><creatorcontrib>Becker, Guillaume</creatorcontrib><creatorcontrib>Monassier, Laurent</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ayme-Dietrich, Estelle</au><au>Da Silva, Sylvia</au><au>Bouabout, Ghina Alame</au><au>Arnoux, Alizée</au><au>Guyonnet, Jérôme</au><au>Becker, Guillaume</au><au>Monassier, Laurent</au><au>Oury, Cécile</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of the spontaneous degenerative mitral valve disease in FVB mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2021-09-02</date><risdate>2021</risdate><volume>16</volume><issue>9</issue><spage>e0257022</spage><epage>e0257022</epage><pages>e0257022-e0257022</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The development of new non-surgical treatments dedicated to mitral valve degeneration is limited by the absence of relevant spontaneous and rapidly progressing animal experimental models.
We characterized the spontaneous mitral valve degeneration in two inbred FVB mouse strains compared to C57BL/6J and investigated a contribution of the serotonergic system.
Males and females FVB/NJ and FVB/NRj were compared to the putative C57BL/6J control at 12, 16, 20 and 24 weeks of age. Body weight, systolic blood pressure, heart rate, urinary 5-hydroxyindoleacetic acid (5-HIAA), whole blood and plasma serotonin, tail bleeding time, blood cell count, plasma TGF-β1 and plasma natriuretic peptide concentrations were measured. Myocardium and mitral valves were characterized by histology. mRNA mitral expression of 5-HT2A and 5-HT2B receptors was measured in the anterior leaflet. Cardiac anatomy and function were assessed by echocardiography.
Compared to C57BL/6J, FVB mice strains did not significantly differ regarding body weight increase, arterial blood pressure and heart rate. A progressive augmentation of plasma pro-ANP was observed in FVB mice. Nevertheless, no cardiac hypertrophy or left-ventricular fibrosis were observed. Accordingly, plasma TGF-β1 was not different among the three strains. Conversely, FVB mice demonstrated a high prevalence of fibromyxoid highly cellularized and enriched in glycosaminoglycans lesions, inducing major mitral leaflets thickening without increase in length. The increased thickness was correlated with urinary 5-HIAA and blood platelet count. Whole blood serotonin concentration was similar in the two strains but, in FVB, a reduction of plasma serotonin was observed together with an increase of the bleeding time. Finally, echocardiography identified left atrial and left ventricular remodeling associated with thickening of both mitral leaflets and mitral insufficient in 30% of FVB mice but no systolic protrusion of mitral leaflets towards the atrium.
The FVB mouse strain is highly prone to spontaneous mitral myxomatous degeneration. A contribution of the peripheral serotonergic system is suggested.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>34473777</pmid><doi>10.1371/journal.pone.0257022</doi><tpages>e0257022</tpages><orcidid>https://orcid.org/0000-0001-8341-4986</orcidid><orcidid>https://orcid.org/0000-0002-0613-3803</orcidid><orcidid>https://orcid.org/0000-0003-2710-0960</orcidid><orcidid>https://orcid.org/0000-0002-1714-0267</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2021-09, Vol.16 (9), p.e0257022-e0257022 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2568584190 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animal models Animal research Animals Atria Atrial Natriuretic Factor - blood Biology and Life Sciences Bleeding Bleeding Time Blood cells Blood levels Blood Pressure Body weight Cardiology and cardiovascular system Cardiovascular disease Coronary vessels Degeneration Disease Models, Animal Echocardiography Echocardiography - methods Female Fibrosis Gene expression Genetic aspects Glycosaminoglycans Heart Rate Heart valve diseases Heart valves Histology Human health and pathology Hydroxyindoleacetic Acid - urine Hypertrophy Inbreeding Laboratories Life Sciences Male Medicine and Health Sciences Mice Mice, Inbred C57BL Mitral valve Mitral Valve Insufficiency - blood Mitral Valve Insufficiency - diagnostic imaging Mitral Valve Insufficiency - physiopathology Mitral Valve Insufficiency - urine mRNA Myocardium Pathophysiology Platelet Count Pulmonary arteries Receptor mechanisms Rheumatic heart disease Serotonin Serotonin - blood Serotonin S2 receptors Thickening Transforming Growth Factor beta1 - blood Transforming growth factor-b1 Transforming growth factors Ventricle Ventricular Remodeling |
| title | Characterization of the spontaneous degenerative mitral valve disease in FVB mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T11%3A07%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Characterization%20of%20the%20spontaneous%20degenerative%20mitral%20valve%20disease%20in%20FVB%20mice&rft.jtitle=PloS%20one&rft.au=Ayme-Dietrich,%20Estelle&rft.date=2021-09-02&rft.volume=16&rft.issue=9&rft.spage=e0257022&rft.epage=e0257022&rft.pages=e0257022-e0257022&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0257022&rft_dat=%3Cgale_plos_%3EA674089540%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2568584190&rft_id=info:pmid/34473777&rft_galeid=A674089540&rft_doaj_id=oai_doaj_org_article_52a824897d2b417f9971833ec6db8e9c&rfr_iscdi=true |