دورية أكاديمية
أعرض في EDS

Imbalanced expression of Vcan mRNA splice form proteins alters heart morphology and cellular protein profiles.

التفاصيل البيبلوغرافية
العنوان: Imbalanced expression of Vcan mRNA splice form proteins alters heart morphology and cellular protein profiles.
المؤلفون: Burns TA; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Dours-Zimmermann MT; Institute of Surgical Pathology, University Hospital Zurich, Zurich, Switzerland., Zimmermann DR; Institute of Surgical Pathology, University Hospital Zurich, Zurich, Switzerland., Krug EL; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Comte-Walters S; Department of Cell and Molecular Pharmacology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Reyes L; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Davis MA; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Schey KL; Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, Tennessee, United States of America., Schwacke JH; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Kern CB; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America., Mjaatvedt CH; Departments of Regenerative Medicine & Cell Biology, Medical University of South Carolina, Charleston, South Carolina, United States of America.
المصدر: PloS one [PLoS One] 2014 Feb 20; Vol. 9 (2), pp. e89133. Date of Electronic Publication: 2014 Feb 20 (Print Publication: 2014).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Gene Expression Regulation*, Heart/*anatomy & histology , Myocardium/*cytology , Myocardium/*metabolism , Versicans/*genetics, Animals ; Aorta/cytology ; Aorta/pathology ; Extracellular Matrix/metabolism ; Female ; Heart Septal Defects/genetics ; Heart Septal Defects/metabolism ; Heart Septal Defects/pathology ; Heart Valves/cytology ; Heart Valves/pathology ; Mice ; Myocardium/pathology ; Pregnancy ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proteomics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Versicans/metabolism
مستخلص: The fundamental importance of the proteoglycan versican to early heart formation was clearly demonstrated by the Vcan null mouse called heart defect (hdf). Total absence of the Vcan gene halts heart development at a stage prior to the heart's pulmonary/aortic outlet segment growth. This creates a problem for determining the significance of versican's expression in the forming valve precursors and vascular wall of the pulmonary and aortic roots. This study presents data from a mouse model, Vcan ((tm1Zim)), of heart defects that results from deletion of exon 7 in the Vcan gene. Loss of exon 7 prevents expression of two of the four alternative splice forms of the Vcan gene. Mice homozygous for the exon 7 deletion survive into adulthood, however, the inability to express the V2 or V0 forms of versican results in ventricular septal defects, smaller cushions/valve leaflets with diminished myocardialization and altered pulmonary and aortic outflow tracts. We correlate these phenotypic findings with a large-scale differential protein expression profiling to identify compensatory alterations in cardiac protein expression at E13.5 post coitus that result from the absence of Vcan exon 7. The Vcan ((tm1Zim)) hearts show significant changes in the relative abundance of several cytoskeletal and muscle contraction proteins including some previously associated with heart disease. These alterations define a protein fingerprint that provides insight to the observed deficiencies in pre-valvular/septal cushion mesenchyme and the stability of the myocardial phenotype required for alignment of the outflow tract with the heart ventricles.
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معلومات مُعتمدة: C06 RR018823 United States RR NCRR NIH HHS; N01-HV-28282 United States HV NHLBI NIH HHS
المشرفين على المادة: 0 (Protein Isoforms)
0 (RNA, Messenger)
126968-45-4 (Versicans)
تواريخ الأحداث: Date Created: 20140304 Date Completed: 20150127 Latest Revision: 20211021
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3930639
DOI: 10.1371/journal.pone.0089133
PMID: 24586547
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0089133