دورية أكاديمية
أعرض في EDS

The Heparan Sulfate Proteoglycan Glypican-6 Is Upregulated in the Failing Heart, and Regulates Cardiomyocyte Growth through ERK1/2 Signaling.

التفاصيل البيبلوغرافية
العنوان: The Heparan Sulfate Proteoglycan Glypican-6 Is Upregulated in the Failing Heart, and Regulates Cardiomyocyte Growth through ERK1/2 Signaling.
المؤلفون: Melleby AO; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway., Strand ME; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway., Romaine A; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway., Herum KM; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway., Skrbic B; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway.; Department of Cardiothoracic Surgery, Oslo University Hospital, Oslo, Norway., Dahl CP; Center for Heart Failure Research, University of Oslo, Oslo, Norway.; Research Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway., Sjaastad I; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway.; Division of Molecular and Cellular Biology, Sunnybrook Research Institute and Department of Medical Biophysics, University of Toronto, Toronto, Canada., Fiane AE; Department of Cardiothoracic Surgery, Oslo University Hospital, Oslo, Norway., Filmus J; Division of Molecular and Cellular Biology, Sunnybrook Research Institute and Department of Medical Biophysics, University of Toronto, Toronto, Canada., Christensen G; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway., Lunde IG; Institute for Experimental Medical Research, Oslo University Hospital and University of Oslo, Oslo, Norway.; Center for Heart Failure Research, University of Oslo, Oslo, Norway.
المصدر: PloS one [PLoS One] 2016 Oct 21; Vol. 11 (10), pp. e0165079. Date of Electronic Publication: 2016 Oct 21 (Print Publication: 2016).
نوع المنشور: Journal Article
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: MAP Kinase Signaling System* , Up-Regulation*, Glypicans/*metabolism , Heart Failure/*metabolism , Myocytes, Cardiac/*metabolism, Animals ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; NIH 3T3 Cells ; Rats ; Rats, Wistar
مستخلص: Pressure overload is a frequent cause of heart failure. Heart failure affects millions of patients worldwide and is a major cause of morbidity and mortality. Cell surface proteoglycans are emerging as molecular players in cardiac remodeling, and increased knowledge about their regulation and function is needed for improved understanding of cardiac pathogenesis. Here we investigated glypicans (GPC1-6), a family of evolutionary conserved heparan sulfate proteoglycans anchored to the extracellular leaflet of the cell membrane, in experimental and clinical heart failure, and explored the function of glypican-6 in cardiac cells in vitro. In mice subjected to pressure overload by aortic banding (AB), we observed elevated glypican-6 levels during hypertrophic remodeling and dilated, end-stage heart failure. Consistently, glypican-6 mRNA was elevated in left ventricular myocardium from explanted hearts of patients with end-stage, dilated heart failure with reduced ejection fraction. Glypican-6 levels correlated negatively with left ventricular ejection fraction in patients, and positively with lung weight after AB in mice. Glypican-6 mRNA was expressed in both cardiac fibroblasts and cardiomyocytes, and the corresponding protein displayed different sizes in the two cell types due to tissue-specific glycanation. Importantly, adenoviral overexpression of glypican-6 in cultured cardiomyocytes increased protein synthesis and induced mRNA levels of the pro-hypertrophic signature gene ACTA1 and the hypertrophy and heart failure signature genes encoding natriuretic peptides, NPPA and NPPB. Overexpression of GPC6 induced ERK1/2 phosphorylation, and co-treatment with the ERK inhibitor U0126 attenuated the GPC6-induced increase in NPPA, NPPB and protein synthesis. In conclusion, our data suggests that glypican-6 plays a role in clinical and experimental heart failure progression by regulating cardiomyocyte growth through ERK signaling.
Competing Interests: The authors have declared that no competing interests exist.
References: J Biol Chem. 2006 Sep 15;281(37):26884-92. (PMID: 16807244)
Physiol Genomics. 2004 Feb 13;16(3):301-8. (PMID: 14625378)
Nat Genet. 1996 Mar;12(3):241-7. (PMID: 8589713)
Crit Rev Eukaryot Gene Expr. 2001;11(1-3):23-45. (PMID: 11693963)
Biochem J. 2000 Apr 1;347 Pt 1:275-84. (PMID: 10727428)
Exp Clin Cardiol. 2003 Winter;8(4):173-83. (PMID: 19649217)
Am J Hum Genet. 2009 Jun;84(6):760-70. (PMID: 19481194)
Cardiovasc Res. 2015 Apr 1;106(1):32-42. (PMID: 25694587)
Annu Rev Cell Biol. 1992;8:365-93. (PMID: 1335744)
OMICS. 2012 Mar;16(3):79-89. (PMID: 22401653)
Clinics (Sao Paulo). 2007 Aug;62(4):531-4. (PMID: 17823719)
Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):7440-5. (PMID: 23589880)
Genes Dis. 2014 Sep;1(1):87-105. (PMID: 25401122)
Circulation. 2002 Mar 26;105(12):1503-8. (PMID: 11914262)
Int J Cancer. 2003 Feb 10;103(4):455-65. (PMID: 12478660)
Matrix Biol. 2003 Apr;22(2):163-77. (PMID: 12782143)
Cardiovasc Res. 2015 May 1;106(2):217-26. (PMID: 25587045)
Dev Dyn. 2008 Nov;237(11):3200-9. (PMID: 18924235)
Cardiovasc Diabetol. 2011 Apr 25;10 :35. (PMID: 21518435)
Cancer Res. 2007 Sep 1;67(17):8149-55. (PMID: 17804727)
Cold Spring Harb Perspect Biol. 2011 Jul 01;3(7):null. (PMID: 21690215)
J Biochem. 2010 Jan;147(1):35-51. (PMID: 19762341)
J Biol Chem. 1998 Sep 4;273(36):22936-42. (PMID: 9722514)
Nat Rev Drug Discov. 2007 Feb;6(2):127-39. (PMID: 17268484)
Genome Biol. 2008;9(5):224. (PMID: 18505598)
Glycoconj J. 2006 Nov;23(7-8):555-63. (PMID: 17006646)
Am J Med Genet. 1999 Apr 23;83(5):378-81. (PMID: 10232747)
J Biol Chem. 1999 Sep 17;274(38):26968-77. (PMID: 10480909)
Am J Med Genet. 1994 Feb 1;49(3):263-5. (PMID: 8209882)
Bone. 2013 Aug;55(2):367-76. (PMID: 23624389)
Biochim Biophys Acta. 2013 Dec;1832(12):2414-24. (PMID: 24036209)
Dev Biol. 2001 Mar 1;231(1):31-46. (PMID: 11180950)
J Appl Physiol (1985). 2011 Nov;111(5):1278-89. (PMID: 21474694)
Nat Rev Cardiol. 2011 Jan;8(1):30-41. (PMID: 21060326)
J Cell Sci. 2014 Apr 1;127(Pt 7):1565-75. (PMID: 24496449)
PLoS One. 2011;6(12):e28302. (PMID: 22164265)
J Biol Chem. 2005 Dec 16;280(50):41201-6. (PMID: 16227623)
FEBS J. 2013 May;280(10):2228-47. (PMID: 23374111)
Mech Dev. 2005 Jul;122(7-8):928-38. (PMID: 15925496)
Biochem J. 2008 Mar 15;410(3):503-11. (PMID: 17967162)
J Histochem Cytochem. 2010 May;58(5):429-41. (PMID: 20124094)
Pediatr Radiol. 2004 Jan;34(1):75-82. (PMID: 14566439)
J Clin Invest. 2001 Aug;108(4):497-501. (PMID: 11518720)
Am J Med Genet. 1991 Apr 1;39(1):91-6. (PMID: 1867270)
Ann Thorac Surg. 2005 Sep;80(3):1028-32. (PMID: 16122479)
Cell Mol Life Sci. 2011 Mar;68(6):923-9. (PMID: 18087675)
Dev Biol. 2000 Sep 1;225(1):179-87. (PMID: 10964473)
Hypertension. 2013 Feb;61(2):352-60. (PMID: 23248151)
Genomics. 1999 May 1;57(3):455-8. (PMID: 10329016)
J Mol Cell Cardiol. 2015 Nov;88:133-44. (PMID: 26449522)
J Biol Chem. 2000 Dec 1;275(48):37895-901. (PMID: 10984495)
Am J Med. 2009 Nov;122(11):1023-8. (PMID: 19854330)
J Biol Chem. 2009 May 1;284(18):11806-14. (PMID: 19244235)
J Mol Cell Cardiol. 2013 Jan;54:73-81. (PMID: 23178899)
المشرفين على المادة: 0 (Glypicans)
0 (glypican 6 protein, mouse)
تواريخ الأحداث: Date Created: 20161022 Date Completed: 20170620 Latest Revision: 20181113
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5074531
DOI: 10.1371/journal.pone.0165079
PMID: 27768722
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0165079