Document Detail


DMPK dosage alterations result in atrioventricular conduction abnormalities in a mouse myotonic dystrophy model.
MedLine Citation:
PMID:  10021468     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Myotonic dystrophy (DM) is the most common form of muscular dystrophy and is caused by expansion of a CTG trinucleotide repeat on human chromosome 19. Patients with DM develop atrioventricular conduction disturbances, the principal cardiac manifestation of this disease. The etiology of the pathophysiological changes observed in DM has yet to be resolved. Haploinsufficiency of myotonic dystrophy protein kinase (DMPK), DM locus-associated homeodomain protein (DMAHP) and/or titration of RNA-binding proteins by expanded CUG sequences have been hypothesized to underlie the multi-system defects observed in DM. Using an in vivo murine electrophysiology study, we show that cardiac conduction is exquisitely sensitive to DMPK gene dosage. DMPK-/- mice develop cardiac conduction defects which include first-, second-, and third-degree atrioventricular (A-V) block. Our results demonstrate that the A-V node and the His-Purkinje regions of the conduction system are specifically compromised by DMPK loss. Importantly, DMPK+/- mice develop first-degree heart block, a conduction defect strikingly similar to that observed in DM patients. These results demonstrate that DMPK dosage is a critical element modulating cardiac conduction integrity and conclusively link haploinsufficiency of DMPK with cardiac disease in myotonic dystrophy.
Authors:
C I Berul; C T Maguire; M J Aronovitz; J Greenwood; C Miller; J Gehrmann; D Housman; M E Mendelsohn; S Reddy
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of clinical investigation     Volume:  103     ISSN:  0021-9738     ISO Abbreviation:  J. Clin. Invest.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-04-13     Completed Date:  1999-04-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7802877     Medline TA:  J Clin Invest     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  R1-7     Citation Subset:  AIM; IM    
Affiliation:
Department of Cardiology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. berul@cardio.tch.harvard.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Cholinergic Agents
Disease Models, Animal
Female
Gene Dosage*
Heart Block / genetics*,  physiopathology
Male
Mice
Mutagenesis
Myocardium / pathology
Myotonic Dystrophy / genetics*,  physiopathology
Protein-Serine-Threonine Kinases / genetics,  physiology*
Sympatholytics
Grant Support
ID/Acronym/Agency:
HL-03607/HL/NHLBI NIH HHS; HL-41484/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cholinergic Agents; 0/Sympatholytics; EC 2.7.1.-/myotonic dystrophy protein kinase; EC 2.7.11.1/Protein-Serine-Threonine Kinases
Comments/Corrections

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