Document Detail


Vitamin D signaling pathway plays an important role in the development of heart failure after myocardial infarction.
MedLine Citation:
PMID:  23429874     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Accumulating evidence suggests that vitamin D deficiency plays a crucial role in heart failure. However, whether vitamin D signaling itself plays an important role in cardioprotection is poorly understood. In this study, we examined the mechanism of modulating vitamin D signaling on progression to heart failure after myocardial infarction (MI) in mice. Vitamin D signaling was activated by administration of paricalcitol (PC), an activated vitamin D analog. Wild-type (WT) mice underwent sham or MI surgery and then were treated with either vehicle or PC. Compared with vehicle group, PC attenuated development of heart failure after MI associated with decreases in biomarkers, apoptosis, inflammation, and fibrosis. There was also improvement of cardiac function with PC treatment after MI. Furthermore, vitamin D receptor (VDR) mRNA and protein levels were restored by PC treatment. Next, to explore whether defective vitamin D signaling exhibited deleterious responses after MI, WT and VDR knockout (KO) mice underwent sham or MI surgery and were analyzed 4 wk after MI. VDR KO mice displayed a significant decline in survival rate and cardiac function compared with WT mice after MI. VDR KO mice also demonstrated a significant increase in heart failure biomarkers, apoptosis, inflammation, and fibrosis. Vitamin D signaling promotes cardioprotection after MI through anti-inflammatory, antifibrotic and antiapoptotic mechanisms.
Authors:
Soochan Bae; Sylvia S Singh; Hyeon Yu; Ji Yoo Lee; Byung Ryul Cho; Peter M Kang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-02-21
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  114     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2013 Apr 
Date Detail:
Created Date:  2013-04-16     Completed Date:  2013-10-17     Revised Date:  2014-04-15    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  979-87     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects
Biological Markers / metabolism
Cells, Cultured
Chemokine CCL2 / metabolism
Collagen Type I / metabolism
Collagen Type III / metabolism
Disease Models, Animal
Ergocalciferols / pharmacology*
Fibrosis
Heart Failure / etiology,  genetics,  metabolism,  pathology,  physiopathology,  prevention & control*
Inflammation Mediators / metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Infarction / complications,  drug therapy*,  genetics,  metabolism,  pathology,  physiopathology
Myocardium / metabolism*,  pathology
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Receptors, Calcitriol / agonists*,  deficiency,  genetics,  metabolism*
Recovery of Function
Signal Transduction / drug effects*
Time Factors
Tumor Necrosis Factor-alpha / metabolism
Ventricular Function, Left / drug effects
Vitamins / pharmacology*
Grant Support
ID/Acronym/Agency:
R01 HL65742/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Ccl2 protein, mouse; 0/Chemokine CCL2; 0/Collagen Type I; 0/Collagen Type III; 0/Ergocalciferols; 0/Inflammation Mediators; 0/RNA, Messenger; 0/Receptors, Calcitriol; 0/Tumor Necrosis Factor-alpha; 0/Vitamins; 0/collagen type I, alpha 1 chain; 131918-61-1/paricalcitol
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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