Differential MicroRNA Expression Profile in Myxomatous Mitral Valve Prolapse and Fibroelastic Deficiency Valves

Autor: Juan Wang, Chin Cheng Woo, Vitaly Sorokin, Abby S.Y. Wee, Arthur Mark Richards, Edgar Lik Wui Tay, Yei Tsung Chen, Lieng H. Ling, Quek Wei Yong
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Male
Pathology
Decorin
030204 cardiovascular system & hematology
degererative mitral valve disease (DMVD)
Extracellular matrix
lcsh:Chemistry
0302 clinical medicine
Mitral valve
Mitral valve prolapse
Gene Regulatory Networks
3' Untranslated Regions
lcsh:QH301-705.5
Spectroscopy
Mitral Valve Prolapse
biology
microRNA
General Medicine
Middle Aged
fibroelastic deficiency (FED)
Computer Science Applications
Extracellular Matrix
medicine.anatomical_structure
Mitral Valve
Female
ACTA2
medicine.medical_specialty
Catalysis
Article
Inorganic Chemistry
03 medical and health sciences
ESM1
medicine
Humans
Computer Simulation
Physical and Theoretical Chemistry
Molecular Biology
Mitral regurgitation
Gene Expression Profiling
Organic Chemistry
myxomatous mitral valve prolapse (MMVP)
medicine.disease
MicroRNAs
030104 developmental biology
Gene Expression Regulation
lcsh:Biology (General)
lcsh:QD1-999
biology.protein
Desmin
Zdroj: International Journal of Molecular Sciences, Vol 17, Iss 5, p 753 (2016)
International Journal of Molecular Sciences; Volume 17; Issue 5; Pages: 753
International Journal of Molecular Sciences
ISSN: 1422-0067
Popis: Myxomatous mitral valve prolapse (MMVP) and fibroelastic deficiency (FED) are two common variants of degenerative mitral valve disease (DMVD), which is a leading cause of mitral regurgitation worldwide. While pathohistological studies have revealed differences in extracellular matrix content in MMVP and FED, the molecular mechanisms underlying these two disease entities remain to be elucidated. By using surgically removed valvular specimens from MMVP and FED patients that were categorized on the basis of echocardiographic, clinical and operative findings, a cluster of microRNAs that expressed differentially were identified. The expressions of has-miR-500, -3174, -17, -1193, -646, -1273e, -4298, -203, -505, and -939 showed significant differences between MMVP and FED after applying Bonferroni correction (p < 0.002174). The possible involvement of microRNAs in the pathogenesis of DMVD were further suggested by the presences of in silico predicted target sites on a number of genes reported to be involved in extracellular matrix homeostasis and marker genes for cellular composition of mitral valves, including decorin (DCN), aggrecan (ACAN), fibromodulin (FMOD), α actin 2 (ACTA2), extracellular matrix protein 2 (ECM2), desmin (DES), endothelial cell specific molecule 1 (ESM1), and platelet/ endothelial cell adhesion molecule 1 (PECAM1), as well as inverse correlations of selected microRNA and mRNA expression in MMVP and FED groups. Our results provide evidence that distinct molecular mechanisms underlie MMVP and FED. Moreover, the microRNAs identified may be targets for the future development of diagnostic biomarkers and therapeutics.
Databáze: OpenAIRE
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