Open Accessmi RNA ‐940 reduction contributes to human Tetralogy of Fallot development
Author(s) -
Liang Dandan,
Xu Xinran,
Deng Fangfei,
Feng Jing,
Zhang Hong,
Liu Ying,
Zhang Yangyang,
Pan Lei,
Liu Yi,
Zhang Dasheng,
Li Jun,
Liang Xingqun,
Sun Yunfu,
Xiao Junjie,
Chen YiHan
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12309
Subject(s) - tetralogy of fallot , reduction (mathematics) , rna , medicine , cardiology , biology , heart disease , biochemistry , gene , geometry , mathematics
Tetralogy of Fallot ( TOF ) is a complex congenital heart defect and the micro RNA s regulation in TOF development is largely unknown. Herein, we explored the role of mi RNA s in TOF . Among 75 dysregulated mi RNA s identified from human heart tissues, mi RNA ‐940 was the most down‐regulated one. Interestingly, mi RNA ‐940 was most highly expressed in normal human right ventricular out‐flow tract comparing to other heart chambers. As TOF is caused by altered proliferation, migration and/or differentiation of the progenitor cells of the secondary heart field, we isolated Sca‐1 + human cardiomyocyte progenitor cells (h CMPC ) for mi RNA ‐940 function analysis. mi RNA ‐940 reduction significantly promoted h CMPC s proliferation and inhibited h CMPC s migration. We found that JARID 2 is an endogenous target regulated by mi RNA ‐940. Functional analyses showed that JARID 2 also affected h CMPC s proliferation and migration. Thus, decreased mi RNA ‐940 affects the proliferation and migration of the progenitor cells of the secondary heart field by targeting JARID 2 and potentially leads to TOF development.