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High‐affinity folate receptor in cardiac neural crest migration: A gene knockdown model using siRNA
Author(s) -
Rosenquist Thomas H.,
Chaudoin Tammy,
Finnell Richard H.,
Bennett Gregory D.
Publication year - 2010
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22270
Subject(s) - neural crest , biology , neural tube , gene knockdown , small interfering rna , microbiology and biotechnology , mitosis , receptor , heart development , immunolabeling , cell , medicine , andrology , rna , embryo , gene , immunology , genetics , immunohistochemistry , embryonic stem cell
Folate supplementation reduces the incidence of congenital heart defects, but the nature of this protective mechanism remains unclear. Immunolabeling demonstrated that the neural tube and neural crest (NC) cells were rich in the high‐affinity folate receptor FOLR1and during the early stages of development FOLR1 was found principally in these cells. Suppression of Folr1 expression in the nascent cardiac NC by site‐directed short‐interfering RNA (siRNA) altered cardiac NC cell mitosis and subsequent migration patterns leading to abnormal development of the pharyngeal arch arteries (PAA) and outflow tract. qPCR analysis demonstrated that the siRNA treatment significantly reduced Folr1 24 hr after treatment. These treatments also significantly reduced mitosis in the neural tube, but adjacent, nontreated areas were unaffected. In summary, a brief reduction in the expression of Folr1 during a critical stage of NC development had long‐term consequences for the development of the PAA and outflow tract. Developmental Dynamics 239:1136–1144, 2010. © 2010 Wiley‐Liss, Inc.