Expression of insulin-like growth factor binding proteins during mouse cochlear development

Authors

  • Takayuki Okano,

    1. Laboratory of Cochlear Development, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland
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  • Matthew W. Kelley

    Corresponding author
    1. Laboratory of Cochlear Development, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland
    • Correspondence to: Matthew W. Kelley, 35 Convent Drive, Porter Neuroscience Research Center, Building 35, 2A-100, Bethesda, MD, 20892. E-mail: kelleymt@nidcd.nih.gov

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Abstract

Background: Insulin-like growth factor (IGF) signaling plays important roles in growth and cellular differentiation in the cochlear sensory epithelium. However, the roles of IGF binding proteins (IGFBPs), a family of IGF modulators, remain to be elucidated in this system. To begin to examine the role of IGFBPs, we used reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization to determine the temporal and spatial patterns of expression for Igfbps within the developing mouse cochlea. Results: RT-PCR analysis indicates that Igfpb2–5 are expressed in the cochlea between embryonic day (E) 13.5 and postnatal day (P) 0. In addition, the expression of each Igfbp significantly increased between E13.5 and P0. In situ hybridization indicates that Igfbp2, 3, 4, and 5 have distinct and complementary expression patterns in the developing cochlea. Moreover, expression patterns of Igfbp3 and 5 demonstrate contrasting gradients along the basal-to-apical axis of the cochlea. Conclusions: Igfbp2–5 are expressed in distinct and complementary patterns during cochlear development. These data suggest that IGFBPs may act to precisely regulate activation of IGF signaling in the developing cochlea in a cell type-specific manner, contributing to cellular patterning and differentiation in the cochlea. Developmental Dynamics 242:1210–1221, 2013. © 2013 Wiley Periodicals, Inc.

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