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Induction of cell growth by insulin and insulin‐like growth factor‐I is associated with jun expression in the otic vesicle
Author(s) -
León Yolanda,
Sanz Carmen,
Giráldez Fernando,
VarelaNieto Isabel
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19980831)398:3<323::aid-cne2>3.0.co;2-1
Subject(s) - growth factor , insulin , biology , cell growth , microbiology and biotechnology , insulin like growth factor , inositol , vesicle , endocrinology , medicine , chemistry , receptor , biochemistry , membrane
The present report investigates the cellular mechanisms involved in the regulation of cell proliferation by insulin and insulin‐like growth factor‐I (IGF‐I) in the developing inner ear. The results show that insulin and IGF‐I stimulate cell proliferation in the otic vesicle. This effect is associated with the induction of the expression of the nuclear proto‐oncogene c‐ jun. The temporal profile of Jun expression coincided with the proliferative period of growth of the otic vesicle. IGF‐I promoted the hydrolysis of a membrane glycosyl‐phosphatidylinositol, which was characterised as the endogenous precursor for inositol phosphoglycan (IPG). Both purified IPG and a synthetic analogue, 6‐ O ‐(2‐amino‐2‐deoxy‐α‐D‐glucopyranosyl)‐D‐ myo‐ inositol‐1,2‐cyclic phosphate (C3), were able to mimic the effects of IGF‐I on Jun expression. Anti‐IPG antibodies blocked the effects of IGF‐I, which were rescued by the addition of IPG or its analogue. These results suggest that the sequence involving the hydrolysis of membrane glycolipids and the expression of c‐ jun and c‐ fos proto‐oncogenes is part of the mechanism that activates cell division in response to insulin and IGF‐I during early organogenesis of the avian inner ear. The implications of these observations for otic development and regeneration are briefly discussed. J. Comp. Neurol. 398:323–332, 1997. © 1998 Wiley‐Liss, Inc.