Premium
Expression patterns of epidermal growth factor receptor and fibroblast growth factor receptor 1 mRNA in fetal human brain
Author(s) -
Fu Lijuan,
AbuKhalil Amir,
Morrison Richard S.,
Geschwind Daniel H.,
Kornblum Harley I.
Publication year - 2003
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/cne.10727
Subject(s) - biology , epidermal growth factor , subventricular zone , fibroblast growth factor , receptor , human brain , neuroscience , progenitor cell , microbiology and biotechnology , stem cell , genetics
Factors that interact with the epidermal growth factor and fibroblast growth factor receptors have numerous effects in the central nervous system (CNS), inducing the proliferation of CNS stem cells and astrocytes and the survival and differentiation of neurons. Both receptors are expressed in the embryonic rodent brain in proliferative and nonproliferative regions, suggesting roles in numerous developmental processes. However, the roles of these factors in human brain development are not known. In the current study, we examined the expression of human epidermal growth factor receptor (HEGFR) and human fibroblast growth factor receptor 1 (HFGFR1) mRNAs in the human fetal brain. The expression of both receptors is strikingly conserved relative to previously reported patterns in the rodent. In the germinal zones, the sites of cellular proliferation, HFGFR1 was expressed primarily in the ventricular zone, whereas HEGFR was expressed in the subventricular zone, suggesting different roles in CNS progenitor proliferation. Differential expression was also observed in other brain areas examined, including the hippocampus and the cerebellum. The current study suggests that HEGFR and HFGFR1 are likely to play different roles during human brain development, but that these roles will be similar to those observed in the rodent brain. J. Comp. Neurol. 462:265–273, 2003. © 2003 Wiley‐Liss, Inc.