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Neuregulins and ErbB receptors in cultured neonatal astrocytes
Author(s) -
Francis Amy,
Raabe Timothy D.,
Wen Duanzhi,
DeVries George H.
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990815)57:4<487::aid-jnr8>3.0.co;2-w
Subject(s) - neuregulin , paracrine signalling , biology , astrocyte , autocrine signalling , gene isoform , receptor tyrosine kinase , erbb , receptor , microbiology and biotechnology , signal transduction , neuroglia , central nervous system , neuroscience , gene , biochemistry
Neuregulins (NRGs) are a family of growth factors involved in signaling between neurons and glial cells of the peripheral and central nervous system. NRGs are synthesized and secreted by a number of cell types including Schwann cells, neurons, and oligodendrocytes. NRG transduction signals are mediated by the erbB family of receptor tyrosine kinases. These NRGs may be important for paracrine or autocrine signaling during development, injury, and the normal functioning of the central nervous system. In this study, we characterize the NRGs and erbB receptors expressed by cultured neonatal rat astrocytes. Using immunoblotting protocols with pan‐specific antibodies, we identified eleven NRG molecular weight isoforms from approximately 16 kDa to 105 kDa in cultured neonatal rat astrocytes. Immunocyotchemistry with isoform‐specific antibodies revealed the expression of both major isoform families (NRGα, NRGβ). Additionally, astrocyte‐conditioned media contained two molecular weight isoforms of NRGs. We detected mRNA expression of NRGα and NRGβ in astrocytes by amplifying mRNA transcripts with reverse transcription polymerase chain reaction. Furthermore, we confirm that cultured astrocytes express all four erbB receptors as detected by immunocytochemical and immunoblotting techniques. These data indicate that astrocytes contain and secrete NRGs. J. Neurosci. Res. 57:487–494, 1999. © 1999 Wiley‐Liss, Inc.