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The Human Brain Has Distinct Regional Expression Patterns of Estrogen Receptor α mRNA Isoforms Derived from Alternative Promoters
Author(s) -
Österlund Marie K.,
Grandien Kaj,
Keller Eva,
Hurd Yasmin L.
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0751390.x
Subject(s) - promoter , gene isoform , biology , in situ hybridization , gene expression , estrogen receptor alpha , untranslated region , estrogen receptor , forebrain , estrogen receptor beta , regulation of gene expression , messenger rna , gene , microbiology and biotechnology , genetics , neuroscience , central nervous system , cancer , breast cancer
The human estrogen receptor (ER) α gene is transcribed from multiple promoters, generating mRNA isoforms with unique 5′ ends in the untranslated region. In the present study, alternative promoters were shown to regulate the ERα gene expression in different neuronal populations of the human brain. By using in situ hybridization histochemistry, the A and B promoters, but not the C promoter, in the ERα gene were found to be active in the human forebrain. The mRNA isoform transcribed from the A promoter was expressed in low levels in most of the brain areas where ERα mRNA was present. In contrast, the B promoter mRNA isoform was more restricted, localized predominantly in high‐expressing ERα mRNA regions. The gross anatomical distribution of the different mRNA isoforms analyzed with RT‐PCR generally supported the results obtained by the in situ hybridization. Estrogen is known to modulate many different brain functions, such as neuroendocrine events associated with reproduction, mood, and cognition, likely to be mediated by different neuronal populations. Thus, the current findings of alternative ERα promoter expression in distinct neuronal populations suggest that multiple promoter usage is a possible mechanism to achieve differentiated regulation of the ERα expression, dependent on the cell phenotype and consequently the functions mediated by the specific neuron.