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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00363.2001
Submitted on July 31, 2001
Accepted on June 11, 2002
1 Departament de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Hospital Clinic, Barcelona, Catalonia, Spain
2 Departament de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Hospital Clinic, Barcelona, Catalonia, Spain; Departament de Medicina, Universitat de Barcelona, Servei d'Otorinolaringologia, Hospital Clinic, Barcelona, Catalonia, Spain
3 Departament de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Hospital Clinic, Barcelona, Catalonia, Spain; Departament de Medicina, Universitat de Barcelona, Servei de Pneumologia i Al.lergia Respiratoria - Institut Clinic de Pneumologia i Cirurgia Toracica, Hospital Clinic, Barcelona, Catalonia, Spain
4 Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA
* To whom correspondence should be addressed. E-mail: lpujols{at}medicina.ub.es.
Alternative splicing of the human glucocorticoid receptor (GR) primary transcript generates two protein isoforms: GR
and GRß. We investigated the expression of both GR isoforms in healthy human cells and tissues. GR mRNA abundance (x106 cDNA copies/µg total RNA) was: brain (3.83 ± 0.80) > skeletal muscle > macrophages > lung > kidney > liver > heart > eosinophils > peripheral blood mononuclear cells (PBMCs) > nasal mucosa > neutrophils > colon (0.33 ± 0.04). GRß mRNA was much less expressed than GR mRNA. Its abundance (x103 cDNA copies/µg total RNA) was: eosinophils (1.55 ± 0.58) > PBMCs > liver 
skeletal muscle > kidney > macrophages > lung > neutrophils > brain nasal mucosa > heart (0.15 ± 0.08). GRß mRNA was not found in colon. While GR protein was detected in all cells and tissues, GRß was not detected in any specimen. Our results suggest that in physiological conditions the default splicing pathway is the one leading to GR. The alternative splicing event leading to GRß is minimally activated.
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