Expression of glucocorticoid receptor α- and β-isoforms in human cells and tissues

American Journal of Physiology - Cell Physiology - Tập 283 Số 4 - Trang C1324-C1331 - 2002
Laura Pujols1, Joaquim Mullol1,2, Jordi Roca‐Ferrer1, Alfons Torrego1,3, Antoni Xaubet1,3, John A. Cidlowski4, César Picado1,3
1Institut d'Investigacions Biomèdiques August Pi i Sunyer,
2Servei d'Otorinolaringologia, and
3Servei de Pneumologia i Al.lèrgia Respiratòria-Institut Clı́nic de Pneumologia i Cirurgia Toràcica, Hospital Clı́nic, Departament de Medicina, Universitat de Barcelona, 08036 Barcelona, Spain; and
4Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, 27709

Tóm tắt

Alternative splicing of the human glucocorticoid receptor (GR) primary transcript generates two protein isoforms: GR-α and GR-β. We investigated the expression of both GR isoforms in healthy human cells and tissues. GR-α mRNA abundance (×106 cDNA copies/μg total RNA) was as follows: 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). GR-β mRNA was much less expressed than GR-α mRNA. Its abundance (×103 cDNA copies/μg total RNA) was as follows: eosinophils (1.55 ± 0.58) > PBMCs > liver ≥ skeletal muscle > kidney > macrophages > lung > neutrophils > brain ≥ nasal mucosa > heart (0.15 ± 0.08). GR-β mRNA was not found in colon. While GR-α protein was detected in all cells and tissues, GR-β was not detected in any specimen. Our results suggest that, in physiological conditions, the default splicing pathway is the one leading to GR-α. The alternative splicing event leading to GR-β is minimally activated.

Từ khóa


Tài liệu tham khảo

10.1164/ajrccm.154.3.8810618

10.1172/JCI117943

10.1210/edrv-17-3-245

10.1016/0092-8674(95)90201-5

10.1016/S0303-7207(99)00156-2

10.1164/ajrccm/154.2_Pt_2.S28

10.1016/0303-7207(92)90187-B

10.1016/S0300-2896(15)30534-2

10.1067/mai.2000.109054

Dahia PLM, 1997, J Clin Endocrinol Metab, 82, 1088

10.1016/S0165-5728(00)00297-6

10.1007/BF03401643

10.1210/edrv.19.3.0331

10.1016/S0303-7207(99)00072-6

10.1016/S0968-0004(98)01212-2

10.1016/S0021-9258(20)89627-6

10.1126/science.3283939

10.1164/ajrccm.162.1.9911032

10.1016/0303-7207(84)90089-3

10.1164/ajrccm.159.5.9804131

10.1067/mai.2001.116428

10.1074/jbc.272.42.26659

10.1038/318635a0

10.1016/S0016-5085(00)70172-7

10.1016/S0092-8674(00)81177-0

Kayes-Wandover KM, 2000, J Clin Endocrinol Metab, 85, 2519

10.1016/S0091-6749(96)70311-1

10.1084/jem.186.9.1567

10.1002/(SICI)1097-4598(199710)20:10<1318::AID-MUS17>3.0.CO;2-Z

10.1006/cimm.1998.1293

10.1111/j.1476-5381.1994.tb17093.x

10.1074/jbc.274.39.27857

10.1074/jbc.271.16.9550

10.1016/S0039-128X(99)00059-8

10.1210/endo.138.11.5501

10.1016/0300-9084(91)90074-B

Ozaki T, 1982, Clin Exp Immunol, 47, 505

10.1007/BF00734576

10.1016/0091-6749(81)90186-X

10.1165/ajrcmb.24.1.4024

10.1016/S0303-7207(98)00208-1

Schleimer RP., 1990, Am Rev Respir Dis, 141, S59

10.1152/ajpcell.1994.266.3.C729

10.1006/bbrc.1998.9980

10.1016/S0968-0004(00)01604-2

10.1067/mai.2000.106486

10.1084/jem.193.5.585

10.1046/j.1468-1331.1999.640469.x

10.1016/S0304-3940(00)01325-2

10.1016/S0039-128X(00)00205-1

10.1073/pnas.121455098

10.1111/j.1365-2222.1994.tb00240.x