Cited by 20Asthma and respiratory diseasesEstrogen and related hormone effectsAdrenal Hormones and Disorders

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Expression of c-fos, rather than c-jun or glucocorticoid-receptor mRNA, correlates with decreased glucocorticoid response of peripheral blood mononuclear cells in asthma

Abstract

Resolution of the molecular mechanism(s) underlying glucocorticoid (GC) resistance is an important clinical problem when performing individualized GC therapy according to the GC response of peripheral cells in asthma. In order to investigate the mechanism(s) underlying the individual differences of lymphocyte GC response, we examined the relationship between lymphocyte sensitivity to GC in vitro and the expression of mRNAs for GC receptor (GR) alpha, GRbeta, c-fos and c-jun, which are reported to be implicated in the regulation of the pharmacological effects of GCs in asthma patients. Twenty-seven patients with bronchial asthma and 14 healthy subjects were included in the study. IC50s of prednisolone and methylprednisolone on blastogenesis of peripheral blood mononuclear cells (PBMCs) stimulated with concanavalin A in vitro were estimated. Transcripts for GRalpha, c-fos, c-jun and beta-actin genes in PBMCs were quantitatively determined by reverse transcription-competitive polymerase chain reaction (RT-cPCR) procedures. GRbeta mRNA expression was examined with an RT-PCR technique. A statistically significant positive correlation was observed between the IC50s for prednisolone (p <0.002) or methylprednisolone (p <0.001) and expression of c-fos mRNA in PBMCs of asthma patients (n = 27). Thus, the increased expression of c-fos mRNA correlated with the decreased responses of PBMCs to prednisolone and methylprednisolone in vitro. In contrast, the expression of GRalpha and c-jun mR…

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Crossref · 10.1016/s1567-5769(02)00083-8

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Metadata

Authors
Takahashi, E., Onda, K., Hirano, T., Oka, K., Maruoka, N., Tsuyuguchi, M., Matsumura, Y., Niitsuma, T., & Hayashi, T.
Affiliations
  • Tokyo University of Pharmacy and Life Sciences (JP)
  • Tokyo Medical University (JP)
Corresponding author
Onda, Kenji
Venue
International Immunopharmacology
Publisher
Elsevier BV
Published
2002-09
Volume
2
Issue
10
Pages
1419-1427
ISSN
1567-5769 (ISSN-L)
OpenAlex
W1996546697
Cited by
20
References
31
Citations by year
2024: 1 · 2020: 1 · 2018: 2 · 2015: 1 · 2013: 1 · 2012: 1
FWCI
0.60
Type
journal article
Language
en
Open access
closed
Locations
  • International Immunopharmacology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Education, Culture, Sports, Science and Technology (09672337)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Keywords
glucocorticoid resistance, asthma, c-fos, c-Jun, glucocorticoid receptor alpha, glucocorticoid receptor beta, peripheral blood mononuclear cells, prednisolone, methylprednisolone, glucocorticoid response, lymphocyte proliferation, concanavalin A, gene expression
MeSH terms
Adult, Aged, Aged, 80 and over, Asthma, Female, Glucocorticoids, Humans, Leukocytes, Mononuclear, Male, Middle Aged, Receptors, Glucocorticoid, RNA, Messenger, Genes, jun, Genes, fos

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