Differences in Down-Regulation of Glucocorticoid Receptor mRNA by Cortisol, Prednisolone and Dexamethasone in HeLa Cells.

Shimojo, Masako; Hiroi, Naoki; Yakushiji, Fumiatsu; Ueshiba, Hajime; Yamaguchi, Nobuo; Miyachi, Yukitaka

doi:10.1507/endocrj.42.629

Cited by 32 publications

(16 citation statements)

References 26 publications

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“…This effect, which is also observed by others (Shimojo et al, 1995;Cidlowski and Cidlowski, 1981) may be assigned to the NCoR1 complex-mediated ligand-induced repression of the glucocorticoid receptor gene (Ramamoorthy and Cidlowski, 2013).…”

Section: Discussionsupporting

confidence: 78%

The triterpene echinocystic acid and its 3-O-glucoside derivative are revealed as potent and selective glucocorticoid receptor agonists

Georgatza

Gorgogietas

Kylindri

et al. 2016

The International Journal of Biochemistry & Cell Biology

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. (2016) The triterpene echinocystic acid and its 3Oglucoside derivative are revealed as potent and selective glucocorticoid receptor agonists. The International Journal of Biochemistry & Cell Biology, 79 . pp. 277287. ISSN 13572725 It is advisable to refer to the publisher's version if you intend to cite from the work.http://dx.doi.org/10. 1016/j.biocel.2016.08.028 For more information about UCLan's research in this area go to http://www.uclan.ac.uk/researchgroups/ and search for .

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Section: Discussionsupporting

confidence: 78%

The triterpene echinocystic acid and its 3-O-glucoside derivative are revealed as potent and selective glucocorticoid receptor agonists

Georgatza

Gorgogietas

Kylindri

et al. 2016

The International Journal of Biochemistry & Cell Biology

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“…Through a process of autoregulation, GCs downregulate steady‐state expression of GR in both cell lines and tissue . HeLa cells treated long term with dexamethasone showed a 50% downregulation in the level of the GR in both protein and mRNA levels . This decrease in both mRNA and protein seen previously implies that an essential component in the downregulation of GR protein lies at the level of mRNA …”

Section: Discussionmentioning

confidence: 74%

An abnormality in glucocorticoid receptor expression differentiates steroid responders from nonresponders in keloid disease

et al. 2015

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SummaryBackgroundGlucocorticoids (GCs) are first‐line treatment for keloid disease (KD) but are limited by high incidence of resistance, recurrence and undesirable side‐effects. Identifying patient responsiveness early could guide therapy.MethodsNineteen patients with KD were recruited at week 0 (before treatment) and received intralesional steroids. At weeks 0, 2 and 4, noninvasive imaging and biopsies were performed. Responsiveness was determined by clinical response and a significant reduction in vascular perfusion following steroid treatment, using full‐field laser perfusion imaging (FLPI). Responsiveness was also evaluated using (i) spectrophotometric intracutaneous analysis to quantify changes in collagen and melanin and (ii) histology to identify changes in epidermal thickness and glycosaminoglycan (GAG) expression. Biopsies were used to quantify changes in glucocorticoid receptor (GR) expression using quantitative reverse transcriptase polymerase chain reaction, immunoblotting and immunohistochemistry.ResultsAt week 2, the FLPI was used to separate patients into steroid responsive (n = 12) and nonresponsive groups (n = 7). All patients demonstrated a significant decrease in GAG at week 2 (P < 0·05). At week 4, responsive patients exhibited significant reduction in melanin, GAG, epidermal thickness (all P < 0·05) and a continued reduction in perfusion (P < 0·001) compared with nonresponders. Steroid‐responsive patients had increased GR expression at baseline and showed autoregulation of GR compared with nonresponders, who showed no change in GR transcription or protein.ConclusionsThis is the first demonstration that keloid response to steroids can be measured objectively using noninvasive imaging. FLPI is a potentially reliable tool to stratify KD responsiveness. Altered GR expression may be the mechanism gating therapeutic response.

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“…In non-lymphoid cell lines and in peripheral blood mononuclear cells of children with auto-immune disorders, with no apoptotic response upon GC exposure, a decrease in GR mRNA expression and receptor number was observed after exposure to GC. [32][33][34][35][36][37] Contrary to the down-regulation in those non-lymphoid cell lines, up-regulation of the GR upon GC exposure is reported in leukemic and lymphoid cell lines. In the leukemic T cell line, CCRF-CEM, an up-regulation of GR mRNA was shown in the first few hours after exposure to GC.…”

Section: Number Of Glucocorticoid Receptorsmentioning

confidence: 90%

“…Another important target gene, known to be up-regulated in a leukemic cell line but down-regulated in cells not undergoing apoptosis after GC exposure is the GR gene itself. 29,[32][33][34]36,39 The relationship between the potency to upregulate the GR number and sensitivity to GC in ALL is currently the subject of study in different laboratories.…”

Section: Genes Regulated By Gcmentioning

confidence: 99%

Molecular determinants of glucocorticoid sensitivity and resistance in acute lymphoblastic leukemia

et al. 2003

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Glucocorticoids (GC) are probably the most important drugs in the treatment of ALL. Despite the extensive use of GC for many years, little is known about the molecular mechanisms of sensitivity and resistance. This review summarizes the knowledge on GC cytotoxicity in leukemia. The relevance of polymorphisms, splice variants and the number and regulation of the GC receptor are discussed. The role of multidrug resistance proteins, glutathione and glutathione S-transferase is evaluated, as well as the influence of the different heat-shock chaperone (hsp 90 and 70) and co-chaperone proteins (BAG-1 and others) which form a complex together with the GC receptor. Finally, the transactivation and transrepression (via NF-kappa B and AP-1 binding) of a wide range of genes (like c-myc) which initiates the final apoptosis pathway are discussed and suggestions for future directions of research in ALL patients are given.

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Differences in Down-Regulation of Glucocorticoid Receptor mRNA by Cortisol, Prednisolone and Dexamethasone in HeLa Cells.

Cited by 32 publications

References 26 publications

The triterpene echinocystic acid and its 3-O-glucoside derivative are revealed as potent and selective glucocorticoid receptor agonists

The triterpene echinocystic acid and its 3-O-glucoside derivative are revealed as potent and selective glucocorticoid receptor agonists

An abnormality in glucocorticoid receptor expression differentiates steroid responders from nonresponders in keloid disease

Molecular determinants of glucocorticoid sensitivity and resistance in acute lymphoblastic leukemia

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