Hormone-induced changes in nuclear receptor stoichiometry in HL60 cells correlate with induction of monocyte or neutrophil differentiation

McTernan, P. G.; Sheppard, M. C.; Williams, Gareth R.

doi:10.1677/joe.0.1560135

Cited by 11 publications

(7 citation statements)

References 43 publications

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“…Treatment of HL60 cells with 100 nM ATRA (an RAR agonist) or 9-cis-retinoic acid (a dual RAR\RXR agonist) for 120 h provoked 70-80 % of the cells to differentiate into neutrophils, as did the specific RXR and RAR agonists AGN194204 and TTNPB respectively (100 nM) ( Figure 5A). A pan-specific RAR antagonist (AGN194310 ; 100 nM) greatly inhibited the differentiation induced by either ATRA (P 0.03) or 9-cisretinoic acid (P 0.001 ; Figure 5C), supporting previous evidence that RAR plays an essential role in HL60 neutrophil differentiation [42]. The RXR-specific antagonist AGN195393 (100 nM) slightly reduced ATRA-mediated neutrophil differentiation (P" 0.05), but inhibited neutrophil differentiation in- duced by 100 nM 9-cis-retinoic acid by " 50 % (P 0.02 ; Figure 5C).…”

Section: The Retinoid Receptors Rar and Rxr Are Involved In Atra-and supporting

confidence: 84%

“…There are two types of retinoid receptor (RAR and RXR), both of which have at least three isoforms [45], and a single VDR [46]. HL60 cells express both classes of retinoid receptor [42]. The retinoid receptors differ in their ligand specificities : RARs bind ATRA and 9-cis-retinoic acid, while RXRs bind only 9-cis-retinoic acid [45].…”

Section: Figure 9 Immunoblots and Rt-pcr Showing The Presence Of (A mentioning

confidence: 99%

“…It is thought that retinoid-induced neutrophilic differentiation of HL60 cells is driven by RXR\RAR heterodimers [42], and that VDR\RXR heterodimers mediate 1α,25(OH) # D $ -induced monocytic differentiation [19,42]. A selective RAR antagonist prevented ATRA-and 9-cis-retinoic acid-mediated differentiation and STS induction, and a specific RXR antagonist blocked STS induction in response to 9-cis-retinoic acid or 1α,25(OH) # D $ , but not to ATRA.…”

Section: Figure 9 Immunoblots and Rt-pcr Showing The Presence Of (A mentioning

confidence: 99%

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Up-regulation of steroid sulphatase activity in HL60 promyelocytic cells by retinoids and 1α,25-dihydroxyvitamin D3

Hughes

Twist

Durham

et al. 2001

Biochemical Journal

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HL60 promyeloid cells express both classes of oestrogen receptor (ERα and ERβ). We show that hydrolysis of oestrone sulphate by steroid sulphatase is a major source of oestrone in HL60 cells, and that most of the released oestrone is not metabolized further to 17β-oestradiol. Treatment of HL60 cells with retinoids or 1α,25-dihydroxyvitamin D3 increased steroid sulphatase mRNA and activity in parallel with the induction of CD11b, an early marker of myeloid differentiation that is expressed before the differentiating cells stop proliferating. Use of agonists and antagonists against retinoid receptor-α and retinoid receptor-X revealed that both classes of retinoid receptor can drive steroid sulphatase up-regulation. Steroid sulphatase activity fluctuates during the cell cycle, being highest around the transition from G1 to S phase. During the differentiation of HL60 cells induced by all-trans-retinoic acid or 1α,25-dihydroxyvitamin D3, there is increased conversion of 17β-oestradiol into oestrone by an oxidative 17β-hydroxysteroid dehydrogenase. Treatment of Caco-2 colon adenocarcinoma cells with all-trans-retinoic acid or 1α,25-dihydroxyvitamin D3 also increases 17β-oestradiol oxidation to oestrone. An increase in local oestrone production therefore occurs in multiple cell types following treatment with retinoids and 1α,25-dihydroxyvitamin D3. The possible involvement of locally produced oestrogenic steroids in regulating the proliferation and differentiation of myeloid cells is discussed.

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Section: The Retinoid Receptors Rar and Rxr Are Involved In Atra-and supporting

confidence: 84%

Section: Figure 9 Immunoblots and Rt-pcr Showing The Presence Of (A mentioning

confidence: 99%

Section: Figure 9 Immunoblots and Rt-pcr Showing The Presence Of (A mentioning

confidence: 99%

See 1 more Smart Citation

Up-regulation of steroid sulphatase activity in HL60 promyelocytic cells by retinoids and 1α,25-dihydroxyvitamin D3

Hughes

Twist

Durham

et al. 2001

Biochemical Journal

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“…Western blotting. Western blot analysis was performed using a method previously described (19). In brief, after gel electrophoresis and electroblotting, filters were incubated overnight at 4°C with continual motion, using specific primary antibodies (1:5,000 for HSL and 1:500 for LPL).…”

Section: Methodsmentioning

confidence: 99%

Insulin and Rosiglitazone Regulation of Lipolysis and Lipogenesis in Human Adipose Tissue In Vitro

et al. 2002

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Lipolysis is an important process determining fuel metabolism, and insulin regulates this process in adipose tissue. The aim of this study was to investigate the long-term effects of insulin, an insulin enhancer (rosiglitazone [RSG]), and insulin in combination with RSG on the regulation of lipolysis and lipogenesis in human abdominal subcutaneous fat. Lipolysis and lipogenesis were assessed by protein expression studies of hormone-sensitive lipase (HSL) (84 kDa) and lipoprotein lipase (LPL) (56 kDa), respectively. In addition, lipolytic rate was assessed by glycerol release assay and tumor necrosis factor (TNF)-␣ release measured by enzyme-linked immunosorbent assay (n ‫؍‬ 12). In subcutaneous adipocytes, increasing insulin doses stimulated LPL expression, with maximal stimulation at 100 nmol/l insulin (control, 1.0 ؎ 0.0 [mean ؎ SE, protein expression relative to control]; 1 nmol/l insulin, 0.87 ؎ 0.13; 100 nmol/l insulin, 1.68 ؎ 0.19; P < 0.001). In contrast, insulin at the 100 nmol/l dose reduced the expression of HSL (100 nmol/l insulin, 0.49 ؎ 0.05; P < 0.05), while no significant reduction was observed at other doses. Higher doses of insulin stimulated both HSL (1,000 nmol/l insulin, 1.4 ؎ 0.07; P < 0.01) and LPL (control 1.00 ؎ 0.0; 1,000 nmol/l insulin, 2.66 ؎ 0.27; P < 0.01) protein expression. Cotreatment with RSG induced an increased dose response to insulin for LPL and HSL (P < 0.05); RSG alone also increased LPL and HSL expression (P < 0.05). Insulin stimulated TNF-␣ secretion in a dose-dependent manner (P < 0.01); the addition of RSG (10 ؊8 mol/l) reduced TNF-␣ secretion (P < 0.05). In summary, chronic treatment of human adipocytes with insulin stimulates lipolysis and LPL protein expression. The addition of RSG reduced the lipolytic rate and TNF-␣ secretion. The increase in lipolysis is not explained by changes in HSL expression. These data, therefore, may explain in part why hyperinsulinemia coexists with increased circulating nonesterified free fatty acids and increased adiposity in obese and/or type 2 diabetic patients.

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“…23 In brief, equal amounts (20 g) of protein were loaded onto a 10% gel. After gel electrophoresis and electroblotting, filters were incubated overnight at 4°C with continual motion, with a primary antibody of 1:250 for AGT.…”

Section: Western Blottingmentioning

confidence: 99%

Insulin-Mediated Upregulation of the Renin Angiotensin System in Human Subcutaneous Adipocytes Is Reduced by Rosiglitazone

et al. 2005

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Background-Obesity-associated hypertension is likely to be due to multiple mechanisms. Identification of the renin-angiotensin system (RAS) within adipose tissue does, however, suggest a potential causal role for it in obesity-associated hypertension. Obese patients are often hyperinsulinemic, but mechanisms underlying insulin upregulation of the RAS in adipose tissue are unclear. Tumor necrosis factor-␣ (TNF-␣), an inducer of angiotensinogen in hepatocytes, is elevated in hyperinsulinemic, obese individuals and may provide a link in mediating insulin upregulation of the RAS in adipose tissue. Furthermore, thiazolidinediones lower blood pressure in vivo, and downregulation of the RAS in adipose tissue may contribute to this effect. We therefore examined the effect of rosiglitazone (RSG) on the insulin-mediated upregulation of the RAS. Methods and Results-Sera were obtained from the arterial circulation and from venous blood by draining subcutaneous abdominal adipose tissue. Isolated human abdominal subcutaneous adipocytes (nϭ12) were treated with insulin (1 to 1000 nmol/L), insulin in combination with RSG (10 nmol/L), and RSG (10 nmol/L) alone to determine angiotensinogen expression and angiotensin II, bradykinin, and TNF-␣ secretion. Subcutaneous adipocytes were also treated with TNF-␣ (10 to 100 ng/mL) to examine the direct effect on angiotensinogen expression and angiotensin II secretion. The findings showed that the arteriovenous difference in angiotensin II levels was significant (Ͼ23%; PϽ0.001). Insulin increased TNF-␣ secretion in a concentration-dependent manner (PϽ0.01), whereas RSG (10 nmol/L) significantly reduced the insulin-mediated rise in TNF-␣ (PϽ0.001), as well as angiotensin and angiotensin II. TNF-␣ also increased angiotensinogen and angiotensin II in isolated adipocytes. Conclusions-The present in vivo data suggest that human subcutaneous adipose tissue is a significant source of angiotensin II. This study also demonstrates a potential TNF-␣-mediated mechanism through which insulin may stimulate the RAS and may contribute to explain obesity-associated hypertension. RSG downregulates the RAS in subcutaneous adipose tissue, and this effect may contribute to the long-term effect of RSG on blood pressure.

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Hormone-induced changes in nuclear receptor stoichiometry in HL60 cells correlate with induction of monocyte or neutrophil differentiation

Cited by 11 publications

References 43 publications

Up-regulation of steroid sulphatase activity in HL60 promyelocytic cells by retinoids and 1α,25-dihydroxyvitamin D3

Up-regulation of steroid sulphatase activity in HL60 promyelocytic cells by retinoids and 1α,25-dihydroxyvitamin D3

Insulin and Rosiglitazone Regulation of Lipolysis and Lipogenesis in Human Adipose Tissue In Vitro

Insulin-Mediated Upregulation of the Renin Angiotensin System in Human Subcutaneous Adipocytes Is Reduced by Rosiglitazone

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