Does 4-tert-octylphenol affect estrogen signaling pathways in bank vole Leydig cells and tumor mouse Leydig cells in vitro?

Kotula–Balak, Małgorzata; Chojnacka, Katarzyna; Hejmej, Anna; Galas, Jerzy; Satola, Monika; Bilińska, Barbara

doi:10.1016/j.reprotox.2013.03.007

Cited by 28 publications

(20 citation statements)

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“…Detection of amplification products of tested genes and the reference genes ( Actb, B2m , Rn18s, and Gapdh ) was performed with 10 ng cDNA, 0.5 μM primers, and SYBR Green master mix (Applied Biosystems) in a final volume of 20 μL as described previously (Kotula‐Balak et al ., ). Amplifications were performed as follows: 55 °C for 2 min, 94 °C for 10 min, followed by annealing temperature for 30 and 45 sec 72 °C to determine the cycle threshold (Ct) for quantitative measurement.…”

Section: Methodsmentioning

confidence: 99%

Notch signaling regulates nuclear androgen receptor AR and membrane androgen receptor ZIP9 in mouse Sertoli cells

et al. 2019

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Background Notch signaling pathway is involved in contact‐dependent communication between the cells of seminiferous epithelium, and its proper activity is important for undisturbed spermatogenesis. Objectives The aim was to assess the effect of Notch pathway inhibition on the expression of nuclear (AR) and membrane (ZIP9) androgen receptors and androgen‐regulated genes, claudin‐5 and claudin‐11, in TM4 mouse Sertoli cell line. Materials and methods DAPT (γ‐secretase inhibitor) treatment and recombination signal binding protein silencing were employed to reduce Notch signaling, whereas immobilized ligands were used to activate Notch pathway in TM4 cells. To reveal specific effect of each androgen receptor, AR or ZIP9 silencing was performed. Results Notch pathway inhibition increased the expression of AR and ZIP9 mRNA and proteins (p < 0.01; p < 0.05) in TM4 cells, whereas incubation with Notch ligands, rDLL1 or rJAG1, reduced AR (p < 0.01; p < 0.001) and ZIP9 (p < 0.05; p < 0.01) expressions, respectively. Testosterone enhanced the expression of both receptors (p < 0.05; p < 0.01). Androgen‐regulated claudin‐5 and claudin‐11 (p < 0.01; p < 0.001) and cAMP (p < 0.001) were elevated in Notch‐inhibited cells, while activation of Notch signaling by DLL1 or JAG1 reduced claudin‐11 or claudin‐5 level (p < 0.01; p < 0.001), respectively. Discussion Our findings indicate opposite effect of Notch and androgen signaling on the expression of androgen receptors in TM4 cells. We demonstrated that AR expression is regulated by DLL1‐mediated Notch signaling, whereas JAG1 is involved in the regulation of ZIP9. The expression of both claudins and cAMP production is under inhibitory influence of Notch pathway. The effects of Notch signaling on claudin‐5 and claudin‐11 expression are mediated by ZIP9 and AR, respectively. Conclusion Notch signaling may be considered as an important pathway controlling Sertoli cell physiology, and its alterations may contribute to disturbed response of Sertoli cells to androgens.

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Section: Methodsmentioning

confidence: 99%

Notch signaling regulates nuclear androgen receptor AR and membrane androgen receptor ZIP9 in mouse Sertoli cells

et al. 2019

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“…A negative RT reaction (RT enzyme was replaced by water) was performed to detect residual DNA contamination. The RT+ and RT− samples were then subjected to PCR amplification performed in a Veriti Thermal Cycler (Applied Biosystems) with a temperature-cycling program of 10 min at 25 °C, 2 h at 37 °C and 5 min at 85 °C, as described previously (Kotula-Balak et al 2013 ). Samples were kept at −20 °C until further analysis.…”

Section: Methodsmentioning

confidence: 99%

“…Detection of amplification products for ERRα, β, γ and GAPDH was performed with 10 ng cDNA, 0.5 μM primers and SYBR Green master mix (Applied Biosystems) in a final volume of 20 μL. Amplifications were performed as follows: 55 °C for 2 min, 94 °C for 10 min, followed by 40 cycles of 30 s at 62 °C and 45 s 72 °C to determine the cycle threshold (Ct) for the quantitative measurement described previously (Kotula-Balak et al 2013 ). To confirm amplification specificity, the PCR products from each primer pair were subjected to melting curve analysis and subsequent agarose gel electrophoresis.…”

Section: Methodsmentioning

confidence: 99%

“…Control and delor-treated Leydig cell culture media (100 μl) were collected for determination of sex steroid content (testosterone and estradiol, respectively) using the radioimmunological technique described elsewhere (Dufau et al 1972 ; Hotchkiss et al 1971 ; Kotula-Balak et al 2011 , 2013 ; Starowicz et al 2015 ). Testosterone levels were assessed using [1,2,6,7- 3 H]-testosterone (specific activity 110 Ci/mmol; American Radiolabeled Chemicals) as a tracer and rabbit antibody against testosterone-3-0-CMO:BSA (a gift from Dr. B. Ričařova, Institute of Radiology, Czech Academy of Sciences, Prague, Czech Republic).…”

Section: Methodsmentioning

confidence: 99%

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Chlorinated biphenyls effect on estrogen-related receptor expression, steroid secretion, mitochondria ultrastructure but not on mitochondrial membrane potential in Leydig cells

et al. 2017

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To characterize polychlorinated biphenyls (PCBs) action on Leydig cells, PCBs congeners, low-chlorinated (delor 103; d103) and high-chlorinated ones (delor 106; d106) were selected. The cells were treated according to PCBs dose (d103 or d106 0.2 ng/ml in low doses:, or 2 ng/ml in high doses) and type (d103 + d106 in low doses or 103 + 106 in high doses). After 24 h treatment with PCBs, a distinct increase in estrogen-related receptors (ERRs type α, β and γ) expression was revealed. However, the dose- and type-dependent PCBs effect was mostly exerted on ERRα expression. A similar increase in ERRs expression was demonstrated by estradiol but not testosterone, which was without an effect on ERRs. PCBs caused no decrease in the membrane potential status of Leydig cells (either in dose or type schedule) but had severe effects on the mitochondria number and structure. Moreover, PCBs markedly increased calcium (Ca2+) concentration and sex steroid secretion (both androgens and estrogens were elevated). These findings suggest a similar estrogenic action of PCBs congeners (d103 and d106) on Leydig cell function. We report dose- and type-specific effects of PCBs only on Leydig cell ERRs expression. Both delors showed common effects on the mitochondria ultrastructural and functional status. Based on our results, ERRα seems to be the most sensitive to hormonal modulation. The increases in Ca2+ and sex steroid secretion may be due to the activation of ERRs by PCBs binding and/or direct effect of PCBs on ERRs mRNA/protein expression. Nevertheless, to confirm the existence of possible relationships between ERRs signaling (including PCBs as ligands) and mitochondria function in Leydig cells, further intensive studies are needed.

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“…Drug studies using Cx46 hemichannels expressed in Xenopus oocytes are not currently available. The concentrations of endocrine disruptors used in this study were determined based on the results of the previous studies [ 28 , 29 , 30 , 31 , 32 , 33 ]. Bisphenol A (BPA) was first examined to determine whether it has the potency to affect Cx46 hemichannel currents ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Bisphenol A and 4-tert-Octylphenol Inhibit Cx46 Hemichannel Currents

2015

Korean J Physiol Pharmacol

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Connexins (Cx) are membrane proteins and monomers for forming gap junction (GJ) channels. Cx46 and Cx50 are also known to function as conductive hemichannels. As part of an ongoing effort to find GJ-specific blocker(s), endocrine disruptors were used to examine their effect on Cx46 hemichannels expressed in Xenopus oocytes. Voltage-dependent gating of Cx46 hemichannels was characterized by slowly activating outward currents and relatively fast inward tail currents. Bisphenol A (BPA, 10 nM) reduced outward currents of Cx46 hemichannels up to ~18% of control, and its effect was reversible (n=5). 4-tert-Octylphenol (OP, 1 µM) reversibly reduced outward hemichannel currents up to ~28% (n=4). However, overall shapes of Cx46 hemichannel current traces (outward and inward currents) were not changed by these drugs. These results suggest that BPA and OP are likely to occupy the pore of Cx46 hemichannels and thus obstruct the ionic fluxes. This finding provides that BPA and OP are potential candidates for GJ channel blockers.

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Does 4-tert-octylphenol affect estrogen signaling pathways in bank vole Leydig cells and tumor mouse Leydig cells in vitro?

Cited by 28 publications

References 81 publications

Notch signaling regulates nuclear androgen receptor AR and membrane androgen receptor ZIP9 in mouse Sertoli cells

Notch signaling regulates nuclear androgen receptor AR and membrane androgen receptor ZIP9 in mouse Sertoli cells

Chlorinated biphenyls effect on estrogen-related receptor expression, steroid secretion, mitochondria ultrastructure but not on mitochondrial membrane potential in Leydig cells

Bisphenol A and 4-tert-Octylphenol Inhibit Cx46 Hemichannel Currents

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