Regulation of the cholesterol ester cycle and progesterone synthesis by juvenile hormone in MA-10 Leydig tumor cells
We had previously reported that juvenile hormone III (JH III) and the JH analogue 2-(4-phenoxy phenoxy)-ethoxytetrahydropyran exert inhibitory effects on progesterone synthesis by blocking cAMP production in hCG-stimulated MA-10 Leydig tumor cells. In the present study, the effects of JH analogue up...
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1995
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| LEADER | 13084caa a22010457a 4500 | ||
|---|---|---|---|
| 001 | PAPER-19047 | ||
| 003 | AR-BaUEN | ||
| 005 | 20230518205024.0 | ||
| 008 | 190411s1995 xx ||||fo|||| 00| 0 eng|d | ||
| 024 | 7 | |2 scopus |a 2-s2.0-0028894178 | |
| 024 | 7 | |2 cas |a 20 hydroxycholesterol, 29913-75-5; 25 hydroxycholesterol, 2140-46-7; 3 decyldimethylsilyl n [2 (4 methylphenyl) 1 phenylethyl]propionamide, 78934-83-5; 3(or 17)beta hydroxysteroid dehydrogenase, 9015-81-0; aminoglutethimide, 125-84-8; bucladesine, 16980-89-5, 362-74-3; cholesterol esterase, 9026-00-0; cholesterol monooxygenase (side chain cleaving), 37292-81-2; chorionic gonadotropin, 9002-61-3; pregnenolone, 145-13-1; 2-(4-phenoxyphenoxy)ethoxytetrahydropyran; 25-hydroxycholesterol, 2140-46-7; Bucladesine, 362-74-3; Cholesterol Esterase, EC 3.1.1.13; Cholesterol Esters; Cholesterol, 57-88-5; Hydroxycholesterols; juvenile hormone III, 5255-04-9; Juvenile Hormones; Progesterone, 57-83-0; Pyrans; Sesquiterpenes | |
| 040 | |a Scopus |b spa |c AR-BaUEN |d AR-BaUEN | ||
| 030 | |a JSBBE | ||
| 100 | 1 | |a Vladusic, E.A. | |
| 245 | 1 | 0 | |a Regulation of the cholesterol ester cycle and progesterone synthesis by juvenile hormone in MA-10 Leydig tumor cells |
| 260 | |c 1995 | ||
| 270 | 1 | 0 | |m Vladusic, E.A.; Instituto de Biología y Medicina Experimental (IBYME)-CONICET Obligado 2490, Buenos Aires, 1428, Argentina |
| 506 | |2 openaire |e Política editorial | ||
| 504 | |a Vladusic, Bussmann, Visconti, Stoka, Rodriguez, Gros, Charreau, Effects of juvenile hormone on mammalian steroidogenesis (1994) J. Steroid Biochem. Molec. Biol., 50, pp. 181-187 | ||
| 504 | |a Freeman, Ascoli, Studies on the source of cholesterol used for steroid biosynthesis in cultured Leydig tumor cells (1982) J. Biol. Chem., 257, pp. 14,231-14,238 | ||
| 504 | |a Freeman, Ascoli, Desensitization of steroidogenesis in cultured Leydig tumor cells: role of cholesterol (1982) Proc. Natn. Acad. Sci. U.S.A., 79, pp. 7796-7800 | ||
| 504 | |a Freeman, Ascoli, The low-density lipoprotein pathway of cultured Leydig tumor cells (1983) Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 754, pp. 71-81 | ||
| 504 | |a Freeman, Regulation of the cholesterol ester cycle of cultured Leydig tumor cells (1987) Eur. J. Biochem., 164, pp. 351-356 | ||
| 504 | |a Freeman, Cyclic AMP mediated modification of cholesterol traffic in Leydig tumor cells (1987) J. Biol. Chem., 262, pp. 13,061-13,068 | ||
| 504 | |a Freeman, Plasma membrane cholesterol: removal and insertion into the membrane and utilization as substrate for steroidogenesis (1989) Endocrinology, 124, pp. 2527-2534 | ||
| 504 | |a Rodriguez, Gros, Stoka, Synthesis and activity of juvenile hormone analogues (JHA) (1989) Z. Naturforsch, 44 b, p. 983 | ||
| 504 | |a Ascoli, Characterization of several clonal lines of cultured Leydig tumor cells: gonadotropin receptors and steroidogenic responses (1981) Endocrinology, 108, pp. 88-95 | ||
| 504 | |a Freeman, Ascoli, Desensitization to gonadotropins in cultured Leydig tumor cells involves loss of gonadotropin receptors and decreased capacity for steroidogenesis (1981) Proc. Natn. Acad. Sci. U.S.A., 78, pp. 6309-6313 | ||
| 504 | |a Nagy, Freeeman, Cholesterol movement between the plasma membrane and the cholesteryl ester droplets of cultured Leydig tumor cells (1990) Biochem. J., 271, pp. 809-814 | ||
| 504 | |a Gocze, Freeman, A Cholesteryl ester hydrolase inhibitor blocks cholesterol translocation into the mitochondria of MA-10 Leydig tumor cells (1992) Endocrinology, 131, pp. 2972-2978 | ||
| 504 | |a Resko, Norman, Niswender, Spies, The relationship between progestins and gonadotropins during the late luteal phase of the menstrual cycle in Rhesus monkeys (1974) Endocrinology, 94, pp. 128-135 | ||
| 504 | |a Steiner, Pagliara, Chase, Kipnis, Radioimmunoassay for cyclic nucleotides (1972) J. Biol. Chem., 247, pp. 1114-1120 | ||
| 504 | |a Lowry, Rosebrough, Farr, Randall, Protein measurement with the folin phenol reagent (1951) J. Biol. Chem., 193, pp. 265-275 | ||
| 504 | |a Kim, Sah, Doong, Grodzinsky, Fluorometric assay of DNA in cartilage explants using Hoechst 33258 (1988) Anal. Biochem., 174, pp. 168-176 | ||
| 504 | |a Ross, Go, Heider, Rothblat, Selective inhibition of acyl coenzyme A: cholesterol acyltransferase by compound 58-035 (1984) J. Biol. Chem., 259, pp. 815-819 | ||
| 504 | |a Nagy, Freeman, Effect of cholesterol transport inhibitors on steroidogenesis and plasma membrane cholesterol transport in cultured MA-10 Leydig tumor cells (1990) Endocrinology, 126, pp. 2267-2276 | ||
| 504 | |a Toaff, Schleyer, Strauss, Metabolism of 25-hydroxycholesterol by rat luteal mitochondria and dispersed cells (1982) Endocrinology, 111, pp. 1785-1792 | ||
| 504 | |a Quinn, Georgion, Payne, Differences in the control of sterol metabolism between mouse and rat Leydig cells (1985) Endocrinology, 116, pp. 2300-2305 | ||
| 504 | |a Simpson, Cholesterol side-chain cleavage, cytochrome P450, and the control of steroidogenesis (1979) Molec. Cell. Endocrinol., 13, pp. 213-227 | ||
| 504 | |a Lange, Ramos, Analysis of the distribution of cholesterol in the intact cell (1983) J. Biol. Chem., 258, pp. 15,130-15,134 | ||
| 520 | 3 | |a We had previously reported that juvenile hormone III (JH III) and the JH analogue 2-(4-phenoxy phenoxy)-ethoxytetrahydropyran exert inhibitory effects on progesterone synthesis by blocking cAMP production in hCG-stimulated MA-10 Leydig tumor cells. In the present study, the effects of JH analogue upon the biosynthetic pathway of progesterone synthesis have been examined. Our results demonstrated that JH analogue inhibited progesterone production even in the presence of 20-hydroxycholesterol or 25-hydroxycholesterol. Furthermore, although JH analogue inhibited pregnenolone production in hCG-stimulated MA-10 cells the activity of the 3β-hydroxysteroid dehydrogenase (3β-HSD) was unaffected. These data suggest that JH analogue might inhibit the steroidogenic pathway in Leydig tumor cells by inhibiting the activity of the cholesterol side chain cleavage (CSCC) enzymatic complex. The JH analogue was also evaluated for inhibitory actions on cholesterol availability. An important effect of this compound was the interference with the cellular process of plasma membrane cholesterol internalization. Moreover, JH analogue inhibited not only the use of cholesterol ester for steroid biosynthesis under Bt2cAMP stimulation, but also the cholesterol ester hydrolase (CEH) activity in MA-10 Leydig tumor cells. © 1995. |l eng | |
| 536 | |a Detalles de la financiación: hydroxylatedc ompoundsn or hCG could revert the resynthesiiss lost to steroidogenesaisn d results in a inhibitory effect of the JH analogue. Both these net ester hydrolysis. The presence of JH analogue hydroxylatedc ompoundspassed though the plasma in Bt2cAMP-stimulatedce lls blocked this net ester membranea nd entered the mitochondriato become hydrolysis effect. Control experimentsw ere carried substrateso f the CSCC enzymes [19,20]T. hese out using Bt2cAMP in combination with amino-studies employedc oncentrationosf the inhibitor that gluthetimidea, CSCC inhibitor, with a similar inhibi-almost completelyb lockedsteroidogenesis. tory effect on net ester hydrolysis.T he blocking of Moreover,w ith the use of pregnenolonme etabolism steroidogenesuiss inga minogluthetimiddeid not affect inhibitors such as cyanoketone,w e determined a the increasesi n the activities of CEH and ACAT decreasei n pregnenolonep roductionin stimulated caused by BtzcAMP [5]T. o determinew hetherthe cells treatedw ith the JH analogue. inhibitory effect observedi n the presenceo f the JH These results, togethe.rw ith the previous determi-analogueis similar to the aminogluthetimideeff ect,w e nation of 3/3-HSD activity, led us to suggestt hat the determinedth e cholesteroel sterh ydrolasea ctivityof inhibitory effect could be related to an effect on intact ceils. These experimentws ere carried out using the CSCC enzymaticc omplex.In these studies,h ow-the 58-035 ACAT inhibitor, which preventsc holes-ever, a direct estimationo f CSCC activity was not terol ester resynthesis[ 17]a, nd CEH activity was performed. determined as the percentageo f cholesterol ester The availabilityo f c]holesterofol r steroidogenesis hydrolysed. The addition of both 58-035 and JH is regulatedb y several processesi,n cludingcellular analogueto Bt2 cAMP-stimulatedce llsdid not alter the uptakev ia lipoproteinre ceptorsr,e leasefr om esterified cholesteroel ster mass and decreasedC E hydrolysis storesi n lipid dropletsb y a cAMP-sensitivech olesterol to basal levels, indicating that JH analogue effects esteraset,r ansportt o mitochondriaa, nd translocation CEH activity. acrosst he outer to the inner mitochondriaml embrane [211. The proportion of cell cholesteroli n the plasma membrane,a nd the easy way in which radiolabeled cholesterocla nbe introducedse lectiveliyn tothis mem- brane, makes this molecule a strong candidatea s a plasma membranem arker[22]. In non-stimulatecde lls, most cholesteroils trans- ported to the plasma membrane where it remains indefinitelyS. teroidh ormone-synthesizicnegl ls divert cholesterolo, rdinarilyd estinedf or insertion into the membranet,o wardsthe steroid biosyntheticp athway and cause plasma membrane cholesterolt o become internalized [6].W e have found that JH analogue modifiedt he level of pH]cholesteruosl edto radiolabel the plasmam embranes,u ggestingth at the presenceo f the JH analoguea ffectedt he processd escribeda bove. Blocking of free cholesterouls agew ouldbe expectedto significantllyi mit steroidh ormones ynthesibs y MA-10 cells. Since the use of plasraam embranec holesteroal nd cholesteryel stersr equiresa functionings teroidogenic pathway, it seems likely that the inhibition of the pathway would account for the major effect of this compoundo n steroidogenesiDs.u ring the acute phase of steroidogenes(is0 --4h), cholesterosl toresprovide 73% of all suhstrate[ 5]. Cholesterol esters act as a readily available and rapidly mobilized source of cholesteroflo r steroido- genesis. Stimulation of MA-10 cells with trophic hormoneso r BtzcAMP, producesa n increasein choles- terol ester hydrolase( CEH) and ACAT activities [5]. This leads to an increasei:n the cholesteroel stercycle turnover. Thus, stimulatedce llsare able to convertc holesterol into steroidh ormonesc; onsequentlys,u bstratfeo r ester Acknowledgements--This work was supportedb y Fundaci6n Antorchaasn dC ONICET. We alsow antt o thankD r M. Ascolif or providingt he MA-10 Leydig cells and Dr B. Yamaguchif rom Sandoz,A rgentinafo r the provisiono f the ACAT inhibitor5 8035. | ||
| 593 | |a Instituto de Biología y Medicina Experimental (IBYME)-CONICET Obligado 2490, Buenos Aires, 1428, Argentina | ||
| 690 | 1 | 0 | |a 2 (4 PHENOXYPHENOXY)ETHOXYTETRAHYDROPYRAN |
| 690 | 1 | 0 | |a 20 HYDROXYCHOLESTEROL |
| 690 | 1 | 0 | |a 25 HYDROXYCHOLESTEROL |
| 690 | 1 | 0 | |a 3 DECYLDIMETHYLSILYL N [2 (4 METHYLPHENYL) 1 PHENYLETHYL]PROPIONAMIDE |
| 690 | 1 | 0 | |a 3(OR 17)BETA HYDROXYSTEROID DEHYDROGENASE |
| 690 | 1 | 0 | |a AMINOGLUTETHIMIDE |
| 690 | 1 | 0 | |a BUCLADESINE |
| 690 | 1 | 0 | |a CHOLESTEROL ESTERASE |
| 690 | 1 | 0 | |a CHOLESTEROL MONOOXYGENASE (SIDE CHAIN CLEAVING) |
| 690 | 1 | 0 | |a CHORIONIC GONADOTROPIN |
| 690 | 1 | 0 | |a ENZYME INHIBITOR |
| 690 | 1 | 0 | |a JUVENILE HORMONE DERIVATIVE |
| 690 | 1 | 0 | |a PREGNENOLONE |
| 690 | 1 | 0 | |a UNCLASSIFIED DRUG |
| 690 | 1 | 0 | |a ANIMAL CELL |
| 690 | 1 | 0 | |a ARTICLE |
| 690 | 1 | 0 | |a CHOLESTEROL TRANSPORT |
| 690 | 1 | 0 | |a CONTROLLED STUDY |
| 690 | 1 | 0 | |a ENZYME ACTIVITY |
| 690 | 1 | 0 | |a LEYDIG CELL TUMOR |
| 690 | 1 | 0 | |a MALE |
| 690 | 1 | 0 | |a NONHUMAN |
| 690 | 1 | 0 | |a PROGESTERONE SYNTHESIS |
| 690 | 1 | 0 | |a STEROIDOGENESIS |
| 690 | 1 | 0 | |a BUCLADESINE |
| 690 | 1 | 0 | |a CELL MEMBRANE |
| 690 | 1 | 0 | |a CHOLESTEROL |
| 690 | 1 | 0 | |a CHOLESTEROL ESTERASE |
| 690 | 1 | 0 | |a CHOLESTEROL ESTERS |
| 690 | 1 | 0 | |a HYDROXYCHOLESTEROLS |
| 690 | 1 | 0 | |a JUVENILE HORMONES |
| 690 | 1 | 0 | |a LEYDIG CELL TUMOR |
| 690 | 1 | 0 | |a PROGESTERONE |
| 690 | 1 | 0 | |a PYRANS |
| 690 | 1 | 0 | |a SESQUITERPENES |
| 690 | 1 | 0 | |a SUPPORT, NON-U.S. GOV'T |
| 653 | 0 | 0 | |a compound 58035, sandoz, Argentina |
| 700 | 1 | |a Pignataro, O.P. | |
| 700 | 1 | |a Bussmann, L.E. | |
| 700 | 1 | |a Charreau, E.H. | |
| 773 | 0 | |d 1995 |g v. 52 |h pp. 83-90 |k n. 1 |p J. Steroid Biochem. Mol. Biol. |x 09600760 |w (AR-BaUEN)CENRE-5799 |t Journal of Steroid Biochemistry and Molecular Biology | |
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| 856 | 4 | 0 | |u https://doi.org/10.1016/0960-0760(94)00149-G |y DOI |
| 856 | 4 | 0 | |u https://hdl.handle.net/20.500.12110/paper_09600760_v52_n1_p83_Vladusic |y Handle |
| 856 | 4 | 0 | |u https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_09600760_v52_n1_p83_Vladusic |y Registro en la Biblioteca Digital |
| 961 | |a paper_09600760_v52_n1_p83_Vladusic |b paper |c PE | ||
| 962 | |a info:eu-repo/semantics/article |a info:ar-repo/semantics/artículo |b info:eu-repo/semantics/publishedVersion | ||