Sequence of pig 17β-hydroxysteroid dehydrogenase Type3 cDNA and its expression in mammalian cells

Ohno, Shuji; Honda, Yoshiyuki; Nakajima, Yonako; Nakajin, Shizuo

doi:10.1016/j.jsbmb.2006.06.012

Cited by 5 publications

(3 citation statements)

References 22 publications

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“…Real‐time PCR analyses were performed using TaqMan Gene Expression Master mix and porcine‐specific TaqMan Gene Expression Assays (Applied Biosystems) for 3 β ‐HSD (Ss03391751_m1), CYP17 (Ss03394947_m1), 17 β ‐HSD1 (Ss04245957_g1) and 17 β ‐HSD3 (Custom Plus TaqMan RNA Assay based on 17 β ‐HSD3 cDNA sequence according to Ohno et al. ()) with endogenous control for glyceraldehyde‐3‐phosphate dehydrogenase (Ss03373286_u1) following manufacturer's instructions. The amplifications were performed with the StepOne ™ Real‐Time PCR System (Applied Biosystems) according to the recommended cycling program (2 min at 50°C, 10 min at 95°C, 40 cycles of 15 s at 95°C and 1 min at 60°C).…”

Section: Methodsmentioning

confidence: 99%

Altered Expression of 3β‐HSD, CYP17 and 17β‐HSD in the Foetal Porcine Gonads in Response to Anti‐androgen Flutamide Exposure

Knapczyk-Stwora

Grzesiak

Słomczyńska

2014

Reprod Domestic Animals

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We investigated whether the limited access to androgens during late prenatal period alters expression of steroidogenic enzymes involved in androgen production: 3β-hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD), cytochrome P450 17α-hydroxylase/17,20-lyase (CYP17) and 17β-hydroxysteroid dehydrogenase type 1 (17β-HSD1) or type 3 (17β-HSD3) in the foetal porcine gonads. Pregnant gilts were injected with anti-androgen flutamide (for seven days, 50 mg/day/kg bw) or corn oil (control) starting at 83 (GD90) or 101 (GD108) gestational day. To assess 3β-HSD, CYP17 and 17β-HSD1 or 17β-HSD3 expression, real-time PCR and immunohistochemistry were performed. In testes from flutamide-treated foetuses, increased 3β-HSD and CYP17 mRNA expression was observed in the GD90 group, while decreased 3β-HSD and 17β-HSD3 mRNA expression and increased CYP17 mRNA expression were found in the GD108 group. CYP17 and 17β-HSD3 were localized in Leydig cells. Following flutamide administration, the intensity of CYP17 immunostaining was higher in both treated groups, while 17β-HSD3 intensity was lower in the GD108 group. In ovaries from flutamide-treated foetuses in the GD90 group, mRNA level for 3β-HSD was elevated, but it was diminished for CYP17 and 17β-HSD1. In the GD108 group, flutamide treatment led to lower mRNA level for 3β-HSD but higher for CYP17. 3β-HSD was found in granulosa cells, while CYP17 was localized within egg nests and oocytes of forming follicles. Following flutamide treatment, the intensity of 3β-HSD and CYP17 immunostaining was higher in the GD90 and GD108 groups, respectively. Immunohistochemical staining for 3β-HSD was restricted to the ovary. Concluding, diminished androgen action in the porcine foetal gonads during late gestation induces changes in steroidogenic enzymes expression, which may led to changes in gonadal function. However, it seems that androgens exert diverse biological effects depending on the gestational period.

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Section: Methodsmentioning

confidence: 99%

Altered Expression of 3β‐HSD, CYP17 and 17β‐HSD in the Foetal Porcine Gonads in Response to Anti‐androgen Flutamide Exposure

Knapczyk-Stwora

Grzesiak

Słomczyńska

2014

Reprod Domestic Animals

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“…Recently, the pig 17b-HSD3 enzyme has been sequenced, cloned and expressed. As it has a similar substrate profile to the human enzyme and a higher amino acid homology to the human enzyme, at 82%, than that of rats and mice, microsomes from pig testicular homogenates may also have the potential to be used as a ready source of 17b-HSD3 for inhibitor studies (Ohno et al 2006).…”

Section: Inhibitors Of 17b-hsd3mentioning

confidence: 99%

Design and validation of specific inhibitors of 17 -hydroxysteroid dehydrogenases for therapeutic application in breast and prostate cancer, and in endometriosis

Day¹,

Tutill²,

Purohit³

et al. 2008

Endocrine Related Cancer

115

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Abstract17b-Hydroxysteroid dehydrogenases (17b-HSDs) are enzymes that are responsible for reduction or oxidation of hormones, fatty acids and bile acids in vivo, regulating the amount of the active form that is available to bind to its cognate receptor. All require NAD(P)(H) for activity. Fifteen 17b-HSDs have been identified to date, and with one exception, 17b-HSD type 5 (17b-HSD5), an aldo-keto reductase, they are all short-chain dehydrogenases/reductases, although overall homology between the enzymes is low. Although named as 17b-HSDs, reflecting the major redox activity at the 17b-position of the steroid, the activities of these 15 enzymes vary, with several of the 17b-HSDs able to reduce and/or oxidise multiple substrates at various positions. These activities are involved in the progression of a number of diseases, including those related to steroid metabolism. Despite the success of inhibitors of steroidogenic enzymes in the clinic, such as those of aromatase and steroid sulphatase, the development of inhibitors of 17b-HSDs is at a relatively early stage, as at present none have yet reached clinical trials. However, many groups are now working on inhibitors specific for several of these enzymes for the treatment of steroid-dependent diseases, including breast and prostate cancer, and endometriosis, with demonstrable efficacy in in vivo disease models. In this review, the recent advances in the validation of these enzymes as targets for the treatment of these diseases, with emphasis on 17b-HSD1, 3 and 5, the development of specific inhibitors, the models used for their evaluation, and their progress towards the clinic will be discussed.

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“…They also have the ketosteroid reductase function. The 3βHSDs in human are reported to have two isozymes, and 17βHSDs have nine isoforms (Ohno et al, 2006). Each of them is from a distinct gene (Payne and Hales, 2004).…”

Section: Introductionmentioning

confidence: 99%

Investigation on the transcription factors of porcine 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase genes

Dong¹,

Bai²,

Yi³

et al. 2012

Gene

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Sequence of pig 17β-hydroxysteroid dehydrogenase Type3 cDNA and its expression in mammalian cells

Cited by 5 publications

References 22 publications

Altered Expression of 3β‐HSD, CYP17 and 17β‐HSD in the Foetal Porcine Gonads in Response to Anti‐androgen Flutamide Exposure

Altered Expression of 3β‐HSD, CYP17 and 17β‐HSD in the Foetal Porcine Gonads in Response to Anti‐androgen Flutamide Exposure

Design and validation of specific inhibitors of 17 -hydroxysteroid dehydrogenases for therapeutic application in breast and prostate cancer, and in endometriosis

Investigation on the transcription factors of porcine 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase genes

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