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Increased Exposure to Estrogens Disturbs Maturation, Steroidogenesis, and Cholesterol Homeostasis via Estrogen Receptor α in Adult Mouse Leydig Cells

Deteriorated male reproductive health has been connected to overexposure to estrogens or to imbalanced androgen-estrogen ratio. Transgenic male mice expressing human aromatase (AROM+ mice) serve as an apt model for the study of the consequences of an altered androgen-estrogen ratio. Our previous stu... Full description

Journal Title: ENDOCRINOLOGY 2009-06, Vol.150 (6), p.2865-2872
Main Author: Strauss, Leena
Other Authors: Kallio, Jenny , Desai, Nimisha , Pakarinen, Pirjo , Miettinen, Tatu , Gylling, Helena , Albrecht, Martin , Mäkelä, Sari , Mayerhofer, Artur , Poutanen, Matti
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Chevy Chase, MD: Endocrine Society
ID: ISSN: 0013-7227
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title: Increased Exposure to Estrogens Disturbs Maturation, Steroidogenesis, and Cholesterol Homeostasis via Estrogen Receptor α in Adult Mouse Leydig Cells
format: Article
creator:
  • Strauss, Leena
  • Kallio, Jenny
  • Desai, Nimisha
  • Pakarinen, Pirjo
  • Miettinen, Tatu
  • Gylling, Helena
  • Albrecht, Martin
  • Mäkelä, Sari
  • Mayerhofer, Artur
  • Poutanen, Matti
subjects:
  • Abridged Index Medicus
  • Animals
  • Aromatase - genetics
  • Aromatase - metabolism
  • Biological and medical sciences
  • Cholesterol - metabolism
  • Estradiol Dehydrogenases - metabolism
  • Estrogen Receptor alpha - genetics
  • Estrogen Receptor alpha - metabolism
  • Estrogen Receptor beta - genetics
  • Estrogen Receptor beta - metabolism
  • Estrogens - metabolism
  • Estrogens - pharmacology
  • Follicle Stimulating Hormone - blood
  • Fundamental and applied biological sciences. Psychology
  • Homeostasis - drug effects
  • Homeostasis - physiology
  • Leydig Cells - drug effects
  • Leydig Cells - metabolism
  • Luteinizing Hormone - blood
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Models, Animal
  • Phosphoproteins - metabolism
  • Sexual Maturation - drug effects
  • Sexual Maturation - physiology
  • Steroid 17-alpha-Hydroxylase - metabolism
  • Steroids - metabolism
  • Testosterone - metabolism
  • Vertebrates: endocrinology
ispartof: ENDOCRINOLOGY, 2009-06, Vol.150 (6), p.2865-2872
description: Deteriorated male reproductive health has been connected to overexposure to estrogens or to imbalanced androgen-estrogen ratio. Transgenic male mice expressing human aromatase (AROM+ mice) serve as an apt model for the study of the consequences of an altered androgen-estrogen ratio. Our previous studies with AROM+ mice showed that low androgen levels together with high estrogen levels result in cryptorchidism and infertility. In the present study, the AROM+ mice were shown to have severe abnormalities in the structure and function of Leydig cells before the appearance of spermatogenic failure. Decreased expression of adult-type Leydig cell markers (Ptgds, Vcam1, Insl3, Klk21, -24 and -27, Star, Cyp17a1, and Hsd17b3) indicated an immature developmental stage of the Leydig cells, which appears to be the first estrogen-dependent alteration. Genes involved in steroidogenesis (Star, Cyp17a1, and Hsd17b3) were suppressed despite normal LH levels. The low expression level of kallikreins 21, 24, and 27 potentially further inhibited Leydig cell function via remodeling extracellular matrix composition. In connection with disrupted steroidogenesis, Leydig cells showed enlarged mitochondria, a reduced amount of smooth endoplasmic reticulum, and an accumulation of cholesterol and precursors for cholesterol synthesis. The results of studies with AROM+ mice crossed with estrogen receptor α or β (ERα and ERβ, respectively) knockout mice lead to the conclusion that the structural and functional disorders caused by estrogen exposure were mediated via ERα, whereas ERβ was not involved. Imbalance in androgen-estrogen ratio has several effects on Leydig cell structure and function.
language: eng
source:
identifier: ISSN: 0013-7227
fulltext: no_fulltext
issn:
  • 0013-7227
  • 1945-7170
url: Link


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titleIncreased Exposure to Estrogens Disturbs Maturation, Steroidogenesis, and Cholesterol Homeostasis via Estrogen Receptor α in Adult Mouse Leydig Cells
creatorStrauss, Leena ; Kallio, Jenny ; Desai, Nimisha ; Pakarinen, Pirjo ; Miettinen, Tatu ; Gylling, Helena ; Albrecht, Martin ; Mäkelä, Sari ; Mayerhofer, Artur ; Poutanen, Matti
creatorcontribStrauss, Leena ; Kallio, Jenny ; Desai, Nimisha ; Pakarinen, Pirjo ; Miettinen, Tatu ; Gylling, Helena ; Albrecht, Martin ; Mäkelä, Sari ; Mayerhofer, Artur ; Poutanen, Matti
descriptionDeteriorated male reproductive health has been connected to overexposure to estrogens or to imbalanced androgen-estrogen ratio. Transgenic male mice expressing human aromatase (AROM+ mice) serve as an apt model for the study of the consequences of an altered androgen-estrogen ratio. Our previous studies with AROM+ mice showed that low androgen levels together with high estrogen levels result in cryptorchidism and infertility. In the present study, the AROM+ mice were shown to have severe abnormalities in the structure and function of Leydig cells before the appearance of spermatogenic failure. Decreased expression of adult-type Leydig cell markers (Ptgds, Vcam1, Insl3, Klk21, -24 and -27, Star, Cyp17a1, and Hsd17b3) indicated an immature developmental stage of the Leydig cells, which appears to be the first estrogen-dependent alteration. Genes involved in steroidogenesis (Star, Cyp17a1, and Hsd17b3) were suppressed despite normal LH levels. The low expression level of kallikreins 21, 24, and 27 potentially further inhibited Leydig cell function via remodeling extracellular matrix composition. In connection with disrupted steroidogenesis, Leydig cells showed enlarged mitochondria, a reduced amount of smooth endoplasmic reticulum, and an accumulation of cholesterol and precursors for cholesterol synthesis. The results of studies with AROM+ mice crossed with estrogen receptor α or β (ERα and ERβ, respectively) knockout mice lead to the conclusion that the structural and functional disorders caused by estrogen exposure were mediated via ERα, whereas ERβ was not involved. Imbalance in androgen-estrogen ratio has several effects on Leydig cell structure and function.
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subjectAbridged Index Medicus ; Animals ; Aromatase - genetics ; Aromatase - metabolism ; Biological and medical sciences ; Cholesterol - metabolism ; Estradiol Dehydrogenases - metabolism ; Estrogen Receptor alpha - genetics ; Estrogen Receptor alpha - metabolism ; Estrogen Receptor beta - genetics ; Estrogen Receptor beta - metabolism ; Estrogens - metabolism ; Estrogens - pharmacology ; Follicle Stimulating Hormone - blood ; Fundamental and applied biological sciences. Psychology ; Homeostasis - drug effects ; Homeostasis - physiology ; Leydig Cells - drug effects ; Leydig Cells - metabolism ; Luteinizing Hormone - blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Models, Animal ; Phosphoproteins - metabolism ; Sexual Maturation - drug effects ; Sexual Maturation - physiology ; Steroid 17-alpha-Hydroxylase - metabolism ; Steroids - metabolism ; Testosterone - metabolism ; Vertebrates: endocrinology
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1Kallio, Jenny
2Desai, Nimisha
3Pakarinen, Pirjo
4Miettinen, Tatu
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6Albrecht, Martin
7Mäkelä, Sari
8Mayerhofer, Artur
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1ENDOCRINOLOGY
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descriptionDeteriorated male reproductive health has been connected to overexposure to estrogens or to imbalanced androgen-estrogen ratio. Transgenic male mice expressing human aromatase (AROM+ mice) serve as an apt model for the study of the consequences of an altered androgen-estrogen ratio. Our previous studies with AROM+ mice showed that low androgen levels together with high estrogen levels result in cryptorchidism and infertility. In the present study, the AROM+ mice were shown to have severe abnormalities in the structure and function of Leydig cells before the appearance of spermatogenic failure. Decreased expression of adult-type Leydig cell markers (Ptgds, Vcam1, Insl3, Klk21, -24 and -27, Star, Cyp17a1, and Hsd17b3) indicated an immature developmental stage of the Leydig cells, which appears to be the first estrogen-dependent alteration. Genes involved in steroidogenesis (Star, Cyp17a1, and Hsd17b3) were suppressed despite normal LH levels. The low expression level of kallikreins 21, 24, and 27 potentially further inhibited Leydig cell function via remodeling extracellular matrix composition. In connection with disrupted steroidogenesis, Leydig cells showed enlarged mitochondria, a reduced amount of smooth endoplasmic reticulum, and an accumulation of cholesterol and precursors for cholesterol synthesis. The results of studies with AROM+ mice crossed with estrogen receptor α or β (ERα and ERβ, respectively) knockout mice lead to the conclusion that the structural and functional disorders caused by estrogen exposure were mediated via ERα, whereas ERβ was not involved. Imbalance in androgen-estrogen ratio has several effects on Leydig cell structure and function.
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0Abridged Index Medicus
1Animals
2Aromatase - genetics
3Aromatase - metabolism
4Biological and medical sciences
5Cholesterol - metabolism
6Estradiol Dehydrogenases - metabolism
7Estrogen Receptor alpha - genetics
8Estrogen Receptor alpha - metabolism
9Estrogen Receptor beta - genetics
10Estrogen Receptor beta - metabolism
11Estrogens - metabolism
12Estrogens - pharmacology
13Follicle Stimulating Hormone - blood
14Fundamental and applied biological sciences. Psychology
15Homeostasis - drug effects
16Homeostasis - physiology
17Leydig Cells - drug effects
18Leydig Cells - metabolism
19Luteinizing Hormone - blood
20Male
21Mice
22Mice, Inbred C57BL
23Mice, Knockout
24Mice, Transgenic
25Models, Animal
26Phosphoproteins - metabolism
27Sexual Maturation - drug effects
28Sexual Maturation - physiology
29Steroid 17-alpha-Hydroxylase - metabolism
30Steroids - metabolism
31Testosterone - metabolism
32Vertebrates: endocrinology
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5Gylling, Helena
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8Mayerhofer, Artur
9Poutanen, Matti
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titleIncreased Exposure to Estrogens Disturbs Maturation, Steroidogenesis, and Cholesterol Homeostasis via Estrogen Receptor α in Adult Mouse Leydig Cells
authorStrauss, Leena ; Kallio, Jenny ; Desai, Nimisha ; Pakarinen, Pirjo ; Miettinen, Tatu ; Gylling, Helena ; Albrecht, Martin ; Mäkelä, Sari ; Mayerhofer, Artur ; Poutanen, Matti
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1Animals
2Aromatase - genetics
3Aromatase - metabolism
4Biological and medical sciences
5Cholesterol - metabolism
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7Estrogen Receptor alpha - genetics
8Estrogen Receptor alpha - metabolism
9Estrogen Receptor beta - genetics
10Estrogen Receptor beta - metabolism
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12Estrogens - pharmacology
13Follicle Stimulating Hormone - blood
14Fundamental and applied biological sciences. Psychology
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18Leydig Cells - metabolism
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21Mice
22Mice, Inbred C57BL
23Mice, Knockout
24Mice, Transgenic
25Models, Animal
26Phosphoproteins - metabolism
27Sexual Maturation - drug effects
28Sexual Maturation - physiology
29Steroid 17-alpha-Hydroxylase - metabolism
30Steroids - metabolism
31Testosterone - metabolism
32Vertebrates: endocrinology
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5Gylling, Helena
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abstractDeteriorated male reproductive health has been connected to overexposure to estrogens or to imbalanced androgen-estrogen ratio. Transgenic male mice expressing human aromatase (AROM+ mice) serve as an apt model for the study of the consequences of an altered androgen-estrogen ratio. Our previous studies with AROM+ mice showed that low androgen levels together with high estrogen levels result in cryptorchidism and infertility. In the present study, the AROM+ mice were shown to have severe abnormalities in the structure and function of Leydig cells before the appearance of spermatogenic failure. Decreased expression of adult-type Leydig cell markers (Ptgds, Vcam1, Insl3, Klk21, -24 and -27, Star, Cyp17a1, and Hsd17b3) indicated an immature developmental stage of the Leydig cells, which appears to be the first estrogen-dependent alteration. Genes involved in steroidogenesis (Star, Cyp17a1, and Hsd17b3) were suppressed despite normal LH levels. The low expression level of kallikreins 21, 24, and 27 potentially further inhibited Leydig cell function via remodeling extracellular matrix composition. In connection with disrupted steroidogenesis, Leydig cells showed enlarged mitochondria, a reduced amount of smooth endoplasmic reticulum, and an accumulation of cholesterol and precursors for cholesterol synthesis. The results of studies with AROM+ mice crossed with estrogen receptor α or β (ERα and ERβ, respectively) knockout mice lead to the conclusion that the structural and functional disorders caused by estrogen exposure were mediated via ERα, whereas ERβ was not involved. Imbalance in androgen-estrogen ratio has several effects on Leydig cell structure and function.
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pmid19196801
doi10.1210/en.2008-1311
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