The Experts below are selected from a list of 261 Experts worldwide ranked by ideXlab platform
Matsuto Mochizuki - One of the best experts on this subject based on the ideXlab platform.
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Immunohistochemical evidence for the presence of tumor necrosis factor-alpha in the infant and adult human ovary.
Endocrine journal, 1995Co-Authors: Hitoshi Kondo, Takeshi Maruo, Matsuto MochizukiAbstract:The cytologic localization and cellular levels of tumor necrosis factor-α (TNFα) in the human ovary during follicular growth and regression were examined by the avidin/biotin immunoperoxidase method with a specific antibody to human recombinant TNFα. In the infant ovary, TNFα immunostaining was present only in the oocyte within the primordial follicles. TNFα immunostaining was also present within the oocyte in primordial follicles of the adult ovary. Positive immunostaining for TNFα in granulosa cells became apparent in preantral follicles, while that in theca interna cells began to appear at the antral follicle stage. The staining intensity of the oocyte increased as the oocyte reached the preovulatory stage. The intensity of immunostaining for TNFα in the granulosa and thecal cells increased as the follicle became larger and matured. In corpora lutea, the immunostaining for TNFα persisted in the granulosa lutein and theca lutein cells and intensified in the mid luteal phase. In the regressing corpora lutea, TNFct immunostaining in the luteal cells decreased as the regression advanced. Regressed corpora lutea with a central core of scar tissue were bordered by macrophage-like cells which exhibited intense immunostaining for TNFα. In the cortex region, the Corpus Albicans was negative for TNFα immunostaining, whereas macrophage-like cells peripheral to the Corpus Albicans exhibited intense immunostaining for TNFα. In the medullary region, the Corpus Albicans and surrounding stromal cells were totally negative for TNFα. By contrast, in the early atretic stage, the degenerating oocyte showed weak immunostaining for TNFα, while the granulosa and theca interna cells showed moderate immunostaining for TNFα. In the late atretic stage, the immunostaining for TNFα in the scattered granulosa cells became negligible, whereas the theca interna cells showed intense immunostaining for TNFα. The results obtained indicate that the oocyte is the primary intrafollicular site of TNFα localization within the ovary and that TNFα may participate in regulating follicular growth, regression and aresia.
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Expression of transforming growth factor-alpha in the human ovary during follicular growth, regression and atresia.
Endocrine journal, 1994Co-Authors: Takeshi Maruo, Hitoshi Kondo, Cecilia A. Ladines-llave, Takashi Samoto, Matsuto MochizukiAbstract:The cytologic localization and cellular levels of TGF alpha in the human ovary during follicular growth and regression were examined by avidin/biotin immunoperoxidase techniques with a monoclonal antibody to TGF alpha. In primordial follicles, only the oocyte showed intense immunostaining for TGF alpha, whereas the flattened pregranulosa cells were negative for the immunostaining. The earliest stage of follicular growth at which immunostaining for TGF alpha in granulosa cells and theca interna cells became apparent was the preantral stage. With the increase in the size of follicles, the intensity of TGF alpha immunostaining in the oocyte decreased, whereas the staining intensity of the granulosa and theca cells increased. The immunostaining for TGF alpha in granulosa and theca interna cells persisted in the Corpus luteum, and further intensified during the midluteal phase. In the regressing Corpus luteum, the immunostaining was present only in the peripheral theca lutein cells adjacent to the central scar tissue. The Corpus Albicans was negative for the immunostaining. Stromal cells exhibited weak staining for TGF alpha. In atretic follicles, the theca interna cells exhibited intense staining for TGF alpha without appreciable staining in the scattered granulosa cells. This is the first report to demonstrate that TGF alpha expression in the oocyte is maximal in primordial follicles, whereas TGF alpha expression in granulosa and theca cells increases with the progress of follicles and reaches its maximum in the lutein cells during the mid luteal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
Yukihiro Hasegawa - One of the best experts on this subject based on the ideXlab platform.
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Ovarian histological findings in an adult patient with the steroidogenic acute regulatory protein (StAR) deficiency reveal the impairment of steroidogenesis by lipoid deposition.
Endocrine journal, 2008Co-Authors: Uiko Kaku, Hironobu Sasano, Takashi Suzuki, Kaori Kameyama, Masako Izawa, Makoto Yamada, Junko Miyamoto, Yukihiro HasegawaAbstract:Context: The steroidogenic acute regulatory protein (StAR) is essential for the production of steroid hormones. The mutations in the StAR gene typically cause congenital lipoid adrenal hyperplasia (lipoid CAH), characterized by severe adrenal insufficiency in both sexes and complete female external genitalia in genetic males. Affected 46, XX females feminize at puberty and menstruate but have progressive hypergonadotropic hypogonadism. It has been hypothesized that the cholesterol accumulation in the steroidogenic cells destroys the residual steroidogenic capacity and progressive ovarian failure occurs (two-hit model). Additionally, ovulation and luteinization in the patients is supposed to be impaired. However, those hypotheses have not been confirmed histologically. Objective: We examined whether pathological findings of the ovary in a patient of lipoid CAH corresponded with two-hit model, and whether ovulation and luteinization occurred or not in the patient. Subject: The ovary in an adult 46, XX female with a homozygous nonsense mutation (Q258X) in the StAR gene was examined. When the patient was age 22 yr, the ovary was resected because of enlargement with polycysts and subsequent torsion. Result: The affected ovary demonstrated remarkable lipoid deposition and changes of the mitochondrial ultrastructure. Immunohistochemical examination showed decrease of steroidogenic enzymes such as P450 cholesterol side-chain cleavage (P450scc). Additionally, we detected Corpus Albicans in the affected ovary. Conclusion: This is the first detailed report on ovarian histology in an adult 46, XX female with a null type mutation of the StAR gene (Q258X), which indicates the evidence of the impairment of ovarian StAR-independent steroidogenesis by lipoid deposition.
Takashi Suzuki - One of the best experts on this subject based on the ideXlab platform.
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Ovarian histological findings in an adult patient with the steroidogenic acute regulatory protein (StAR) deficiency reveal the impairment of steroidogenesis by lipoid deposition.
Endocrine journal, 2008Co-Authors: Uiko Kaku, Hironobu Sasano, Takashi Suzuki, Kaori Kameyama, Masako Izawa, Makoto Yamada, Junko Miyamoto, Yukihiro HasegawaAbstract:Context: The steroidogenic acute regulatory protein (StAR) is essential for the production of steroid hormones. The mutations in the StAR gene typically cause congenital lipoid adrenal hyperplasia (lipoid CAH), characterized by severe adrenal insufficiency in both sexes and complete female external genitalia in genetic males. Affected 46, XX females feminize at puberty and menstruate but have progressive hypergonadotropic hypogonadism. It has been hypothesized that the cholesterol accumulation in the steroidogenic cells destroys the residual steroidogenic capacity and progressive ovarian failure occurs (two-hit model). Additionally, ovulation and luteinization in the patients is supposed to be impaired. However, those hypotheses have not been confirmed histologically. Objective: We examined whether pathological findings of the ovary in a patient of lipoid CAH corresponded with two-hit model, and whether ovulation and luteinization occurred or not in the patient. Subject: The ovary in an adult 46, XX female with a homozygous nonsense mutation (Q258X) in the StAR gene was examined. When the patient was age 22 yr, the ovary was resected because of enlargement with polycysts and subsequent torsion. Result: The affected ovary demonstrated remarkable lipoid deposition and changes of the mitochondrial ultrastructure. Immunohistochemical examination showed decrease of steroidogenic enzymes such as P450 cholesterol side-chain cleavage (P450scc). Additionally, we detected Corpus Albicans in the affected ovary. Conclusion: This is the first detailed report on ovarian histology in an adult 46, XX female with a null type mutation of the StAR gene (Q258X), which indicates the evidence of the impairment of ovarian StAR-independent steroidogenesis by lipoid deposition.
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Localization of steroidogenesis and steroid receptors in human Corpus luteum. Classification of human Corpus luteum (CL) into estrogen-producing degenerating CL, and nonsteroid-producing degenerating CL
Seminars in reproductive endocrinology, 1997Co-Authors: Hironobu Sasano, Takashi SuzukiAbstract:In the analysis of the regulation of human Corpus luteum, it is very important to localize the sites of specific steroid hormone production to obtain a better understanding of luteal function. We have examined expression of steroidogenic enzymes, steroid receptors, and adrenal 4 binding protein (Ad4BP), a transcription factor of steroidogenesis, in Corpus luteum of normal cycling human ovary. Corpus luteum can be classified into four different stages from ovulation to complete regression or fibrosis based on these findings: (1) Corpus luteum, (2) steroid-producing degenerating Corpus luteum or SPDCL, (3) nonsteroid producing or NSPDCL, and (4) Corpus Albicans. Corpus luteum in the luteal phase is characterized as follows: (a) the expression of P450scc (cholesterol side chain cleavage), 3 beta HSD (hydroxysteroid dehydrogenase), and Ad4BP in almost all the luteinized granulosa and theca cells, consistent with active progesterone biosynthesis; (b) expression of estrogen-producing P450arom (aromatase) in luteinized granulosa cells, indicating active estrogen production and that of P450c17 (17 alpha hydroxylase) in luteinized theca cells, and (c) expression of progesterone receptor (PR) and androgen receptor (AR) in both luteinized granulosa and theca cells. SPDCL correspond to Corpus luteum undergoing regression or degeneration in the following cycle and are characterized as follows: (a) absence of all the steroidogenic enzymes and Ad4BP in the luteinized granulosa cells, suggestive of hormonally inactive nature of these cells and (b) marked expression of P450scc, 3 beta HSD, P450c17 and Ad4BP in luteinized theca cells. NSPDCL is characterized as the absence of all the steroidogenic enzymes and sporadic expression of Ad4BP in luteinized theca cells. These findings indicate that luteal cells remain even after losing expression of steroidogenic enzymes, consistent with a prolonged process of degeneration or regression of human Corpus luteum. In Corpus Albicans, all the cells were replaced by fibrosis and steroidogenic enzymes; steroid receptors and Ad4BP were not expressed at all. Localization of steroidogenesis in human Corpus luteum has thus provided new insights into understanding of its biological features.
Hironobu Sasano - One of the best experts on this subject based on the ideXlab platform.
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Ovarian histological findings in an adult patient with the steroidogenic acute regulatory protein (StAR) deficiency reveal the impairment of steroidogenesis by lipoid deposition.
Endocrine journal, 2008Co-Authors: Uiko Kaku, Hironobu Sasano, Takashi Suzuki, Kaori Kameyama, Masako Izawa, Makoto Yamada, Junko Miyamoto, Yukihiro HasegawaAbstract:Context: The steroidogenic acute regulatory protein (StAR) is essential for the production of steroid hormones. The mutations in the StAR gene typically cause congenital lipoid adrenal hyperplasia (lipoid CAH), characterized by severe adrenal insufficiency in both sexes and complete female external genitalia in genetic males. Affected 46, XX females feminize at puberty and menstruate but have progressive hypergonadotropic hypogonadism. It has been hypothesized that the cholesterol accumulation in the steroidogenic cells destroys the residual steroidogenic capacity and progressive ovarian failure occurs (two-hit model). Additionally, ovulation and luteinization in the patients is supposed to be impaired. However, those hypotheses have not been confirmed histologically. Objective: We examined whether pathological findings of the ovary in a patient of lipoid CAH corresponded with two-hit model, and whether ovulation and luteinization occurred or not in the patient. Subject: The ovary in an adult 46, XX female with a homozygous nonsense mutation (Q258X) in the StAR gene was examined. When the patient was age 22 yr, the ovary was resected because of enlargement with polycysts and subsequent torsion. Result: The affected ovary demonstrated remarkable lipoid deposition and changes of the mitochondrial ultrastructure. Immunohistochemical examination showed decrease of steroidogenic enzymes such as P450 cholesterol side-chain cleavage (P450scc). Additionally, we detected Corpus Albicans in the affected ovary. Conclusion: This is the first detailed report on ovarian histology in an adult 46, XX female with a null type mutation of the StAR gene (Q258X), which indicates the evidence of the impairment of ovarian StAR-independent steroidogenesis by lipoid deposition.
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Localization of steroidogenesis and steroid receptors in human Corpus luteum. Classification of human Corpus luteum (CL) into estrogen-producing degenerating CL, and nonsteroid-producing degenerating CL
Seminars in reproductive endocrinology, 1997Co-Authors: Hironobu Sasano, Takashi SuzukiAbstract:In the analysis of the regulation of human Corpus luteum, it is very important to localize the sites of specific steroid hormone production to obtain a better understanding of luteal function. We have examined expression of steroidogenic enzymes, steroid receptors, and adrenal 4 binding protein (Ad4BP), a transcription factor of steroidogenesis, in Corpus luteum of normal cycling human ovary. Corpus luteum can be classified into four different stages from ovulation to complete regression or fibrosis based on these findings: (1) Corpus luteum, (2) steroid-producing degenerating Corpus luteum or SPDCL, (3) nonsteroid producing or NSPDCL, and (4) Corpus Albicans. Corpus luteum in the luteal phase is characterized as follows: (a) the expression of P450scc (cholesterol side chain cleavage), 3 beta HSD (hydroxysteroid dehydrogenase), and Ad4BP in almost all the luteinized granulosa and theca cells, consistent with active progesterone biosynthesis; (b) expression of estrogen-producing P450arom (aromatase) in luteinized granulosa cells, indicating active estrogen production and that of P450c17 (17 alpha hydroxylase) in luteinized theca cells, and (c) expression of progesterone receptor (PR) and androgen receptor (AR) in both luteinized granulosa and theca cells. SPDCL correspond to Corpus luteum undergoing regression or degeneration in the following cycle and are characterized as follows: (a) absence of all the steroidogenic enzymes and Ad4BP in the luteinized granulosa cells, suggestive of hormonally inactive nature of these cells and (b) marked expression of P450scc, 3 beta HSD, P450c17 and Ad4BP in luteinized theca cells. NSPDCL is characterized as the absence of all the steroidogenic enzymes and sporadic expression of Ad4BP in luteinized theca cells. These findings indicate that luteal cells remain even after losing expression of steroidogenic enzymes, consistent with a prolonged process of degeneration or regression of human Corpus luteum. In Corpus Albicans, all the cells were replaced by fibrosis and steroidogenic enzymes; steroid receptors and Ad4BP were not expressed at all. Localization of steroidogenesis in human Corpus luteum has thus provided new insights into understanding of its biological features.
Hitoshi Kondo - One of the best experts on this subject based on the ideXlab platform.
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Immunohistochemical evidence for the presence of tumor necrosis factor-alpha in the infant and adult human ovary.
Endocrine journal, 1995Co-Authors: Hitoshi Kondo, Takeshi Maruo, Matsuto MochizukiAbstract:The cytologic localization and cellular levels of tumor necrosis factor-α (TNFα) in the human ovary during follicular growth and regression were examined by the avidin/biotin immunoperoxidase method with a specific antibody to human recombinant TNFα. In the infant ovary, TNFα immunostaining was present only in the oocyte within the primordial follicles. TNFα immunostaining was also present within the oocyte in primordial follicles of the adult ovary. Positive immunostaining for TNFα in granulosa cells became apparent in preantral follicles, while that in theca interna cells began to appear at the antral follicle stage. The staining intensity of the oocyte increased as the oocyte reached the preovulatory stage. The intensity of immunostaining for TNFα in the granulosa and thecal cells increased as the follicle became larger and matured. In corpora lutea, the immunostaining for TNFα persisted in the granulosa lutein and theca lutein cells and intensified in the mid luteal phase. In the regressing corpora lutea, TNFct immunostaining in the luteal cells decreased as the regression advanced. Regressed corpora lutea with a central core of scar tissue were bordered by macrophage-like cells which exhibited intense immunostaining for TNFα. In the cortex region, the Corpus Albicans was negative for TNFα immunostaining, whereas macrophage-like cells peripheral to the Corpus Albicans exhibited intense immunostaining for TNFα. In the medullary region, the Corpus Albicans and surrounding stromal cells were totally negative for TNFα. By contrast, in the early atretic stage, the degenerating oocyte showed weak immunostaining for TNFα, while the granulosa and theca interna cells showed moderate immunostaining for TNFα. In the late atretic stage, the immunostaining for TNFα in the scattered granulosa cells became negligible, whereas the theca interna cells showed intense immunostaining for TNFα. The results obtained indicate that the oocyte is the primary intrafollicular site of TNFα localization within the ovary and that TNFα may participate in regulating follicular growth, regression and aresia.
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Expression of transforming growth factor-alpha in the human ovary during follicular growth, regression and atresia.
Endocrine journal, 1994Co-Authors: Takeshi Maruo, Hitoshi Kondo, Cecilia A. Ladines-llave, Takashi Samoto, Matsuto MochizukiAbstract:The cytologic localization and cellular levels of TGF alpha in the human ovary during follicular growth and regression were examined by avidin/biotin immunoperoxidase techniques with a monoclonal antibody to TGF alpha. In primordial follicles, only the oocyte showed intense immunostaining for TGF alpha, whereas the flattened pregranulosa cells were negative for the immunostaining. The earliest stage of follicular growth at which immunostaining for TGF alpha in granulosa cells and theca interna cells became apparent was the preantral stage. With the increase in the size of follicles, the intensity of TGF alpha immunostaining in the oocyte decreased, whereas the staining intensity of the granulosa and theca cells increased. The immunostaining for TGF alpha in granulosa and theca interna cells persisted in the Corpus luteum, and further intensified during the midluteal phase. In the regressing Corpus luteum, the immunostaining was present only in the peripheral theca lutein cells adjacent to the central scar tissue. The Corpus Albicans was negative for the immunostaining. Stromal cells exhibited weak staining for TGF alpha. In atretic follicles, the theca interna cells exhibited intense staining for TGF alpha without appreciable staining in the scattered granulosa cells. This is the first report to demonstrate that TGF alpha expression in the oocyte is maximal in primordial follicles, whereas TGF alpha expression in granulosa and theca cells increases with the progress of follicles and reaches its maximum in the lutein cells during the mid luteal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
