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5 results for “Cyp19A1”
CYP19A1 (Cytochrome P450 Family 19 Subfamily A Member 1) Gene and Pharmacogenetics of Response to Testosterone Therapy
ClinicalTrials.gov study NCT01378299. IPD Sharing: YES. Countries: 1. Publications: 2.
The Immp2l mutation causes ovarian aging through ROS-wnt/β-catenin-estrogen (cyp19a1) pathway: preventive effect of melatonin
<p>Mitochondria play important roles in ovarian follicle development. Mitochondrial dysfunction, including mitochondrial gene deficiency, impairs the ovarian development. Here, we explored the role and mechanism of mitochondrial inner membrane gene <i>Immp2l</i> in ovarian follicle growth and development. Our results revealed that the female Immp2l<sup>-/-</sup> mice were infertile, while the Immp2l<sup>+/- </sup>mice were normal. Body and ovarian weights were reduced in the female Immp2l<sup>-/- </sup>mice, ovarian follicle growth and development were stunted in the secondary follicle stage. Although a few ovarian follicles were ovulated, the oocytes were not fertilized due to mitochondrial dysfunction. Increased oxidative stress, decreased estrogen levels, and altered genes expression of Wnt/β-catenin and steroid hormone synthesis pathways were observed in 28-day-old Immp2l<sup>-/-</sup> mice. The Immp2l mutation accelerated ovarian aging process, as no ovarian follicles were detected in age of 5 months in Immp2l<sup>-/- </sup>mice. All the aforementioned changes in the Immp2l<sup>-/- </sup>mice were reversed by administration of antioxidant melatonin to the Immp2l<sup>-/-</sup> mice. Furthermore, our in vitro study using Immp2l knockdown granulosa cells confirmed that the Immp2l downregulation induced granulosa cell aging by enhancing ROS levels, suppressing <i>Wnt16</i>, increasing β-catenin and decreasing steroid hormone synthesis gene <i>cyp19a1</i> and estrogen levels, accompanied by an increase in the aging phenotype of granulosa cells. Melatonin treatment delayed granulosa cell aging progression. Taken together, Immp2l causes ovarian aging through the ROS-Wnt/β-catenin-estrogen (cyp19a1) pathway, which can be reversed by melatonin treatment.Mitochondria play important roles in ovarian follicle development. Mitochondrial dysfunction, including mitochondrial gene deficiency, impairs the ovarian development. Here, we explored the role and mechanism of mitochondrial inner membrane gene <i>Immp2l</i> in ovarian follicle growth and development. Our results revealed that the female Immp2l<sup>-/-</sup> mice were infertile, while the Immp2l<sup>+/- </sup>mice were normal. Body and ovarian weights were reduced in the female Immp2l<sup>-/- </sup>mice, ovarian follicle growth and development were stunted in the secondary follicle stage. Although a few ovarian follicles were ovulated, the oocytes were not fertilized due to mitochondrial dysfunction. Increased oxidative stress, decreased estrogen levels, and altered genes expression of Wnt/β-catenin and steroid hormone synthesis pathways were observed in 28-day-old Immp2l<sup>-/-</sup> mice. The Immp2l mutation accelerated ovarian aging process, as no ovarian follicles were detected in age of 5 months in Immp2l<sup>-/- </sup>mice. All the aforementioned changes in the Immp2l<sup>-/- </sup>mice were reversed by administration of antioxidant melatonin to the Immp2l<sup>-/-</sup> mice. Furthermore, our in vitro study using Immp2l knockdown granulosa cells confirmed that the Immp2l downregulation induced granulosa cell aging by enhancing ROS levels, suppressing <i>Wnt16</i>, increasing β-catenin and decreasing steroid hormone synthesis gene <i>cyp19a1</i> and estrogen levels, accompanied by an increase in the aging phenotype of granulosa cells. Melatonin treatment delayed granulosa cell aging progression. Taken together, Immp2l causes ovarian aging through the ROS-Wnt/β-catenin-estrogen (cyp19a1) pathway, which can be reversed by melatonin treatment.</p>
The Immp2l mutation causes ovarian aging through ROS-wnt/β-catenin-estrogen (cyp19a1) pathway: preventive effect of melatonin
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Transcriptome response of mouse mammary gland from age 12 to 30 months of age in Esr1 and CYP19A1 genetically engineered mouse models of breast cancer risk in the presence and absence of transgene ind
GEO Series GSE201767. Mus musculus. 48 samples. Type: Expression profiling by high throughput sequencing.
Transcriptome response to anti-hormonals in Esr1 and CYP19A1 genetically engineered mouse models of breast cancer risk during reproductive senescence
GEO Series GSE201326. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing.
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