Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells
Нема приказа
Аутори
Samardzija, DraganaPogrmić-Majkić, Kristina
Fa, Svetlana
Stanić, Bojana
Jasnić, Jovana
Andrić, Nebojša
Чланак у часопису (Објављена верзија)
Метаподаци
Приказ свих података о документуАпстракт
Bisphenol A (BPA) is an endocrine disruptor used in a variety of consumer products. Exposure to BPA leads to alterations in steroidogenesis of ovarian granulosa cells. Here, we analyzed the mechanism by which BPA alters progesterone biosynthesis in immature rat granulosa cells. BPA increased expression of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase in granulosa cells; however, BPA prevented the basal and the FSH-induced progesterone production. BPA caused sequestration of cholesterol to the perinuclear area, as evident by the Filipin staining. BPA decreased mRNA expression of ATP binding cassette transporter-A1 (Abca1) and increased level of sterol regulatory element binding protein 1. Addition of exogenous cell-permeable cholesterol restored the effect of BPA on Abca1 and Star mRNA expression and partially reversed BPA's effect on progesterone production. These results indicate that exposure to BPA disru...pts cholesterol homeostasis leading to decreased progesterone production in immature rat granulosa cells.
Кључне речи:
StAR / Progesterone / Granulosa cells / Cholesterol / Bisphenol A / Abca1Извор:
Molecular and Cellular Endocrinology, 2018, 461, C, 55-63Издавач:
- Elsevier Ireland Ltd, Clare
Финансирање / пројекти:
- Environmental signaling and ovarian diseases susceptibility (EU-FP7-321745)
- Ксенобиотици са хормонском активношћу: репродуктивни, метаболички, развојни одговори и механизам дејства код одабраних модел организама и ћелијских линија (RS-MESTD-Basic Research (BR or ON)-173037)
DOI: 10.1016/j.mce.2017.08.013
ISSN: 0303-7207
PubMed: 28859904
WoS: 000424309100006
Scopus: 2-s2.0-85028673869
Институција/група
Institut za molekularnu genetiku i genetičko inženjerstvoTY - JOUR AU - Samardzija, Dragana AU - Pogrmić-Majkić, Kristina AU - Fa, Svetlana AU - Stanić, Bojana AU - Jasnić, Jovana AU - Andrić, Nebojša PY - 2018 UR - https://imagine.imgge.bg.ac.rs/handle/123456789/1193 AB - Bisphenol A (BPA) is an endocrine disruptor used in a variety of consumer products. Exposure to BPA leads to alterations in steroidogenesis of ovarian granulosa cells. Here, we analyzed the mechanism by which BPA alters progesterone biosynthesis in immature rat granulosa cells. BPA increased expression of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase in granulosa cells; however, BPA prevented the basal and the FSH-induced progesterone production. BPA caused sequestration of cholesterol to the perinuclear area, as evident by the Filipin staining. BPA decreased mRNA expression of ATP binding cassette transporter-A1 (Abca1) and increased level of sterol regulatory element binding protein 1. Addition of exogenous cell-permeable cholesterol restored the effect of BPA on Abca1 and Star mRNA expression and partially reversed BPA's effect on progesterone production. These results indicate that exposure to BPA disrupts cholesterol homeostasis leading to decreased progesterone production in immature rat granulosa cells. PB - Elsevier Ireland Ltd, Clare T2 - Molecular and Cellular Endocrinology T1 - Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells EP - 63 IS - C SP - 55 VL - 461 DO - 10.1016/j.mce.2017.08.013 ER -
@article{ author = "Samardzija, Dragana and Pogrmić-Majkić, Kristina and Fa, Svetlana and Stanić, Bojana and Jasnić, Jovana and Andrić, Nebojša", year = "2018", abstract = "Bisphenol A (BPA) is an endocrine disruptor used in a variety of consumer products. Exposure to BPA leads to alterations in steroidogenesis of ovarian granulosa cells. Here, we analyzed the mechanism by which BPA alters progesterone biosynthesis in immature rat granulosa cells. BPA increased expression of steroidogenic acute regulatory protein (StAR), cholesterol side-chain cleavage enzyme and 3 beta-hydroxysteroid dehydrogenase in granulosa cells; however, BPA prevented the basal and the FSH-induced progesterone production. BPA caused sequestration of cholesterol to the perinuclear area, as evident by the Filipin staining. BPA decreased mRNA expression of ATP binding cassette transporter-A1 (Abca1) and increased level of sterol regulatory element binding protein 1. Addition of exogenous cell-permeable cholesterol restored the effect of BPA on Abca1 and Star mRNA expression and partially reversed BPA's effect on progesterone production. These results indicate that exposure to BPA disrupts cholesterol homeostasis leading to decreased progesterone production in immature rat granulosa cells.", publisher = "Elsevier Ireland Ltd, Clare", journal = "Molecular and Cellular Endocrinology", title = "Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells", pages = "63-55", number = "C", volume = "461", doi = "10.1016/j.mce.2017.08.013" }
Samardzija, D., Pogrmić-Majkić, K., Fa, S., Stanić, B., Jasnić, J.,& Andrić, N.. (2018). Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells. in Molecular and Cellular Endocrinology Elsevier Ireland Ltd, Clare., 461(C), 55-63. https://doi.org/10.1016/j.mce.2017.08.013
Samardzija D, Pogrmić-Majkić K, Fa S, Stanić B, Jasnić J, Andrić N. Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells. in Molecular and Cellular Endocrinology. 2018;461(C):55-63. doi:10.1016/j.mce.2017.08.013 .
Samardzija, Dragana, Pogrmić-Majkić, Kristina, Fa, Svetlana, Stanić, Bojana, Jasnić, Jovana, Andrić, Nebojša, "Bisphenol A decreases progesterone synthesis by disrupting cholesterol homeostasis in rat granulosa cells" in Molecular and Cellular Endocrinology, 461, no. C (2018):55-63, https://doi.org/10.1016/j.mce.2017.08.013 . .