Interleukin-6 inhibits the expression of luteinizing hormone receptor mRNA during the maturation of cultured rat granulosa cells

Tamura, Kazuhiro; Kawaguchi, T.; Kuroda, Hiroshi

doi:10.1677/joe.0.1700121

Cited by 15 publications

(5 citation statements)

References 40 publications

(45 reference statements)

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“…There were several reports on the effect of IL‐6 on follicular development. In one report, the addition of IL‐6 into the rat granulosa cell culture medium inhibited LHR expression . In other reports, IL‐6 inhibited estradiol and progesterone production that were induced by FSH stimulation in the granulosa cells .…”

Section: Luteinizing Hormone Receptor Expression In the Granulosa Cellsmentioning

confidence: 99%

Expression of the gonadotropin receptors during follicular development

Kishi

Kitahara

Imai

et al. 2017

Reprod Medicine & Biology

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BackgroundGonadotropins induce follicular development that leads to ovulation and luteinization. In women, the level of gonadotropins, along with the expression of their receptors, changes dynamically throughout the menstrual cycle. This study aimed to clarify the mechanisms underlying these phenomena.MethodsThe literature was reviewed, including that published by the authors.Main findings (Results)Follicle‐stimulating hormone receptor expression in the granulosa cells was induced by androgens that were derived from growth differentiation factor‐9‐stimulated theca cells. In the theca cells, luteinizing hormone receptor (LHR) expression was noted from their appearance. In the granulosa cells, follicle‐stimulating hormone (FSH) stimulation was essential for LHR expression. However, FSH alone was not sufficient to respond to the luteinizing hormone (LH) surge for oocyte maturation, ovulation, and subsequent luteinization. To achieve these stages, various local factors that were derived from the granulosa and theca cells in response to FSH and LH stimulation had to work synergistically in an autocrine/paracrine manner to strongly induce LHR expression. Following the LH surge, the LHR expression decreased markedly; miRNAs were involved in this transient LHR downregulation. Following ovulation, LHR expression drastically increased again toward luteinization.ConclusionThe expression of gonadotropin receptors is controlled by sophisticated and complicated systems; a breakdown of this system could lead to ovulation disorders.

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Section: Luteinizing Hormone Receptor Expression In the Granulosa Cellsmentioning

confidence: 99%

Expression of the gonadotropin receptors during follicular development

Kishi

Kitahara

Imai

et al. 2017

Reprod Medicine & Biology

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“…IL-6 inhibited FSH-induced LHR expression in rat and porcine GCs (40,41) and suppressed FSH-induced steroidogenesis in rat and bovine GCs (42, 43). Although a report indicated that IL-6 enhanced FSH-induced LHR expression in rat GCs (44), excess IL-6 is commonly associated with aging and believed to affect follicular development negatively (45)(46)(47).…”

Section: Folliculogenesis In the Ovarian Cortexmentioning

confidence: 99%

Chronic low-grade inflammation and ovarian dysfunction in women with polycystic ovarian syndrome, endometriosis, and aging

Orisaka,

Mizutani,

Miyazaki

et al. 2023

Front. Endocrinol.

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The ovarian microenvironment is critical for follicular development and oocyte maturation. Maternal conditions, including polycystic ovary syndrome (PCOS), endometriosis, and aging, may compromise the ovarian microenvironment, follicular development, and oocyte quality. Chronic low-grade inflammation can induce oxidative stress and tissue fibrosis in the ovary. In PCOS, endometriosis, and aging, pro-inflammatory cytokine levels are often elevated in follicular fluids. In women with obesity and PCOS, hyperandrogenemia and insulin resistance induce ovarian chronic low-grade inflammation, thereby disrupting follicular development by increasing oxidative stress. In endometriosis, ovarian endometrioma-derived iron overload can induce chronic inflammation and oxidative stress, leading to ovarian ferroptosis and fibrosis. In inflammatory aging (inflammaging), senescent cells may secrete senescence-associated secretory phenotype factors, causing chronic inflammation and oxidative stress in the ovary. Therefore, controlling chronic low-grade inflammation and fibrosis in the ovary would present a novel therapeutic strategy for improving the follicular microenvironment and minimizing ovarian dysfunction.

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“…GCs from eCG-primed rats were harvested as described previously (14). Cells (2´10 5 cells / well) were plated onto a 24-well tissue culture dish (Asahi Techno Glass, Tokyo) coated with collagen type I in 0.5 ml chemically defined medium [serum-free Dulbecco's Modified Eagle's Medium (Gibco BRL, Grand Island, NY, USA) supplemented with 5 m g / ml transferrin, 40 ng / ml hydrocortisone, 4 mg / ml BSA, 30 ng / ml androstendione, 1 mg / ml fibronectin, 4 m g/ ml insulin, 100 ng / ml FSH, and 10 ng / ml LH] in the absence or presence of T 3 (10 -9 -10 -5 M).…”

Section: Gcs Preparation and Culturementioning

confidence: 99%

Effect of Thyroid Hormone on CYP19 Expression in Ovarian Granulosa Cells From Gonadotropin-Treated Immature Rats

et al. 2004

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Abstract. The present study was designed to determine the mechanisms by which serum estradiol levels are enhanced during gonadotropin-induced ovarian development in hypothyroid immature rats. Thyroidectomized (Tx)-immature rats receiving thyroidectomy on day 22 were treated with 8 IU equine chorionic gonadotropin (eCG) at 26 days of age to induce follicular development in ovaries. Ovaries or ovarian granulosa cells were collected on the first proestrus (day 28). Enhanced expression of aromatase (CYP19) mRNA induced by eCG treatment was inhibited by injection of thyroxine (T 4 : 5 m g´6 times) in Tx rats. Ovarian granulosa cells harvested from Tx rats were cultured for 24 h in chemically defined serum-free medium containing gonadotropin in the presence of 3,5,3'-triidothyronine (T 3 ). Addition of low doses of T 3 (10 -8 , 10 -7 M) to the medium significantly decreased 17b-estradiol (E 2 ) levels, whereas high doses of T 3 (10 -6 , 10 -5 M) did not inhibit the levels. Similar effects of T 3 on CYP19 mRNA expression were observed. These results indicate that augmentation of E 2 production in hypothyroid animals may be mediated, in part, via the stimulation of CYP19 mRNA expression in granulosa cells, which is suppressed by thyroid hormone.

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Interleukin-6 inhibits the expression of luteinizing hormone receptor mRNA during the maturation of cultured rat granulosa cells

Cited by 15 publications

References 40 publications

Expression of the gonadotropin receptors during follicular development

Expression of the gonadotropin receptors during follicular development

Chronic low-grade inflammation and ovarian dysfunction in women with polycystic ovarian syndrome, endometriosis, and aging

Effect of Thyroid Hormone on CYP19 Expression in Ovarian Granulosa Cells From Gonadotropin-Treated Immature Rats

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