Disease relevance of Follicular Atresia

• Hyperinsulinemia leads to increased ovarian androgen production, resulting in follicular atresia and anovulation [1].

High impact information on Follicular Atresia

• The polycystic ovary syndrome results when a primary defect increases one of three variables: the ratio of the serum concentrations of luteinizing hormone to follicle stimulating hormone, the ratio of the intraovarian concentrations of androgen to estrogen, or follicular atresia [2].
• We conclude that CASP gene family members participate in granulosa cell apoptosis during ovarian follicular atresia, and that collapse of the granulosa cell cytoskeleton may result from caspase-3-catalyzed fodrin proteolysis [3].
• Antral follicular atresia increased in a dose-dependent fashion in response to cyclophosphamide (0 mg/kg, 53.5%; 1 mg/kg, 67.3%; 50 mg/kg, 65.7%; 100 mg/kg, 73.9%; 150 mg/kg, 92.2%) [4].
• To help clarify the phenomenon of follicular atresia during ovarian development, we examined cysteine proteinases stored in mosquito Culex pipiens pallens ovaries [5].
• Clusterin protects granulosa cells from apoptotic cell death during follicular atresia [6].

Biological context of Follicular Atresia

• During the periovulatory interval, intrafollicular progesterone (P) prevents follicular atresia and promotes ovulation [7].
• We therefore investigated the proteolytic cleavage of actin and PARP as well as the localization of caspase-3 during follicular atresia (induced by gonadotropin withdrawal) and luteal regression (induced by prostaglandin F2alpha) in the rat ovary [8].
• It also produced follicular atresia, reduced the circulating levels of estradiol, and resulted in reduced incidence of estrus smears [9].
• Effect of alterations in pulsatile luteinizing hormone release on ovarian follicular atresia and steroid secretion on diestrus 1 in the rat estrous cycle [10].
• Autoradiography after pulse labelling with [3H] thymidine was applied to investigate the proliferation processes in the granulosa and theca related to follicular atresia of the dog ovary during metestrus [11].

Anatomical context of Follicular Atresia

• These results indicate that granulosa cells continue to secrete inhibin during the process of follicular atresia, although these cells quickly shut off the secretion of estradiol, and theca cells shut off the secretion of testosterone [12].
• The time course for loss of ability of Graafian follicles to secrete inhibin and estradiol was investigated during induced follicular atresia [12].
• Chronology of events accompanying follicular atresia in hypophysectomized ewes. Changes in levels of steroidogenic enzymes, connexin 43, insulin-like growth factor II/mannose 6 phosphate receptor, extracellular matrix components, and matrix metalloproteinases [13].
• To confirm the lack of involvement of macrophages in the process of follicular atresia and elimination, specially prepared ovarian sections were incubated with antimouse macrophage monoclonal antibodies (F4/80, Mac-1, Mac-2) [14].
• N-Gal NAc, alpha-D-Gal, alpha-L-Fuc, D-Gal (beta-1-3)-D-Gal NAc, and alpha-beta-D Gal NAc linked glyco-conjugates were exposed during follicular atresia in oocyte, zona pellucida and granulosa cells [15].

Associations of Follicular Atresia with chemical compounds

• By contrast, during follicular atresia, thecal tissue retains its capacity to synthesize delta 4 but loses much of its capacity to synthesize E2 [16].
• These data provide the basis for future studies on the role of sex steroid hormones in follicular atresia and the regulation of endonuclease activity by steroid hormones [17].
• Such shifts in the ratio of estrogen to progesterone production are known to be characteristic of follicular atresia [18].
• Evidence that cocaine- and amphetamine-regulated transcript is a novel intraovarian regulator of follicular atresia [19].
• In addition, follicular atresia was induced by either withdrawal of diethylstilbestrol (DES) for 2 days or injection of GnRHa for 2 days in hypophysectomized DES-implanted immature rats [20].

Gene context of Follicular Atresia

• In contrast, follicular atresia is associated with a decrease and a large increase in levels of IGFBP-3 and IGFBPs less than 40 kDa, respectively [21].
• Because androgens enhance recruitment of primordial follicles into the growth pool and cause atresia of late antral follicles, the inappropriately high level of AR probably is related to the follicular atresia and to the early exhaustion of follicles in BERKO mice [22].
• Syndecan-4 expression is associated with follicular atresia in mouse ovary [23].
• The data suggest that a leptin deficiency in mice is associated with impaired folliculogenesis, which results in increased follicular atresia [24].
• Follicular atresia is associated with greater activity of IGFBP-2, -4, -5, and greater concentrations of P4 in follicles, whereas growing dominant and persistent follicles contained greater concentrations of E2, androstenedione (A4), and less IGFBP-2 activity than follicles of other classes [25].

Analytical, diagnostic and therapeutic context of Follicular Atresia

• Since both pentobarbitone-treatment and hypophysectomy result in follicular atresia, but changes in cumulus respiration occurred only in hypophysectomized adult rats, it is concluded that an increase in cumulus respiration is not inherent to the atretic process [26].
• In this study immunohistochemistry was used to localize TGF-beta1 in order to correlate the growth factor expression with morphological follicular atresia during diestrus in mice [27].

References