This prevents the interaction of LRH-1 protein with the CYP19A1 promoter, represses E2 synthesis, promotes pGC apoptosis, and initiates follicular atresia in porcine ovaries.
Histological analysis showed no differences in the proportion of proliferative follicles (pH3 positive), but increased atresia (cleaved caspase-3-positive, or TUNEL-positive) was detected in ovaries of protein-restricted offspring at both ages (P < 0.05).
Histological analysis showed no differences in the proportion of proliferative follicles (pH3-positive), but increased atresia (cleaved caspase-3-positive, or TUNEL-positive) was detected in ovaries of protein-restricted offspring at both ages (p<0.05).
These data provide additional evidence that CHD7 mutations are a significant cause of semicircular canal atresia in children with full or partial CHARGE syndrome.
CHD7 gene mutations were identified in 17 (71%) of 24 children clinically diagnosed to have CHARGE syndrome (C, coloboma of the iris or retina; H, heart defects; A, atresia of the choanae; R, retardation of growth and/or development; G, genital anomalies; and E, ear abnormalities).
Herein, we identified miR-181a as a central component of activin/Smad3-mediated follicle atresia. miR-181a was strikingly upregulated in porcine atretic follicles, which induced the apoptosis of porcine granulosa cells (GCs) in vitro.
This increased rate of entry into the cell cycle was associated with a ≥ 2-fold increase in follicular atresia and the nuclear localization of nuclear factor-kappa-B transcription factor P65; (NFΚB/p65, or RELA).
To detect the effects of vascular endothelial growth factor 120 (VEGF120), follicle-stimulating hormone (FSH), and 2-methoxyestradiol (2ME2) on follicular angiogenesis during development and atresia, we treated sexually immature and mature female mice with VEGF120, FSH, 2ME2, and FSH receptor (FSHR) antagonist singly or in combination via intraperitoneal injection.
More importantly, we identified a novel circRNA, termed circINHA, that was downregulated during atresia in ovarian follicles, and we confirmed a direct interaction between miR-10a-5p and circINHA.
Samples were obtained from 10 newborns operated for small intestinal atresia and from 17 adults undergoing gastroduodenoscopy and/or ileocolonoscopy. mRNA expression of the transporters SGLT1, GLUT1, GLUT2, GLUT5, and GLUT7 was measured in neonate samples proximal and distal of the atresia as well as in adult duodenum, ileum, and colon.
Here, we aimed to illustrate a circRNA involved in the CTGF regulatory pathway during the apoptosis and follicular atresia of pig granulosa cells (GCs).
This prevents the interaction of LRH-1 protein with the CYP19A1 promoter, represses E2 synthesis, promotes pGC apoptosis, and initiates follicular atresia in porcine ovaries.
Our previous studies of AQP8-deficient (AQP8<sup>-/-</sup>) mice demonstrated that AQP8 participates in folliculogenesis, including in the formation of follicles, ovulation, and atresia.