Chicken ovarian follicular atresia: interaction network at organic, cellular, and molecular levels

Abstract

Most of follicles undergo a degenerative process called follicular atresia. This process directly affects the egg production of laying hens and is regulated by external and internal factors. External factors primarily include nutrition and environmental factors. In follicular atresia, internal factors are predominantly regulated at 3 levels; organic, cellular and molecular levels. At the organic level, the hypothalamic-pituitary-ovary (HPO) axis plays an essential role in controlling follicular development. At the cellular level, gonadotropins and cytokines, as well as estrogens, bind to their receptors and activate different signaling pathways, thereby suppressing follicular atresia. By contrast, oxidative stress induces follicular atresia by increasing ROS levels. At the molecular level, granulosa cell (GC) apoptosis is not the only factor triggering follicular atresia. Autophagy is also known to give rise to atresia. Epigenetics also plays a pivotal role in regulating gene expression in processes that seem to be related to follicular atresia, such as apoptosis, autophagy, proliferation, and steroidogenesis. Among these processes, the miRNA regulation mechanism is well-studied. The current review focuses on factors that regulate follicular atresia at organic, cellular and molecular levels and evaluates the interaction network among these levels. Additionally, this review summarizes atretic follicle characteristics, in vitro modeling methods, and factors preventing follicular atresia in laying hens.

Keywords: follicular atresia; interaction network regulation; laying hen; regulation factor.

Figure 1

Anatomy of the reproductive tract (A) and the process of follicular development (B) in chicken. SWF, small white follicles; LWF, large white follicles: SYF, small yellow follicles: POF, postovulatory follicles.

Figure 2

Appearance (A) of atretic or collapsing follicles, and histopathology (B) of folicular atresia in silky black bone chicken. Data are not published from our laboratory. GCs, granulosa cells: TCs, theca cells.

Figure 3

Regulation of reproductive hormones of the HPO axis in chicken. H, hypothalamic: P, pituitary: O, ovary: P4, progesterone; E2, estrogen.

Figure 4

Cell survival factors and signals in GCs.

Figure 5

Apoptosis and autophagy signaling pathways.

Figure 6

Epigenetic regulations of genes expression in follicular atresia and interaction network at organic, cellular, and molecular levels.