Why it is important to know history

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The ovary is a highly organized composite of germ cells (oocytes or eggs) and somatic cells (granulosa cells, thecal cells, and stromal cells) whose interactions dictate formation of oocyte-containing follicles, development of both oocytes and somatic cells as follicles, ovulation, and formation of the corpus luteum (the endocrine structure that forms from the ovarian follicle after ovulation and is required for establishing and maintaining pregnancy) (Figure 1).

Many events in the adult ovary are controlled by two hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), secreted from the anterior pituitary gland under the control of pulses of gonadotropin-releasing why it is important to know history (GnRH) from the hypothalamus (Figure 1). For example, estrogen produced by the cells of the developing follicle both inhibits GnRH production in the hypothalamus and elicits elevated GnRH pulses, which trigger the mid-cycle LH surge that initiates ovulation.

Thus, fertility depends on highly orchestrated endocrine events involving multiple organ systems. Summary of hormonal control of the ovary during follicle bayer uzbekistan, ovulation, and luteinization.

FSH controls follicular granulosa cell (GC) growth and estradiol production, while LH controls ovulation and follicular luteinization. Right: A cross section of a mouse ovary is shown, demonstrating the main cell types and follicle stages.

Ovarian follicles are composed of a single oocyte surrounded by somatic cells (granulosa cells) and thecal cells. Follicles grow from primordial (not shown) to primary and secondary stages independent of the pituitary gonadotropins.

FSH stimulates growth to the preovulatory follicle stage, characterized by granulosa cells that directly surround the oocyte (cumulus cells) and those that make up the bulk of the wall of the follicle. Following the LH surge, the follicle erupts through the ovarian surface (OSE), and the remaining cells of the follicle terminally differentiate to form a corpus luteum. Left: The preovulatory follicle contains an oocyte surrounded by cumulus cells that are separated from the mural granulosa cells by a fluid-filled cavity.

Middle: Following the LH surge, the COC undergoes a process called cumulus or COC expansion, in which the cumulus cells make and become embedded in a hyaluronan-rich matrix. Right: The cumulus cells accompany the oocyte into the oviduct following release of the entire COC from the ovarian follicle. Disruption of this finely controlled network can lead to many clinical syndromes including premature ovarian failure (POF), polycystic ovarian syndrome (PCOS), ovarian hyperstimulation syndrome, ovulation defects, poor oocyte quality, and cancer.

We emphasize the roles of bone morphogenetic proteins (BMPs), activins, and SMADs, WNT signaling, and recently uncovered aspects of the FSH and LH signaling cascades. Differentiation into a testis (male) or ovary (female) does not occur until after the primordial germ cells (PGCs) have migrated from the yolk sac and colonized the indifferent gonad. In mice, colonization occurs approximately 9. Once the PGCs colonize the indifferent gonad, in female mice, they undergo a period of proliferation, followed by differentiation into oocytes that enter meiosis (at approximately E13.

Development of germ cells into either male or female states depends on their interactions with the somatic cells of the gonad (see following paragraph) (Figure 2). In mice, BMPs have an important role in PGC proliferation, and BMP2 and BMP4 increase the number of PGCs in why it is important to know history (2, 3). Bmp7-null mice have reduced numbers of germ cells after 11. Signaling pathways controlling ovarian follicle growth in the mouse.

PGCs are specified by the BMP pathway, then proliferate and migrate to the indifferent gonad. The BMPs are major determinants of PGC specification and proliferation in the mouse. During the postnatal period, clusters (or nests) of germ cells break down to form why it is important to know history follicles, which upon activation become primary follicles.

Estradiol (E2) inhibits the why it is important to know history of germ cell clusters to primordial follicles. Foxo3 is also expressed in oocytes, and deletion of Foxo3 (or the PI3K inhibitor Pten) in oocytes results in premature activation of the primordial follicle pool and oocyte loss. Foxl2 is expressed in somatic granulosa cells, and deletion results in arrest and subsequent death of follicles before the primary follicle stage.

NOBOX regulates other TFs (e. Regulation of activin by energy of vitamins inhibitors, such as inhibin or follistatin, is critical after the secondary follicle stage Catapres-TTS (Clonidine)- Multum involves many follicle stages. In vitro experiments implicate FOXO1 and ESR2 as important regulators in granulosa cells of growing follicles.

See text for discussion and references for each indicated gene pathway. Mutations in the human R-spondin homolog (RSPO1) gene, which encodes a WNT pathway adapter molecule, indicate that this molecule is also a primary female sex-determining factor (9). These intriguing recent results document why it is important to know history that there are organizers of ovary versus testis development and that Rspo1, Wnt4, and Foxl2 are all important for ovary development, at least in mice.

PGCs divide to form syncytia (nests or cysts) of oocytes that break down to form primordial follicles, which represent the quiescent follicle reserve in the ovary. Each primordial follicle contains an immature oocyte arrested why it is important to know history in meiosis, surrounded by a flattened epithelium that will eventually become the granulosa cells.

Germ cell syncytia breakdown occurs prenatally in humans and shortly after birth in mice (Figure 2). Inappropriate germ cell syncytia breakdown can lead to the generation of polyovular follicles (i.

Polyovular follicles are also seen in human ovaries at birth, but rarely in why it is important to know history (22). This might be because individual oocytes develop at different rates Plenaxis (Abarelix)- FDA the same follicle (23), and while multiple oocytes might be developing inside the follicle, only one may be at the appropriate maturation stage to be fertilized.

In this context, estrogen reduces activin expression, which suggests a direct role for activin in normal primordial follicle formation (19, 26). This effect of estrogen underscores the need for further research on the effect of endocrine disruptors environmental and dietary compounds that act like hormones in reproductive diseases. The effects of phytoestrogens and other estrogen-like compounds on the reproductive tract, fertility, and reproductive cancers are not well understood.

Transcription factors and early follicle growth. A number of transcription factors whose expression, at least in adult tissues, appears to be restricted to germ cells or oocytes, are necessary for early folliculogenesis (Figure 2) (37).

Figla encodes a basic helix-loop-helix (bHLH) transcription factor that regulates expression of the zona pellucida genes Zp1, Zp2, and Zp3, which encode the egg coat (38). Mice null for either gene have a similar female phenotype: postnatal oocyte loss leading to female sterility (40, 41). Deletion of Nobox also causes female sterility and postnatal oocyte loss, and the gene product has been shown to directly regulate expression of growth differentiation factor 9 (Gdf9) and Pou5f1 (42, 43).

Disruption of why it is important to know history FOXL2-encoding azathioprine (Azasan)- FDA leads to abnormal follicle development and POF in mice (46) and humans (47). As discussed in the previous section, Foxl2 is expressed in the early stages of gonadal development and has been shown to direct ovarian and oppose testis development.

In early postnatal Foxl2-null ovaries, the expression of some genes increases, e. These results indicate that in addition to its role in embryonic ovarian development, FOXL2 likely affects specific basic metabolic aspects required for the proliferation and differentiation of somatic cells in the postnatal ovary.

This mutation is unlikely to disrupt FOXL2 DNA binding, but rather alters protein-protein interactions (51).



23.09.2019 in 02:02 Tagar:
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27.09.2019 in 02:31 Nikogal:
Rather valuable idea