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- Author: Roberto Romero x
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Developmental Biology Lab. Biology of Reproduction Research Unit, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, México City, México
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Developmental Biology Lab. Biology of Reproduction Research Unit, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, México City, México
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Developmental Biology Lab. Biology of Reproduction Research Unit, Facultad de Estudios Superiores Zaragoza, Universidad Nacional Autónoma de México, México City, México
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In brief
The SCN regulates ovulation by stimulating the preovulatory surge of gonadotropins. This study revealed an additional role in the sensitization of the hypothalamus to estradiol that changes along the estrous cycle and the side of the nucleus.
Abstract
Ovulation is timed by neural signals originating at the suprachiasmatic nucleus (SCN) that trigger ovulation when converge with high estradiol levels, which indicates the maturation of ovarian follicles. We have shown that the hypothalamic regulation of ovulation is asymmetrical and we hypothesized that the paired SCN could contribute to such symmetries. We unilaterally lesioned the SCN of rats at each stage of the estrous cycle and evaluated the acute effects on the progression of their estrous cycle, follicular development and ovulation. Lesions prevented progression of the estrous cycle when performed in estrus/metestrus but not in diestrus/proestrus. Abnormalities in follicular development were observed in the nonovulating lesioned rats and this was independent of the side of the SCN destroyed and the stage of the cycle when surgery was performed. Groups of lesioned rats were then hormonally primed with GnRH or estradiol to assess the neuroendocrine pathway altered by the treatment. GnRH restored ovulation, suggesting that both SCN are needed for proper triggering of the preovulatory surge of GnRH and that unilateral lesion does not impair the sensitivity of the pituitary or the ovary to GnRH and gonadotropins, respectively. With regard to restoring ovulation, estradiol was asymmetrically effective in rats lesioned in estrous, partially effective in rats operated at diestrus and ineffective in rats at metestrus. Our results indicate that the SCN regulates the activity of the hypothalamic–pituitary–ovarian axis not only by modulating the preovulatory surge of GnRH/gonadotropins but also by promoting the hypothalamic integration of estrogenic signals from the ovaries in an asymmetric and stage-dependent fashion.
Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
Division of Obstetrics and Gynecology, School of Medicine, Faculty of Medicine, Pontificia Universidad Catolica de Chile, Santiago, Chile
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, USA
Department of Biochemistry, Microbiology and Immunology, Wayne State University School of Medicine, Detroit, Michigan, USA
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Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan, USA
Department of Epidemiology and Biostatistics, Michigan State University, East Lansing, Michigan, USA
Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan, USA
Center for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan, USA
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In brief
The syndrome of preterm labor comprises multiple established and novel etiologies. This review summarizes the distinct immune mechanisms implicated in preterm labor and birth and highlights potential strategies for its prevention.
Abstract
Preterm birth, the leading cause of neonatal morbidity and mortality worldwide, results from preterm labor, a syndrome that includes multiple etiologies. In this review, we have summarized the immune mechanisms implicated in intra-amniotic inflammation, the best-characterized cause of preterm labor and birth, as well as novel etiologies non-associated with intra-amniotic inflammation (i.e. formally known as idiopathic). While the intra-amniotic inflammatory responses driven by microbes (infection) or alarmins (sterile) have some overlap in the participating cellular and molecular processes, the distinct natures of these two conditions necessitate the implementation of specific approaches to prevent adverse pregnancy and neonatal outcomes. Intra-amniotic infection can be treated with the correct antibiotics, whereas sterile intra-amniotic inflammation could potentially be treated by administering a combination of anti-inflammatory drugs (e.g. betamethasone, inflammasome inhibitors, etc.). Recent evidence also supports the role of fetal T-cell activation as a newly described trigger for preterm labor and birth in a subset of cases diagnosed as idiopathic. Moreover, herein we also provide evidence of two maternally-driven immune mechanisms responsible for preterm births formerly considered to be idiopathic. First, the impairment of maternal Tregs can lead to preterm birth, likely due to the loss of immunosuppressive activity resulting in unleashed effector T-cell responses. Secondly, homeostatic macrophages were shown to be essential for maintaining pregnancy and promoting fetal development, and the adoptive transfer of homeostatic M2-polarized macrophages shows great promise for preventing inflammation-induced preterm birth. Collectively, in this review, we discuss the established and novel immune mechanisms responsible for preterm birth and highlight the potential targets for novel strategies aimed at preventing the multi-etiological syndrome of preterm labor leading to preterm birth.
