Immunohistochemical Localization of Gastrin‐releasing Peptide, Neuronal Nitric Oxide Synthase and Neurone‐specific Enolase in the Uterus of the North American Opossum, <i>Didelphis virginiana</i>

Kumano, Aiko; Sasaki, Motoki; Budipitojo, Teguh; Kitamura, Nobuo; Krause, William J.; Yamada, Junzo

doi:10.1111/j.1439-0264.2005.00604.x

Cited by 2 publications

(1 citation statement)

References 32 publications

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“…36 Studies on marsupials have detected enolase expression on endothelial cells and have suggested its role in placentation. 37 As a result, anti-α-enolase antibodies may interfere with inflammatory environment in endometrium required for implantation and cause infertility thereby. Although α-enolase is discussed here as an AEA antigen, these antibodies are also involved in systemic autoimmune diseases as well as many inflammatory and degenerative diseases.…”

Section: Antiendometrial Autoantibodies In Its Limited Approachmentioning

confidence: 99%

Autoimmune Activation toward Embryo Implantation is Rare in Immune-Privileged Human Endometrium

et al. 2014

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Human embryo implantation represents embryo apposition, adhesion to the endometrial epithelium, and invasion into the stromal extracellular matrix within 1 to 2 days during days 6 to 9 after ovulation. The major molecular mechanisms mediating implantation include adhesion molecules, including mucins, selectins, integrins, and cadherins; extracellular matrix components, such as laminins and collagens and their degrading enzymes; phospholipids and immune regulatory molecules, including prostaglandins, cytokines; and immunosuppressive molecules expressed by invasive trophoblasts and endometrial cells. Many of these molecules are the targets for autoimmune reactions in autoimmune diseases and cancer; however, the relevance of those in immune-mediated implantation failure has not been defined. In this review, we will describe the molecules involved in 2-day event of human embryo implantation, which may also be involved in immune system activation and subsequently cause immune-mediated implantation failure. We speculate that the data in the literature are limited concerning antiendometrial antibodies because the endometrium might be taken as an immune-privileged site that avoids autoimmune activation that might harm the implantation process. Antibodies affecting human fertility in ways other than impairing implantation are outside the scope of the current article and will not be discussed.

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Section: Antiendometrial Autoantibodies In Its Limited Approachmentioning

confidence: 99%

Autoimmune Activation toward Embryo Implantation is Rare in Immune-Privileged Human Endometrium

et al. 2014

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Conditional knockout of leptin receptor in the female reproductive tract reduces fertility due to parturition defects in mice

Kathleen

Arin

Kylie

et al. 2022

Biology of Reproduction

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Leptin is required for fertility, including initiation of estrous cycles. It is therefore challenging to assess the role of leptin signaling during pregnancy. While neuron-specific transgene approaches suggest that leptin signaling in the central nervous system is most important, experiments with pharmacologic inhibition of leptin in the uterus or global replacement of leptin during pregnancy suggest leptin signaling in the reproductive tract may be required. Here, conditional leptin receptor knockout (Lepr cKO) with a progesterone receptor-driven Cre recombinase was used to examine the importance of leptin signaling in pregnancy. Lepr cKO mice have almost no leptin receptor in uterus or cervix, and slightly reduced leptin receptor levels in corpus luteum. Estrous cycles and progesterone concentrations were not affected by Lepr cKO. Numbers of viable embryos did not differ between primiparous control and Lepr cKO dams on days 6.5 and 17.5 of pregnancy, despite a slight reduction in the ratio of embryos to corpora lutea, showing that uterine leptin receptor signaling is not required for embryo implantation. Placentas of Lepr cKO dams had normal weight and structure. However, over four parities, Lepr cKO mice produced 22% fewer live pups than controls, and took more time from pairing to delivery by their fourth parity. Abnormal birth outcomes of either dystocia or dead pups occurred in 33% of Lepr cKO deliveries but zero control deliveries, and the average time to deliver each pup after crouching was significantly increased. Thus, leptin receptor signaling in the reproductive tract is required for normal labor and delivery. Summary sentence. Mice lacking leptin receptor in the reproductive tract produce fewer live pups and have more adverse labor outcomes than controls, but normal numbers of embryos near term, showing that leptin receptor signaling is required for normal parturition.

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Immunohistochemical Localization of Gastrin‐releasing Peptide, Neuronal Nitric Oxide Synthase and Neurone‐specific Enolase in the Uterus of the North American Opossum, Didelphis virginiana

Cited by 2 publications

References 32 publications

Autoimmune Activation toward Embryo Implantation is Rare in Immune-Privileged Human Endometrium

Autoimmune Activation toward Embryo Implantation is Rare in Immune-Privileged Human Endometrium

Conditional knockout of leptin receptor in the female reproductive tract reduces fertility due to parturition defects in mice

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