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      Identification of a novel mammalian post-translational modification, phosphocholine, on placental secretory polypeptides

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          Abstract

          Placental neurokinin B appears to be post-translationally modified by phosphocholine (PC) attached to the aspartyl side chain at residue 4 of the mature peptide. Corticotrophin releasing factor (CRF) was found to be expressed by the rat placenta with the main secreted forms being phosphocholinated proCRF+/− one or two polysaccharide moieties. A combination of high-pressure liquid chromatography (HPLC) and two-site immunometric analysis suggested that PC was also attached to the placental precursors of adrenocorticotrophin, hemokinin, activin and follistatin. However, the fully processed forms of rat placental activin and CRF were free of PC. Formerly, the parasitic filarial nematodes have used PC as a post-translational modification, attached via the polysaccharide moiety of certain secretory glycoproteins to attenuate the host immune system allowing parasite survival, but it is the PC group itself which endows the carrier with the biological activity. The fact that treatment of proCRF peptides with phospholipase C but not endoglycosidase destroyed PC immunoreactivity suggested a simpler mode of attachment of PC to placental peptides than that used by nematodes. Thus, it is possible that by analogy the placenta uses its secreted phosphocholinated hormones to modulate the mother's immune system and help protect the placenta from rejection.

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          Placental transport of immunoglobulin G

          N E Simister (2003)
          Maternal antibodies transported across the placenta protect the newborn. Maternal immunoglobulin G (IgG) concentrations in fetal blood increase from early in the second trimester through term, most antibodies being acquired during the third trimester. IgG1 is the most efficiently transported subclass and IgG2 the least. Transfer across the syncytiotrophoblast of the chorionic villi is mediated by the neonatal Fc receptor, FcRn. Immune complexes are absorbed in the stroma of the villi, probably by FcgammaRI, FcgammaRII, and FcgammaRIII on placental macrophages. The mechanism of IgG transport across the endothelium of fetal capillaries is not understood. Endothelial cells in terminal villi express FcgammaRIIb. However, it is not known whether this receptor transports IgG or prevents transport of immune complexes to the fetus.
          Article 0 comments Cited 189 times – based on 0 reviews     Review now
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            Testicular macrophage modulation of Leydig cell steroidogenesis.

            Dale Hales (2015)
            This review will highlight recent advances in the study of the immuno-endocrinology of the testis, in particular how macrophage-derived inflammatory mediators affect Leydig cell functions. Both the beneficial and deleterious outcomes resulting from macrophage-Leydig cell interactions are discussed. A brief overview of testicular physiology is provided that discusses the functional and anatomical compartmentalization of the testis into the gamete and endocrine compartments where spermatogenesis and testosterone biosynthesis take place, respectively. The process of steroidogenesis including the activities of the steroidogenic enzymes and the role of steroidogenic acute regulatory protein (StAR) are described. The close physical association between Leydig cells and interstitial testicular macrophages suggests that these cells are functionally related. Under normal physiological and non-inflammatory conditions macrophages play an important role in Leydig cell development. If macrophages are absent from the testicular interstitium, Leydig cells fail to develop normally, which suggest that macrophages provide essential growth and differentiation factors for Leydig cells. In contrast, when macrophages are activated and elaborate inflammatory mediators, Leydig cell steroidogenesis is inhibited. Activated macrophages produce pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) that are profoundly inhibitory to Leydig cells and appear to act as transcriptional repressors of steroidogenic enzyme gene expression. Macrophages also produce reactive oxygen species (ROS) such as hydrogen peroxide, which also inhibits Leydig cell functions. ROS appear to act acutely by perturbing Leydig cell mitochondria resulting in the inhibition of StAR protein expression. One important consequence of this immune modulation of Leydig cell function may be manifest behaviorally by switching the affected animal from 'testosterone' behavior, to 'sickness' behavior. Increased interest in immune-endocrine control of reproductive function over the past decade has stimulated research into the molecular and biochemical immunopathophysiology of the reproductive system. As investigations unravel mechanisms underlying reproductive dysfunction caused by inflammation and infection, an understanding of the role that immune-endocrine interactions play in the normal physiology of the reproductive system has emerged.
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              Elevated C-reactive protein levels during first trimester of pregnancy are indicative of preeclampsia and intrauterine growth restriction.

              M.L. Tjoa, J.M.G. van Vugt, A.T.J.J. Go … (2003)
              C-reactive protein (CRP) is a marker of tissue damage and inflammation. Maternal levels of CRP are elevated in overt preeclampsia, but there is still debate about its use as a predictive marker for preeclampsia during the first and second trimesters of pregnancy. In this study, we measured CRP levels during the first trimester of pregnancy in women who later developed preeclampsia or gave birth to a growth-restricted baby. In total, 107 women from a low-risk population participated in the study, six women developed preeclampsia and nine gave birth to a growth-restricted baby. Although there is a large overlap in measured CRP levels between the three groups, mean CRP levels were significantly elevated in women who later developed preeclampsia (P=0.031) or delivered a growth-restricted baby (P=0.041) when compared with women from the control group, matched for maternal and gestational age, parity, and gravidity. This study shows that in a low-risk population, CRP levels are already elevated between weeks 10 and 14 in pregnant women who develop preeclampsia or deliver a growth-restricted baby.
              Article 0 comments Cited 41 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Mol Endocrinol
                Journal ID (publisher-id): JME
                Title: Journal of Molecular Endocrinology
                Publisher: BioScientifica (Bristol )
                ISSN (Print): 0952-5041
                ISSN (Electronic): 1479-6813
                Publication date (Print): September 2007
                Publication date (Electronic preprint): 24 July 2007
                Volume: 39
                Issue: 3
                Pages: 189-198
                Affiliations
                [1]simpleSchool of Biological Sciences, University of Reading Reading RG6 6AJUK
                [1 ]simpleDepartment of Obstetrics and Gynaecology, St George's Hospital London SW17 0QTUK
                [2 ]simpleBruker Daltonics Limited Coventry Coventry CV4 9GHUK
                [3 ]simpleNational Institute for Medical Research Mill Hill, London NW7 1AAUK
                Author notes
                (Correspondence should be addressed to P J Lowry; Email: p.j.lowry@ 123456reading.ac.uk )
                Article
                Publisher ID: JME070007
                DOI: 10.1677/JME-07-0007
                PMC ID: 2189575
                PubMed ID: 17766644
                SO-VID: b707681e-7c9f-4604-b87c-70611fde1edc
                Copyright © © 2007 Society for Endocrinology
                License:

                This is an Open Access article distributed under the terms of the Society for Endocrinology's Re-use Licence which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date revision received : 25 May 2007
                Date accepted : 24 July 2007
                Funding
                Funded by: Wellcome Trust
                Categories
                Subject: Regular Papers

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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