Vaccinia virus infection of cultured human trophoblast

Vaccinia virus infection of cultured human trophoblast

A.40 Placenta (1992), bl LOCALIZATION OF ANTI-HIV MONOCLONAL ANTIBODY REACTIVITY IN NORMAL TROPHOBIAST DURING DEVELOPMENT. T.W. Lyden, P.M. Johnson,...

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A.40

Placenta (1992), bl

LOCALIZATION OF ANTI-HIV MONOCLONAL ANTIBODY REACTIVITY IN NORMAL TROPHOBIAST DURING DEVELOPMENT. T.W. Lyden, P.M. Johnson, J.M. Mwenda and N.S. Rote. Department of Microbiology and Immunology, Wright State University, Dayton Ohio, U.S.A., and Pregnancy Immunology Group, University of Liverpool, Liverpool UK. The differentiation related expression of endogenous retrovirus (ERV) proviral sequences is well documented in the literature. ERV particles have been associated with the normal human and primate placenta by electron microscopy and molecular biology. Based on analysis of potential cross-reactive sites between HERV-3 and HIV, as well as recent reports of HIV-related proviral sequences within the human genome, we have studied the distribution of HIV cross-reactive antigens within normal noninfected human placenta. This study employed a library of anti-HIV antibodies, as well as both positive and negative controls. Two of these anti-HIV antibodies (gp 120 and ~17, AMAC, Inc.) were found to specifically react with normal non-infected human placenta. In first trimester CVS samples a restricted but intense pattern of trophoblast reactivity was observed with both pl7 and gp 120. This reactivity was often cytoplasmic but in many regions became restricted to the apical surface of the cytotrophoblast or the basal aspect of the syncytium. This type of labeling was particularly clear in smaller villi and in regions that appear to be undergoing cytotrophoblast differentiation. Second and third trimester samples showed a high degree of reactivity with anti-HIV p17 in the cytotrophoblast cells. The syncytium had highly restricted cytoplasmic regions which display low activity. Anti-HIV gp120 showed similar patterns of localization in these samples with the overall intensity being lower and the syncytium being less reactive. These data suggest that endogenous placental proteins which are localized to the region associated with trophoblast fusion are cross-reactive with two specific anti-HIV monoclonal antibodies

FUh’CTIONAL ROLE OF COLONY SZIMULATING FACTOR (CSF) - 1 ON NORMAL AND MALIGNANT HUMAN TROPHOBLAST CELLS. Jeff Lysiak’, Nelson I&o’, Ian Connelly’, William Stettler-Stevenson2 and Peeyush Lala’. ‘De artment of Anatomy, University of Western Ontario, London, ON. Canada, N6A X1, and % boratory of Pathology, NCI, Bethesda, MD.

The effects of CSF-1 on the proliferation, KG production and mRNA expression of invasion ating roteins (tissue inhibitor of metalloprotease TIMP 1, TIMP2 and 72 kD type IV co lagenase Yb { normal human first trimester trophoblast & T) ccl1s and two choriocarcinomas (JAR reYd and JEG3) ccl lines were investigated. Proliferative responses were measured from ‘H-TdR uptake after an 8h pulse in cells cubured for 24h in the presence or absence of CSF-1 (10 ng/ml). HT, JAR and JEG3 cells were cultured in the presence or absence of CSF-1 (10 ng/ml) for 24h for the collection of 1) conditioned media, assayed for hCG production by RIA and 2) total RNA, for Northern blot analysis of the invasion regulatory genes. Results revealed that the presence of exogenous CSF-1 had no effect on the proliferation of normal or malignant trophoblast cells. hCG reduction b JAR and JEG3 cells also remained uneffected. Addition of CSF-1 had no effect on # MP1 or T? MP2 mRNA levels but did enhance the 72 kD type IV collagenase mRNA expressed by the normal trophoblast cells. In the choriocarcinomas TIMPl mRNA was undetectable; however, the 1.0 kb TIIvlP2 message was upregulated in JEG3 cells treated with CSF-1. The 72 kD collagenase mRNA remained unchanged in treated JAR cells. Thus, CSF-1 appears to have no effect on normal or malignant trophoblast cell proliferation; it may have an invasion regulatory function which remains to be tested further. (Supported by the MRC and NC1 Canada).

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