Expression of Fibroblast Growth Factors (FGF) and FGF Receptor (FGFR) in the Horse Placenta
Identifieur interne : 001668 ( Istex/Corpus ); précédent : 001667; suivant : 001669Expression of Fibroblast Growth Factors (FGF) and FGF Receptor (FGFR) in the Horse Placenta
Auteurs : C. Pfarrer ; M. Abd-Elnaeim ; W. R. Allen ; S. Wilsher ; D. Schams ; R. LeiserSource :
- Anatomia, Histologia, Embryologia [ 0340-2096 ] ; 2005-12.
Abstract
Members of the fibroblast growth factor family have been shown to stimulate angiogenesis and cell differentiation during embryogenesis and invasive haemochorial placentation. The non‐invasive epitheliochorial horse placenta is characterized by the occurrence of specialized areolae between the microcotyledons, where secretions of endometrial glands are imbibed by the pseudostratified trophoblast cells throughout gestation. Therefore, we hypothesize that trophoblast cells may be programmed differently depending on their location and function. The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. These would represent the classic FGFR binding isoforms that may be involved in angiogenesis mediated by auto‐ and paracrine mechanisms.
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DOI: 10.1111/j.1439-0264.2005.00669_89.x
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The non‐invasive epitheliochorial horse placenta is characterized by the occurrence of specialized areolae between the microcotyledons, where secretions of endometrial glands are imbibed by the pseudostratified trophoblast cells throughout gestation. Therefore, we hypothesize that trophoblast cells may be programmed differently depending on their location and function. The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. These would represent the classic FGFR binding isoforms that may be involved in angiogenesis mediated by auto‐ and paracrine mechanisms.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>C. Pfarrer</name><affiliations><json:string>Department of Veterinary Anatomy, Histology & Embryology, Justus‐Liebig‐University Giessen, Frankfurter Str. 98, Giessen, Germany</json:string></affiliations></json:item><json:item><name>M. 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The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. 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The non‐invasive epitheliochorial horse placenta is characterized by the occurrence of specialized areolae between the microcotyledons, where secretions of endometrial glands are imbibed by the pseudostratified trophoblast cells throughout gestation. Therefore, we hypothesize that trophoblast cells may be programmed differently depending on their location and function. The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. 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The non‐invasive epitheliochorial horse placenta is characterized by the occurrence of specialized areolae between the microcotyledons, where secretions of endometrial glands are imbibed by the pseudostratified trophoblast cells throughout gestation. Therefore, we hypothesize that trophoblast cells may be programmed differently depending on their location and function. The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. These would represent the classic FGFR binding isoforms that may be involved in angiogenesis mediated by auto‐ and paracrine mechanisms.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Expression of Fibroblast Growth Factors (FGF) and FGF Receptor (FGFR) in the Horse Placenta</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abstracts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Expression of Fibroblast Growth Factors (FGF) and FGF Receptor (FGFR) in the Horse Placenta</title></titleInfo><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Pfarrer</namePart><affiliation>Department of Veterinary Anatomy, Histology & Embryology, Justus‐Liebig‐University Giessen, Frankfurter Str. 98, Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Abd‐Elnaeim</namePart><affiliation>Department of Anatomy & Histology, Faculty of Veterinary Medicine, Assiut University, Egypt</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W. R.</namePart><namePart type="family">Allen</namePart><affiliation>Department of Clinical Veterinary Medicine, University of Cambridge, Mertoun Paddocks, Newmarket, Suffolk, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Wilsher</namePart><affiliation>Department of Clinical Veterinary Medicine, University of Cambridge, Mertoun Paddocks, Newmarket, Suffolk, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Schams</namePart><affiliation>Institute of Physiology, Technical University Munich‐Weihenstephan, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Leiser</namePart><affiliation>Department of Veterinary Anatomy, Histology & Embryology, Justus‐Liebig‐University Giessen, Frankfurter Str. 98, Giessen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Blackwell Verlag GmbH</publisher><place><placeTerm type="text">Berlin, Germany</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Members of the fibroblast growth factor family have been shown to stimulate angiogenesis and cell differentiation during embryogenesis and invasive haemochorial placentation. The non‐invasive epitheliochorial horse placenta is characterized by the occurrence of specialized areolae between the microcotyledons, where secretions of endometrial glands are imbibed by the pseudostratified trophoblast cells throughout gestation. Therefore, we hypothesize that trophoblast cells may be programmed differently depending on their location and function. The influence of FGF family members during placentation in the mare was evaluated in tissues from five mares at days 110, 121, 179, 199, and 309 of gestation. Placental samples were perfusion‐fixed and paraffin‐embedded, and immunohistochemistry was performed with antibodies against FGF1 and FGF2 (which have been shown to influence cells of mesenchymal origin), FGF7 which acts on epithelial cells, and an antibody against FGFR which recognizes various receptor isoforms. FGF1 immunostaining occurred in most cells of the placenta throughout gestation, with the strongest expression in vascular structures. FGF2 protein expression differed in relation to location and stage of gestation. Trophoblast and endometrial epithelial cells in the microcotyledons showed strong nuclear expression, whereas areolar trophoblast, fetal and maternal endothelial cells, and smooth muscle cells of large allantochorionic blood vessels all showed cytoplasmic localization of FGF2. Near term, on day 309, FGF2 expression ceased in all types of cells. FGF7 immunoreactivity was observed predominantly in the nuclei of endometrial gland cells and the cytoplasm of trophoblast cells, and to a lesser extent in the endometrial epithelium. FGFR immunoreaction occurred almost exclusively in vascular cells, such as the endothelium and smooth muscle cells of large blood vessels, and staining declined towards term. The nuclear localization of FGF2 and FGF7 suggests the presence of high molecular weight isoforms, which have been shown to be involved in specific autocrine transcription processes, like activation of endometrial glands and differentiation of trophoblast cells. In contrast, the cytoplasmic localization of FGFs indicates the presence of low molecular weight isoforms. These would represent the classic FGFR binding isoforms that may be involved in angiogenesis mediated by auto‐ and paracrine mechanisms.</abstract><relatedItem type="host"><titleInfo><title>Anatomia, Histologia, Embryologia</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0340-2096</identifier><identifier type="eISSN">1439-0264</identifier><identifier type="DOI">10.1111/(ISSN)1439-0264</identifier><identifier type="PublisherID">AHE</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>34</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>39</start><end>40</end></extent></part></relatedItem><identifier type="istex">6D954CD82CAA1E3BC453B55BA995C1797D8A8EC0</identifier><identifier type="DOI">10.1111/j.1439-0264.2005.00669_89.x</identifier><identifier type="ArticleID">AHE669_89_89</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Verlag GmbH</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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