Potentiation of the Maternal Immune System may Modify the Apoptotic Process in Embryos Exposed to Developmental Toxicants

PROBLEM: We have previously shown that teratogen‐induced embryonic maldevelopment may result from excessive apoptosis in affected organs, but the mechanisms underlying this process are not well understood. Here we investigate the ability of maternal immunopotentiation to affect the apoptotic process...

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Veröffentlicht in:American journal of reproductive immunology (1989) 2003-01, Vol.49 (1), p.30-41
Hauptverfasser: Savion, Shoshana, Kamshitsky-Feldman, Anna, Ivnitsky, Irena, Orenstein, Hasida, Shepshelovich, Jeanne, Carp, Howard, Fein, Amos, Torchinsky, Arkady, Toder, Vladimir
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container_issue 1
container_start_page 30
container_title American journal of reproductive immunology (1989)
container_volume 49
creator Savion, Shoshana
Kamshitsky-Feldman, Anna
Ivnitsky, Irena
Orenstein, Hasida
Shepshelovich, Jeanne
Carp, Howard
Fein, Amos
Torchinsky, Arkady
Toder, Vladimir
description PROBLEM: We have previously shown that teratogen‐induced embryonic maldevelopment may result from excessive apoptosis in affected organs, but the mechanisms underlying this process are not well understood. Here we investigate the ability of maternal immunopotentiation to affect the apoptotic process and its regulatory genes p53 and bcl‐2 in embryos exposed to a teratogenic insult. METHOD OF STUDY: Potentiation of the immune system in pregnant females was performed with xenogeneic rat splenocytes or with granulocyte macrophage‐colony stimulating factor (GM‐CSF). The animals were exposed to cyclophosphamide (CP) and the reproductive performance in the various experimental groups was recorded. The level of apoptosis was assessed in the embryonic head and liver by TdT‐mediated dUTP‐biotin nick end labeling and fluorescence‐activated cell sorter (FACS) analysis, while p53 and bcl‐2 expression was evaluated by FACS and immunohistochemistry. RESULTS: In CP‐treated females, a decrease in embryonic weight and an increase in the resorption rate and the percentage of embryos exhibiting head malformations were noted. These effects of CP were accompanied by the appearance of apoptotic cells in the head but not in the liver and an increased expression of p53 in embryonic organs, while bcl‐2 expression was found to be decreased in the head and increased in the liver. Immunopotentiation with rat splenocytes or GM‐CSF was shown to partially normalize the teratogenic effect of CP. It was also found to partially decrease the CP‐induced apoptotic process and exhibited a tendency to normalize the expression of p53 and bcl‐2 in the embryonic head and liver. CONCLUSION: Our results suggest a possible role for maternal immunopotentiation in protecting the embryo from teratogenic insults, possibly through regulation of the CP‐induced apoptotic process and the expression of p53 and bcl‐2.
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Here we investigate the ability of maternal immunopotentiation to affect the apoptotic process and its regulatory genes p53 and bcl‐2 in embryos exposed to a teratogenic insult. METHOD OF STUDY: Potentiation of the immune system in pregnant females was performed with xenogeneic rat splenocytes or with granulocyte macrophage‐colony stimulating factor (GM‐CSF). The animals were exposed to cyclophosphamide (CP) and the reproductive performance in the various experimental groups was recorded. The level of apoptosis was assessed in the embryonic head and liver by TdT‐mediated dUTP‐biotin nick end labeling and fluorescence‐activated cell sorter (FACS) analysis, while p53 and bcl‐2 expression was evaluated by FACS and immunohistochemistry. RESULTS: In CP‐treated females, a decrease in embryonic weight and an increase in the resorption rate and the percentage of embryos exhibiting head malformations were noted. These effects of CP were accompanied by the appearance of apoptotic cells in the head but not in the liver and an increased expression of p53 in embryonic organs, while bcl‐2 expression was found to be decreased in the head and increased in the liver. Immunopotentiation with rat splenocytes or GM‐CSF was shown to partially normalize the teratogenic effect of CP. It was also found to partially decrease the CP‐induced apoptotic process and exhibited a tendency to normalize the expression of p53 and bcl‐2 in the embryonic head and liver. 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Here we investigate the ability of maternal immunopotentiation to affect the apoptotic process and its regulatory genes p53 and bcl‐2 in embryos exposed to a teratogenic insult. METHOD OF STUDY: Potentiation of the immune system in pregnant females was performed with xenogeneic rat splenocytes or with granulocyte macrophage‐colony stimulating factor (GM‐CSF). The animals were exposed to cyclophosphamide (CP) and the reproductive performance in the various experimental groups was recorded. The level of apoptosis was assessed in the embryonic head and liver by TdT‐mediated dUTP‐biotin nick end labeling and fluorescence‐activated cell sorter (FACS) analysis, while p53 and bcl‐2 expression was evaluated by FACS and immunohistochemistry. RESULTS: In CP‐treated females, a decrease in embryonic weight and an increase in the resorption rate and the percentage of embryos exhibiting head malformations were noted. These effects of CP were accompanied by the appearance of apoptotic cells in the head but not in the liver and an increased expression of p53 in embryonic organs, while bcl‐2 expression was found to be decreased in the head and increased in the liver. Immunopotentiation with rat splenocytes or GM‐CSF was shown to partially normalize the teratogenic effect of CP. It was also found to partially decrease the CP‐induced apoptotic process and exhibited a tendency to normalize the expression of p53 and bcl‐2 in the embryonic head and liver. CONCLUSION: Our results suggest a possible role for maternal immunopotentiation in protecting the embryo from teratogenic insults, possibly through regulation of the CP‐induced apoptotic process and the expression of p53 and bcl‐2.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - immunology</subject><subject>bcl-2</subject><subject>Biological and medical sciences</subject><subject>Cyclophosphamide - pharmacology</subject><subject>Embryo, Mammalian - drug effects</subject><subject>Embryo, Mammalian - immunology</subject><subject>Embryo, Mammalian - metabolism</subject><subject>Embryology: invertebrates and vertebrates. Teratology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GM-CSF</subject><subject>Immune System - drug effects</subject><subject>Immune System - immunology</subject><subject>immunopotentiation</subject><subject>Male</subject><subject>Maternal-Fetal Exchange - drug effects</subject><subject>Maternal-Fetal Exchange - immunology</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>p53</subject><subject>Pregnancy</subject><subject>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>teratogenicity</subject><subject>Teratogens - toxicity</subject><subject>Teratology. Teratogens</subject><subject>Tumor Suppressor Protein p53 - biosynthesis</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>1046-7408</issn><issn>8755-8920</issn><issn>1600-0897</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU1v1DAQhiMEoqXwF5AvcEsYf-TrgrQq22VRSytRxNFykrHwksTB9kLy7_F2V-2Vk8f2M-9Yj5OEUMgocPFhl9ECIIWqLjMGwDOgVEA2P0vOHy-exxpEkZYCqrPklfc7gHjOy5fJGWUl53nNzpPlzgYcg1HB2JFYTcJPJDcqoBtVT7bDsB-RfFt8wIEMaiE3tjN6eaBWk52CDaYld8626D0xI1kPjVusJ-t5sh47Eiz5hH-wt9MQx8TIezubVo3Bv05eaNV7fHNaL5LvV-v7y8_p9e1me7m6TtucU0hFXudY1brrOkrLKkcKTYVKcw61xpLrrsGuYp1oCs0qzAtWCKFaVULcsrbiF8n7Y-7k7O89-iAH41vsezWi3XtJqzKHImcRrI5g66z3DrWcnBmUWyQFedAud_JgVx7syoN2-aBdzrH17WnGvhmwe2o8eY7AuxOgfKt67dTYGv_EiYIxATxyH4_cX9Pj8t8PkKsvW3obyxiQHgNM_LL5MUC5X7IoeZnLH183km0E1Fd8Iwv-D7Vsrog</recordid><startdate>200301</startdate><enddate>200301</enddate><creator>Savion, Shoshana</creator><creator>Kamshitsky-Feldman, Anna</creator><creator>Ivnitsky, Irena</creator><creator>Orenstein, Hasida</creator><creator>Shepshelovich, Jeanne</creator><creator>Carp, Howard</creator><creator>Fein, Amos</creator><creator>Torchinsky, Arkady</creator><creator>Toder, Vladimir</creator><general>Munksgaard International Publishers</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>200301</creationdate><title>Potentiation of the Maternal Immune System may Modify the Apoptotic Process in Embryos Exposed to Developmental Toxicants</title><author>Savion, Shoshana ; Kamshitsky-Feldman, Anna ; Ivnitsky, Irena ; Orenstein, Hasida ; Shepshelovich, Jeanne ; Carp, Howard ; Fein, Amos ; Torchinsky, Arkady ; Toder, Vladimir</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5310-4595e89fddd11785e10b8eaf3309fe73fdbed82d4b6f28e562644aca70f282c83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - immunology</topic><topic>bcl-2</topic><topic>Biological and medical sciences</topic><topic>Cyclophosphamide - pharmacology</topic><topic>Embryo, Mammalian - drug effects</topic><topic>Embryo, Mammalian - immunology</topic><topic>Embryo, Mammalian - metabolism</topic><topic>Embryology: invertebrates and vertebrates. Teratology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GM-CSF</topic><topic>Immune System - drug effects</topic><topic>Immune System - immunology</topic><topic>immunopotentiation</topic><topic>Male</topic><topic>Maternal-Fetal Exchange - drug effects</topic><topic>Maternal-Fetal Exchange - immunology</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>p53</topic><topic>Pregnancy</topic><topic>Proto-Oncogene Proteins c-bcl-2 - biosynthesis</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>teratogenicity</topic><topic>Teratogens - toxicity</topic><topic>Teratology. Teratogens</topic><topic>Tumor Suppressor Protein p53 - biosynthesis</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Savion, Shoshana</creatorcontrib><creatorcontrib>Kamshitsky-Feldman, Anna</creatorcontrib><creatorcontrib>Ivnitsky, Irena</creatorcontrib><creatorcontrib>Orenstein, Hasida</creatorcontrib><creatorcontrib>Shepshelovich, Jeanne</creatorcontrib><creatorcontrib>Carp, Howard</creatorcontrib><creatorcontrib>Fein, Amos</creatorcontrib><creatorcontrib>Torchinsky, Arkady</creatorcontrib><creatorcontrib>Toder, Vladimir</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>American journal of reproductive immunology (1989)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Savion, Shoshana</au><au>Kamshitsky-Feldman, Anna</au><au>Ivnitsky, Irena</au><au>Orenstein, Hasida</au><au>Shepshelovich, Jeanne</au><au>Carp, Howard</au><au>Fein, Amos</au><au>Torchinsky, Arkady</au><au>Toder, Vladimir</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potentiation of the Maternal Immune System may Modify the Apoptotic Process in Embryos Exposed to Developmental Toxicants</atitle><jtitle>American journal of reproductive immunology (1989)</jtitle><addtitle>Am J Reprod Immunol</addtitle><date>2003-01</date><risdate>2003</risdate><volume>49</volume><issue>1</issue><spage>30</spage><epage>41</epage><pages>30-41</pages><issn>1046-7408</issn><issn>8755-8920</issn><eissn>1600-0897</eissn><abstract>PROBLEM: We have previously shown that teratogen‐induced embryonic maldevelopment may result from excessive apoptosis in affected organs, but the mechanisms underlying this process are not well understood. Here we investigate the ability of maternal immunopotentiation to affect the apoptotic process and its regulatory genes p53 and bcl‐2 in embryos exposed to a teratogenic insult. METHOD OF STUDY: Potentiation of the immune system in pregnant females was performed with xenogeneic rat splenocytes or with granulocyte macrophage‐colony stimulating factor (GM‐CSF). The animals were exposed to cyclophosphamide (CP) and the reproductive performance in the various experimental groups was recorded. The level of apoptosis was assessed in the embryonic head and liver by TdT‐mediated dUTP‐biotin nick end labeling and fluorescence‐activated cell sorter (FACS) analysis, while p53 and bcl‐2 expression was evaluated by FACS and immunohistochemistry. RESULTS: In CP‐treated females, a decrease in embryonic weight and an increase in the resorption rate and the percentage of embryos exhibiting head malformations were noted. These effects of CP were accompanied by the appearance of apoptotic cells in the head but not in the liver and an increased expression of p53 in embryonic organs, while bcl‐2 expression was found to be decreased in the head and increased in the liver. Immunopotentiation with rat splenocytes or GM‐CSF was shown to partially normalize the teratogenic effect of CP. It was also found to partially decrease the CP‐induced apoptotic process and exhibited a tendency to normalize the expression of p53 and bcl‐2 in the embryonic head and liver. CONCLUSION: Our results suggest a possible role for maternal immunopotentiation in protecting the embryo from teratogenic insults, possibly through regulation of the CP‐induced apoptotic process and the expression of p53 and bcl‐2.</abstract><cop>Oxford, UK</cop><pub>Munksgaard International Publishers</pub><pmid>12733592</pmid><doi>10.1034/j.1600-0897.2003.01140.x</doi><tpages>12</tpages></addata></record>
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identifier ISSN: 1046-7408
ispartof American journal of reproductive immunology (1989), 2003-01, Vol.49 (1), p.30-41
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source MEDLINE; Wiley Online Library Journals Frontfile Complete
subjects Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - immunology
bcl-2
Biological and medical sciences
Cyclophosphamide - pharmacology
Embryo, Mammalian - drug effects
Embryo, Mammalian - immunology
Embryo, Mammalian - metabolism
Embryology: invertebrates and vertebrates. Teratology
Female
Fundamental and applied biological sciences. Psychology
GM-CSF
Immune System - drug effects
Immune System - immunology
immunopotentiation
Male
Maternal-Fetal Exchange - drug effects
Maternal-Fetal Exchange - immunology
Mice
Mice, Inbred ICR
p53
Pregnancy
Proto-Oncogene Proteins c-bcl-2 - biosynthesis
Proto-Oncogene Proteins c-bcl-2 - genetics
Rats
Rats, Long-Evans
teratogenicity
Teratogens - toxicity
Teratology. Teratogens
Tumor Suppressor Protein p53 - biosynthesis
Tumor Suppressor Protein p53 - genetics
title Potentiation of the Maternal Immune System may Modify the Apoptotic Process in Embryos Exposed to Developmental Toxicants
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