Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes
Background Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the ef...
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| Veröffentlicht in: | Molecular biology reports 2022-07, Vol.49 (7), p.5831-5842 |
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| creator | Kobayashi, Tsukasa Takeba, Yuko Ohta, Yuki Ootaki, Masanori Kida, Keisuke Watanabe, Minoru Iiri, Taroh Matsumoto, Naoki |
| description | Background
Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration on the maturation of liver hepatocytes in preterm rats.
Methods and results
Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), hepatocyte growth factor (HGF), thymus cell antigen 1 (Thy-1), cyclin B, and Cyclin-dependent kinase 1 (CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production. The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.
Conclusions
The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in preterm fetuses. |
| doi_str_mv | 10.1007/s11033-022-07358-5 |
| format | Article |
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Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration on the maturation of liver hepatocytes in preterm rats.
Methods and results
Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), hepatocyte growth factor (HGF), thymus cell antigen 1 (Thy-1), cyclin B, and Cyclin-dependent kinase 1 (CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production. The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.
Conclusions
The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in preterm fetuses.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-022-07358-5</identifier><identifier>PMID: 35304682</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Albumin ; Animal Anatomy ; Animal Biochemistry ; Biomedical and Life Sciences ; Birth ; Cell cycle ; Cesarean section ; Cyclin B ; Cyclin-dependent kinases ; Dexamethasone ; Enzyme-linked immunosorbent assay ; Fetuses ; Glucocorticoids ; Hepatocyte growth factor ; Hepatocytes ; Histology ; Life Sciences ; Liver ; Liver diseases ; Low birth weight ; Maturation ; Morphology ; Original Article ; Polymerase chain reaction ; Premature birth ; Reverse transcription</subject><ispartof>Molecular biology reports, 2022-07, Vol.49 (7), p.5831-5842</ispartof><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer Nature B.V.</rights><rights>The Author(s), under exclusive licence to Springer Nature B.V. 2022.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-d0a57efbde12c34e23a9e8205d32a8bd083e7535c2b96466113e9b6491e3d1643</citedby><cites>FETCH-LOGICAL-c419t-d0a57efbde12c34e23a9e8205d32a8bd083e7535c2b96466113e9b6491e3d1643</cites><orcidid>0000-0002-9871-169X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-022-07358-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-022-07358-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35304682$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kobayashi, Tsukasa</creatorcontrib><creatorcontrib>Takeba, Yuko</creatorcontrib><creatorcontrib>Ohta, Yuki</creatorcontrib><creatorcontrib>Ootaki, Masanori</creatorcontrib><creatorcontrib>Kida, Keisuke</creatorcontrib><creatorcontrib>Watanabe, Minoru</creatorcontrib><creatorcontrib>Iiri, Taroh</creatorcontrib><creatorcontrib>Matsumoto, Naoki</creatorcontrib><title>Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Background
Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration on the maturation of liver hepatocytes in preterm rats.
Methods and results
Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), hepatocyte growth factor (HGF), thymus cell antigen 1 (Thy-1), cyclin B, and Cyclin-dependent kinase 1 (CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production. The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.
Conclusions
The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in preterm fetuses.</description><subject>Albumin</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Birth</subject><subject>Cell cycle</subject><subject>Cesarean section</subject><subject>Cyclin B</subject><subject>Cyclin-dependent kinases</subject><subject>Dexamethasone</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fetuses</subject><subject>Glucocorticoids</subject><subject>Hepatocyte growth factor</subject><subject>Hepatocytes</subject><subject>Histology</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver diseases</subject><subject>Low birth weight</subject><subject>Maturation</subject><subject>Morphology</subject><subject>Original Article</subject><subject>Polymerase chain reaction</subject><subject>Premature birth</subject><subject>Reverse transcription</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kD1v2zAQhomgReM4_QMZCgFduqg9fonUGBhJG8BAOjRLFoKiTrYCSXRIavC_Dx27DZCh0-Fwz713eAi5ovCdAqgfkVLgvATGSlBc6lKekQWVipeiVvoDWQAHWgot6Tm5iPEJAARV8hM555KDqDRbkMffASeb7FBshtl550Pqne_bwrZjP_UxBZt6PxXWORwwNxiLtMVitGk-jXxXdHhIyH2xxZ1N3u0zd0k-dnaI-PlUl-Th9ubP6le5vv95t7pel07QOpUtWKmwa1qkzHGBjNsaNQPZcmZ104LmqCSXjjV1JaqKUo51U4maIm9pJfiSfDvm7oJ_njEmM_YxfzvYCf0cDasE1LVSTGX06zv0yc9hyt9lSucsphXNFDtSLvgYA3ZmF_rRhr2hYA7mzdG8yebNq3kj89KXU_TcjNj-W_mrOgP8CMQ8mjYY3m7_J_YFDUSOuQ</recordid><startdate>20220701</startdate><enddate>20220701</enddate><creator>Kobayashi, Tsukasa</creator><creator>Takeba, Yuko</creator><creator>Ohta, Yuki</creator><creator>Ootaki, Masanori</creator><creator>Kida, Keisuke</creator><creator>Watanabe, Minoru</creator><creator>Iiri, Taroh</creator><creator>Matsumoto, Naoki</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9871-169X</orcidid></search><sort><creationdate>20220701</creationdate><title>Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes</title><author>Kobayashi, Tsukasa ; Takeba, Yuko ; Ohta, Yuki ; Ootaki, Masanori ; Kida, Keisuke ; Watanabe, Minoru ; Iiri, Taroh ; Matsumoto, Naoki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-d0a57efbde12c34e23a9e8205d32a8bd083e7535c2b96466113e9b6491e3d1643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Albumin</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Birth</topic><topic>Cell cycle</topic><topic>Cesarean section</topic><topic>Cyclin B</topic><topic>Cyclin-dependent kinases</topic><topic>Dexamethasone</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fetuses</topic><topic>Glucocorticoids</topic><topic>Hepatocyte growth factor</topic><topic>Hepatocytes</topic><topic>Histology</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Liver diseases</topic><topic>Low birth weight</topic><topic>Maturation</topic><topic>Morphology</topic><topic>Original Article</topic><topic>Polymerase chain reaction</topic><topic>Premature birth</topic><topic>Reverse transcription</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kobayashi, Tsukasa</creatorcontrib><creatorcontrib>Takeba, Yuko</creatorcontrib><creatorcontrib>Ohta, Yuki</creatorcontrib><creatorcontrib>Ootaki, Masanori</creatorcontrib><creatorcontrib>Kida, Keisuke</creatorcontrib><creatorcontrib>Watanabe, Minoru</creatorcontrib><creatorcontrib>Iiri, Taroh</creatorcontrib><creatorcontrib>Matsumoto, Naoki</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kobayashi, Tsukasa</au><au>Takeba, Yuko</au><au>Ohta, Yuki</au><au>Ootaki, Masanori</au><au>Kida, Keisuke</au><au>Watanabe, Minoru</au><au>Iiri, Taroh</au><au>Matsumoto, Naoki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2022-07-01</date><risdate>2022</risdate><volume>49</volume><issue>7</issue><spage>5831</spage><epage>5842</epage><pages>5831-5842</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Background
Prenatal glucocorticoid (GC) is clinically administered to pregnant women who are at risk of preterm birth for the maturation of cardiopulmonary function. Preterm and low-birth-weight infants often experience liver dysfunction after birth because their livers are immature. However, the effects of prenatal GC administration on the liver remain unclear. We aimed to investigate the effects of prenatal GC administration on the maturation of liver hepatocytes in preterm rats.
Methods and results
Dexamethasone (DEX) was administered to pregnant Wistar rats on gestational days 17 and 19 before cesarean section. Real-time reverse transcription-polymerase chain reaction (RT-PCR) was performed to determine the mRNA levels of albumin, hepatocyte nuclear factor-4 alpha (HNF4α), hepatocyte growth factor (HGF), thymus cell antigen 1 (Thy-1), cyclin B, and Cyclin-dependent kinase 1 (CDK1) in the liver samples. Immunohistochemical staining and enzyme-linked immunosorbent assay were performed to examine protein production. The hepatocytes enlarged because of growth and prenatal DEX administration. Albumin, HNF4α, and HGF levels increased secondary to growth and prenatal DEX administration. The levels of the cell cycle markers cyclin B and CDK1 gradually decreased during growth and with DEX administration.
Conclusions
The results suggest that prenatal GC administration leads to hepatocyte maturation via expression of HNF4α and HGF in preterm fetuses.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>35304682</pmid><doi>10.1007/s11033-022-07358-5</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-9871-169X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Albumin Animal Anatomy Animal Biochemistry Biomedical and Life Sciences Birth Cell cycle Cesarean section Cyclin B Cyclin-dependent kinases Dexamethasone Enzyme-linked immunosorbent assay Fetuses Glucocorticoids Hepatocyte growth factor Hepatocytes Histology Life Sciences Liver Liver diseases Low birth weight Maturation Morphology Original Article Polymerase chain reaction Premature birth Reverse transcription |
| title | Prenatal glucocorticoid administration accelerates the maturation of fetal rat hepatocytes |
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