In utero exposure to maternal diabetes impairs nephron progenitor differentiation
The incidence of diabetes mellitus has significantly increased among women of childbearing age, and it has been shown that prenatal exposure to maternal diabetes increases the risk of associated congenital anomalies of the kidney. Congenital anomalies of the kidney are among the leading causes of ch...
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| Veröffentlicht in: | American journal of physiology. Renal physiology 2019-11, Vol.317 (5), p.F1318-F1330 |
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| creator | Cerqueira, Débora M Hemker, Shelby L Bodnar, Andrew J Ortiz, Daniella M Oladipupo, Favour O Mukherjee, Elina Gong, Zhenwei Appolonia, Corynn Muzumdar, Radhika Sims-Lucas, Sunder Ho, Jacqueline |
| description | The incidence of diabetes mellitus has significantly increased among women of childbearing age, and it has been shown that prenatal exposure to maternal diabetes increases the risk of associated congenital anomalies of the kidney. Congenital anomalies of the kidney are among the leading causes of chronic kidney disease in children. To better understand the effect of maternal diabetes on kidney development, we analyzed wild-type offspring (DM_Exp) of diabetic
mice (Akita mice). DM_Exp mice at
have a reduction of ~20% in the total nephron number compared with controls, using the gold standard physical dissector/fractionator method. At the molecular level, the expression of the nephron progenitor markers sine oculis homeobox homolog 2 and
was increased in DM_Exp kidneys at
. Conversely, the number of early developing nephrons was diminished in DM_Exp kidneys. This was associated with decreased expression of the intracellular domain of Notch1 and the canonical Wnt target lymphoid enhancer binding factor 1. Together, these data suggest that the diabetic intrauterine environment impairs the differentiation of nephron progenitors into nephrons, possibly by perturbing the Notch and Wnt/β-catenin signaling pathways. |
| doi_str_mv | 10.1152/ajprenal.00204.2019 |
| format | Article |
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mice (Akita mice). DM_Exp mice at
have a reduction of ~20% in the total nephron number compared with controls, using the gold standard physical dissector/fractionator method. At the molecular level, the expression of the nephron progenitor markers sine oculis homeobox homolog 2 and
was increased in DM_Exp kidneys at
. Conversely, the number of early developing nephrons was diminished in DM_Exp kidneys. This was associated with decreased expression of the intracellular domain of Notch1 and the canonical Wnt target lymphoid enhancer binding factor 1. Together, these data suggest that the diabetic intrauterine environment impairs the differentiation of nephron progenitors into nephrons, possibly by perturbing the Notch and Wnt/β-catenin signaling pathways.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00204.2019</identifier><identifier>PMID: 31509011</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Animals, Newborn ; Cell Differentiation ; Diabetes, Gestational ; Female ; Genetic Predisposition to Disease ; Genotype ; Insulin - genetics ; Insulin - metabolism ; Insulin-Secreting Cells - physiology ; Male ; Mice ; Mutation ; Nephrons - growth & development ; Pregnancy ; Stem Cells - metabolism ; Transcription Factors - metabolism</subject><ispartof>American journal of physiology. Renal physiology, 2019-11, Vol.317 (5), p.F1318-F1330</ispartof><rights>Copyright © 2019 the American Physiological Society 2019 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-1b35824f818a79cbb8e61c7c6d5f8cff8fb0fa06c39a433587b7894d439953bd3</citedby><cites>FETCH-LOGICAL-c405t-1b35824f818a79cbb8e61c7c6d5f8cff8fb0fa06c39a433587b7894d439953bd3</cites><orcidid>0000-0001-7115-1381</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31509011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cerqueira, Débora M</creatorcontrib><creatorcontrib>Hemker, Shelby L</creatorcontrib><creatorcontrib>Bodnar, Andrew J</creatorcontrib><creatorcontrib>Ortiz, Daniella M</creatorcontrib><creatorcontrib>Oladipupo, Favour O</creatorcontrib><creatorcontrib>Mukherjee, Elina</creatorcontrib><creatorcontrib>Gong, Zhenwei</creatorcontrib><creatorcontrib>Appolonia, Corynn</creatorcontrib><creatorcontrib>Muzumdar, Radhika</creatorcontrib><creatorcontrib>Sims-Lucas, Sunder</creatorcontrib><creatorcontrib>Ho, Jacqueline</creatorcontrib><title>In utero exposure to maternal diabetes impairs nephron progenitor differentiation</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>The incidence of diabetes mellitus has significantly increased among women of childbearing age, and it has been shown that prenatal exposure to maternal diabetes increases the risk of associated congenital anomalies of the kidney. Congenital anomalies of the kidney are among the leading causes of chronic kidney disease in children. To better understand the effect of maternal diabetes on kidney development, we analyzed wild-type offspring (DM_Exp) of diabetic
mice (Akita mice). DM_Exp mice at
have a reduction of ~20% in the total nephron number compared with controls, using the gold standard physical dissector/fractionator method. At the molecular level, the expression of the nephron progenitor markers sine oculis homeobox homolog 2 and
was increased in DM_Exp kidneys at
. Conversely, the number of early developing nephrons was diminished in DM_Exp kidneys. This was associated with decreased expression of the intracellular domain of Notch1 and the canonical Wnt target lymphoid enhancer binding factor 1. Together, these data suggest that the diabetic intrauterine environment impairs the differentiation of nephron progenitors into nephrons, possibly by perturbing the Notch and Wnt/β-catenin signaling pathways.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Cell Differentiation</subject><subject>Diabetes, Gestational</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Insulin - genetics</subject><subject>Insulin - metabolism</subject><subject>Insulin-Secreting Cells - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mutation</subject><subject>Nephrons - growth & development</subject><subject>Pregnancy</subject><subject>Stem Cells - metabolism</subject><subject>Transcription Factors - metabolism</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUdlKAzEUDaLYWv0CQfLoy9QssyQvghSXQkEEBd9CJpO0KTOTMZkR_XtTu6BPdzv33MM9AFxiNMU4Izdy3XndynqKEEHplCDMj8A4TkiC0zw_jjmnOGFZ8T4CZyGsEUIYE3wKRhRniMdiDF7mLRx67R3UX50Lg9ewd7CRsRWpYWVlqXsdoG06aX2Are5W3rWw826pW9s7HzHG6Kikt7K3rj0HJ0bWQV_s4gS8Pdy_zp6SxfPjfHa3SFSKsj7BJc0YSQ3DTBZclSXTOVaFyqvMMGUMMyUyEuWKcpnSiC3KgvG0SinnGS0rOgG3W95uKBtdqSjAy1p03jbSfwsnrfg_ae1KLN2nyFnBeZpHgusdgXcfgw69aGxQuq5lq90QBCGMFZiQbAOlW6jyLgSvzeEMRmJjhtibIX7NEBsz4tbVX4WHnf336Q-prIqh</recordid><startdate>20191101</startdate><enddate>20191101</enddate><creator>Cerqueira, Débora M</creator><creator>Hemker, Shelby L</creator><creator>Bodnar, Andrew J</creator><creator>Ortiz, Daniella M</creator><creator>Oladipupo, Favour O</creator><creator>Mukherjee, Elina</creator><creator>Gong, Zhenwei</creator><creator>Appolonia, Corynn</creator><creator>Muzumdar, Radhika</creator><creator>Sims-Lucas, Sunder</creator><creator>Ho, Jacqueline</creator><general>American Physiological Society</general><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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7115-1381</orcidid></search><sort><creationdate>20191101</creationdate><title>In utero exposure to maternal diabetes impairs nephron progenitor differentiation</title><author>Cerqueira, Débora M ; Hemker, Shelby L ; Bodnar, Andrew J ; Ortiz, Daniella M ; Oladipupo, Favour O ; Mukherjee, Elina ; Gong, Zhenwei ; Appolonia, Corynn ; Muzumdar, Radhika ; Sims-Lucas, Sunder ; Ho, Jacqueline</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-1b35824f818a79cbb8e61c7c6d5f8cff8fb0fa06c39a433587b7894d439953bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Cell Differentiation</topic><topic>Diabetes, Gestational</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Insulin - genetics</topic><topic>Insulin - metabolism</topic><topic>Insulin-Secreting Cells - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mutation</topic><topic>Nephrons - growth & development</topic><topic>Pregnancy</topic><topic>Stem Cells - metabolism</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cerqueira, Débora M</creatorcontrib><creatorcontrib>Hemker, Shelby L</creatorcontrib><creatorcontrib>Bodnar, Andrew J</creatorcontrib><creatorcontrib>Ortiz, Daniella M</creatorcontrib><creatorcontrib>Oladipupo, Favour O</creatorcontrib><creatorcontrib>Mukherjee, Elina</creatorcontrib><creatorcontrib>Gong, Zhenwei</creatorcontrib><creatorcontrib>Appolonia, Corynn</creatorcontrib><creatorcontrib>Muzumdar, Radhika</creatorcontrib><creatorcontrib>Sims-Lucas, Sunder</creatorcontrib><creatorcontrib>Ho, Jacqueline</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. 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mice (Akita mice). DM_Exp mice at
have a reduction of ~20% in the total nephron number compared with controls, using the gold standard physical dissector/fractionator method. At the molecular level, the expression of the nephron progenitor markers sine oculis homeobox homolog 2 and
was increased in DM_Exp kidneys at
. Conversely, the number of early developing nephrons was diminished in DM_Exp kidneys. This was associated with decreased expression of the intracellular domain of Notch1 and the canonical Wnt target lymphoid enhancer binding factor 1. Together, these data suggest that the diabetic intrauterine environment impairs the differentiation of nephron progenitors into nephrons, possibly by perturbing the Notch and Wnt/β-catenin signaling pathways.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>31509011</pmid><doi>10.1152/ajprenal.00204.2019</doi><orcidid>https://orcid.org/0000-0001-7115-1381</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Physiological Society Paid; Free E-Journal (出版社公開部分のみ）; Alma/SFX Local Collection |
| subjects | Animals Animals, Newborn Cell Differentiation Diabetes, Gestational Female Genetic Predisposition to Disease Genotype Insulin - genetics Insulin - metabolism Insulin-Secreting Cells - physiology Male Mice Mutation Nephrons - growth & development Pregnancy Stem Cells - metabolism Transcription Factors - metabolism |
| title | In utero exposure to maternal diabetes impairs nephron progenitor differentiation |
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