Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells
Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells You-Qing Zhang 1 , Mary Malo Cleary 1 , Yingjie Si 1 , Guoxun Liu 1 , Yuzuru Eto 2 , Marcie Kritzik 1 , Sandrine Dabernat 1 , Ayse G. Kayali 1 and Nora Sarvetnic...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2004-08, Vol.53 (8), p.2024-2033 |
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| creator | ZHANG, You-Qing CLEARY, Mary Malo YINGJIE SI GUOXUN LIU ETO, Yuzuru KRITZIK, Marcie DABERNAT, Sandrine KAYALI, Ayse G SARVETNICK, Nora |
| description | Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic
β-Cells
You-Qing Zhang 1 ,
Mary Malo Cleary 1 ,
Yingjie Si 1 ,
Guoxun Liu 1 ,
Yuzuru Eto 2 ,
Marcie Kritzik 1 ,
Sandrine Dabernat 1 ,
Ayse G. Kayali 1 and
Nora Sarvetnick 1
1 Department of Immunology, The Scripps Research Institute, La Jolla, California
2 Pharmaceutical Research Laboratories, Ajinomoto Co., Kawasaki, Japan
Address correspondence and reprint requests to Nora Sarvetnick, PhD, Department of Immunology, IMM23, The Scripps Research
Institute, La Jolla, CA 92037. E-mail: noras{at}scripps.edu
Abstract
Activins regulate the growth and differentiation of a variety of cells. During pancreatic islet development, activins are
required for the specialization of pancreatic precursors from the gut endoderm during midgestation. In this study, we probed
the role of activin signaling during pancreatic islet cell development and regeneration. Indeed, we found that both activins
and activin receptors are upregulated in duct epithelial cells during islet differentiation. Interestingly, the expression
of endogenous cellular inhibitors of activin signaling, follistatin and Cripto, were also found to be augmented. Inhibition
of activins significantly enhanced survival and expansion of pancreatic epithelial cells but decreased the numbers of differentiated
β-cells. Our results suggest that the homeostasis of growth and terminal differentiation requires a precise context-dependent
regulation of activin signaling. Follistatin participates in this process by promoting expansion of precursor cells during
pancreas growth.
BrdU, bromodeoxyuridine
ICC, islet-like cell cluster
IFN, interferon
FITC, fluorescein isothiocyanate
PCNA, proliferating cell nuclear antigen
PDX, pancreas duodenum homeobox
P-Smad, phosphorylated Smad
rh, recombinant human
TGF, transforming growth factor
TUNEL, transferase-mediated dUTP-biotin nick-end labeling
Footnotes
Accepted May 5, 2004.
Received March 16, 2004.
DIABETES |
| doi_str_mv | 10.2337/diabetes.53.8.2024 |
| format | Article |
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β-Cells
You-Qing Zhang 1 ,
Mary Malo Cleary 1 ,
Yingjie Si 1 ,
Guoxun Liu 1 ,
Yuzuru Eto 2 ,
Marcie Kritzik 1 ,
Sandrine Dabernat 1 ,
Ayse G. Kayali 1 and
Nora Sarvetnick 1
1 Department of Immunology, The Scripps Research Institute, La Jolla, California
2 Pharmaceutical Research Laboratories, Ajinomoto Co., Kawasaki, Japan
Address correspondence and reprint requests to Nora Sarvetnick, PhD, Department of Immunology, IMM23, The Scripps Research
Institute, La Jolla, CA 92037. E-mail: noras{at}scripps.edu
Abstract
Activins regulate the growth and differentiation of a variety of cells. During pancreatic islet development, activins are
required for the specialization of pancreatic precursors from the gut endoderm during midgestation. In this study, we probed
the role of activin signaling during pancreatic islet cell development and regeneration. Indeed, we found that both activins
and activin receptors are upregulated in duct epithelial cells during islet differentiation. Interestingly, the expression
of endogenous cellular inhibitors of activin signaling, follistatin and Cripto, were also found to be augmented. Inhibition
of activins significantly enhanced survival and expansion of pancreatic epithelial cells but decreased the numbers of differentiated
β-cells. Our results suggest that the homeostasis of growth and terminal differentiation requires a precise context-dependent
regulation of activin signaling. Follistatin participates in this process by promoting expansion of precursor cells during
pancreas growth.
BrdU, bromodeoxyuridine
ICC, islet-like cell cluster
IFN, interferon
FITC, fluorescein isothiocyanate
PCNA, proliferating cell nuclear antigen
PDX, pancreas duodenum homeobox
P-Smad, phosphorylated Smad
rh, recombinant human
TGF, transforming growth factor
TUNEL, transferase-mediated dUTP-biotin nick-end labeling
Footnotes
Accepted May 5, 2004.
Received March 16, 2004.
DIABETES</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/diabetes.53.8.2024</identifier><identifier>PMID: 15277382</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>Activin Receptors - physiology ; Activins - antagonists & inhibitors ; Activins - pharmacology ; Activins - physiology ; Animals ; Biological and medical sciences ; Cell Differentiation - drug effects ; Cell Differentiation - physiology ; Cell Division - drug effects ; Cell Division - physiology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Epithelial Cells - cytology ; Epithelial Cells - drug effects ; Follistatin - pharmacology ; Fundamental and applied biological sciences. Psychology ; Humans ; Interferon-gamma - genetics ; Islets of Langerhans - drug effects ; Islets of Langerhans - physiology ; Medical sciences ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Morphology. Functional localizations ; Pancreas - cytology ; Pancreatic beta cells ; Physiological aspects ; Recombinant Proteins - pharmacology ; Transforming growth factors ; Vertebrates: endocrinology</subject><ispartof>Diabetes (New York, N.Y.), 2004-08, Vol.53 (8), p.2024-2033</ispartof><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 American Diabetes Association</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c520t-31955ef409902e2d1516cda1d6e53ad76c5f7ee2e5d0da661d0b31f5fe131ca83</citedby><cites>FETCH-LOGICAL-c520t-31955ef409902e2d1516cda1d6e53ad76c5f7ee2e5d0da661d0b31f5fe131ca83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15986518$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15277382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ZHANG, You-Qing</creatorcontrib><creatorcontrib>CLEARY, Mary Malo</creatorcontrib><creatorcontrib>YINGJIE SI</creatorcontrib><creatorcontrib>GUOXUN LIU</creatorcontrib><creatorcontrib>ETO, Yuzuru</creatorcontrib><creatorcontrib>KRITZIK, Marcie</creatorcontrib><creatorcontrib>DABERNAT, Sandrine</creatorcontrib><creatorcontrib>KAYALI, Ayse G</creatorcontrib><creatorcontrib>SARVETNICK, Nora</creatorcontrib><title>Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic
β-Cells
You-Qing Zhang 1 ,
Mary Malo Cleary 1 ,
Yingjie Si 1 ,
Guoxun Liu 1 ,
Yuzuru Eto 2 ,
Marcie Kritzik 1 ,
Sandrine Dabernat 1 ,
Ayse G. Kayali 1 and
Nora Sarvetnick 1
1 Department of Immunology, The Scripps Research Institute, La Jolla, California
2 Pharmaceutical Research Laboratories, Ajinomoto Co., Kawasaki, Japan
Address correspondence and reprint requests to Nora Sarvetnick, PhD, Department of Immunology, IMM23, The Scripps Research
Institute, La Jolla, CA 92037. E-mail: noras{at}scripps.edu
Abstract
Activins regulate the growth and differentiation of a variety of cells. During pancreatic islet development, activins are
required for the specialization of pancreatic precursors from the gut endoderm during midgestation. In this study, we probed
the role of activin signaling during pancreatic islet cell development and regeneration. Indeed, we found that both activins
and activin receptors are upregulated in duct epithelial cells during islet differentiation. Interestingly, the expression
of endogenous cellular inhibitors of activin signaling, follistatin and Cripto, were also found to be augmented. Inhibition
of activins significantly enhanced survival and expansion of pancreatic epithelial cells but decreased the numbers of differentiated
β-cells. Our results suggest that the homeostasis of growth and terminal differentiation requires a precise context-dependent
regulation of activin signaling. Follistatin participates in this process by promoting expansion of precursor cells during
pancreas growth.
BrdU, bromodeoxyuridine
ICC, islet-like cell cluster
IFN, interferon
FITC, fluorescein isothiocyanate
PCNA, proliferating cell nuclear antigen
PDX, pancreas duodenum homeobox
P-Smad, phosphorylated Smad
rh, recombinant human
TGF, transforming growth factor
TUNEL, transferase-mediated dUTP-biotin nick-end labeling
Footnotes
Accepted May 5, 2004.
Received March 16, 2004.
DIABETES</description><subject>Activin Receptors - physiology</subject><subject>Activins - antagonists & inhibitors</subject><subject>Activins - pharmacology</subject><subject>Activins - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Differentiation - physiology</subject><subject>Cell Division - drug effects</subject><subject>Cell Division - physiology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Epithelial Cells - cytology</subject><subject>Epithelial Cells - drug effects</subject><subject>Follistatin - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Interferon-gamma - genetics</subject><subject>Islets of Langerhans - drug effects</subject><subject>Islets of Langerhans - physiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, Transgenic</subject><subject>Morphology. Functional localizations</subject><subject>Pancreas - cytology</subject><subject>Pancreatic beta cells</subject><subject>Physiological aspects</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Transforming growth factors</subject><subject>Vertebrates: endocrinology</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkt-KEzEUxoMobq2-gBcyNwoiU_Onmcxclm5dCwUFV_BuSJOT6ZFppiaprs_g2_ggPpMp7bK7UM5FQvh930lOPkJeMjrhQqj3FvUaEsSJFJN6wimfPiIj1oimFFx9e0xGlDJeMtWoC_Isxu-U0irXU3LBJFdK1HxE_iz9BteYcPDF4IqZSfgTffEFO6979F2x9HZvIBaftTcBdEJTLHaYNtCj7os59H2xuNlpHw8O2tviErfoMW6y5hpC3mfsEp2DAD6hvu10z-_f3_LgE5-TJ073EV6c1jH5-mFxPf9Yrj5dLeezVWkkp6kUrJES3JQ2DeXALZOsMlYzW4EU2qrKSKcAOEhLra4qZulaMCcdMMGMrsWYvDn67sLwYw8xtVuMJt9Aexj2sa0qJdU0j3hMyiPY6R5a9G5IQZsOPATdDx4c5uMZy5OXjZLTzE_O8LksbNGcFbx9IMhMgpvU6X2MbX21esjyI2vCEGMA1-4CbnX43TLaHvLQ3uahlaKt20MesujV6an79RbsneQUgAy8PgE6Gt27kL8F4z2uqSvJDjN7d-Q22G1-YYC7bmfa_gdnq9Cv</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>ZHANG, You-Qing</creator><creator>CLEARY, Mary Malo</creator><creator>YINGJIE SI</creator><creator>GUOXUN LIU</creator><creator>ETO, Yuzuru</creator><creator>KRITZIK, Marcie</creator><creator>DABERNAT, Sandrine</creator><creator>KAYALI, Ayse G</creator><creator>SARVETNICK, Nora</creator><general>American Diabetes Association</general><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>8GL</scope><scope>7X8</scope></search><sort><creationdate>20040801</creationdate><title>Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells</title><author>ZHANG, You-Qing ; CLEARY, Mary Malo ; YINGJIE SI ; GUOXUN LIU ; ETO, Yuzuru ; KRITZIK, Marcie ; DABERNAT, Sandrine ; KAYALI, Ayse G ; SARVETNICK, Nora</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c520t-31955ef409902e2d1516cda1d6e53ad76c5f7ee2e5d0da661d0b31f5fe131ca83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Activin Receptors - physiology</topic><topic>Activins - antagonists & inhibitors</topic><topic>Activins - pharmacology</topic><topic>Activins - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Differentiation - physiology</topic><topic>Cell Division - drug effects</topic><topic>Cell Division - physiology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Epithelial Cells - cytology</topic><topic>Epithelial Cells - drug effects</topic><topic>Follistatin - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Interferon-gamma - genetics</topic><topic>Islets of Langerhans - drug effects</topic><topic>Islets of Langerhans - physiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, Transgenic</topic><topic>Morphology. Functional localizations</topic><topic>Pancreas - cytology</topic><topic>Pancreatic beta cells</topic><topic>Physiological aspects</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Transforming growth factors</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ZHANG, You-Qing</creatorcontrib><creatorcontrib>CLEARY, Mary Malo</creatorcontrib><creatorcontrib>YINGJIE SI</creatorcontrib><creatorcontrib>GUOXUN LIU</creatorcontrib><creatorcontrib>ETO, Yuzuru</creatorcontrib><creatorcontrib>KRITZIK, Marcie</creatorcontrib><creatorcontrib>DABERNAT, Sandrine</creatorcontrib><creatorcontrib>KAYALI, Ayse G</creatorcontrib><creatorcontrib>SARVETNICK, Nora</creatorcontrib><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>Gale In Context: High School</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ZHANG, You-Qing</au><au>CLEARY, Mary Malo</au><au>YINGJIE SI</au><au>GUOXUN LIU</au><au>ETO, Yuzuru</au><au>KRITZIK, Marcie</au><au>DABERNAT, Sandrine</au><au>KAYALI, Ayse G</au><au>SARVETNICK, Nora</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>53</volume><issue>8</issue><spage>2024</spage><epage>2033</epage><pages>2024-2033</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic
β-Cells
You-Qing Zhang 1 ,
Mary Malo Cleary 1 ,
Yingjie Si 1 ,
Guoxun Liu 1 ,
Yuzuru Eto 2 ,
Marcie Kritzik 1 ,
Sandrine Dabernat 1 ,
Ayse G. Kayali 1 and
Nora Sarvetnick 1
1 Department of Immunology, The Scripps Research Institute, La Jolla, California
2 Pharmaceutical Research Laboratories, Ajinomoto Co., Kawasaki, Japan
Address correspondence and reprint requests to Nora Sarvetnick, PhD, Department of Immunology, IMM23, The Scripps Research
Institute, La Jolla, CA 92037. E-mail: noras{at}scripps.edu
Abstract
Activins regulate the growth and differentiation of a variety of cells. During pancreatic islet development, activins are
required for the specialization of pancreatic precursors from the gut endoderm during midgestation. In this study, we probed
the role of activin signaling during pancreatic islet cell development and regeneration. Indeed, we found that both activins
and activin receptors are upregulated in duct epithelial cells during islet differentiation. Interestingly, the expression
of endogenous cellular inhibitors of activin signaling, follistatin and Cripto, were also found to be augmented. Inhibition
of activins significantly enhanced survival and expansion of pancreatic epithelial cells but decreased the numbers of differentiated
β-cells. Our results suggest that the homeostasis of growth and terminal differentiation requires a precise context-dependent
regulation of activin signaling. Follistatin participates in this process by promoting expansion of precursor cells during
pancreas growth.
BrdU, bromodeoxyuridine
ICC, islet-like cell cluster
IFN, interferon
FITC, fluorescein isothiocyanate
PCNA, proliferating cell nuclear antigen
PDX, pancreas duodenum homeobox
P-Smad, phosphorylated Smad
rh, recombinant human
TGF, transforming growth factor
TUNEL, transferase-mediated dUTP-biotin nick-end labeling
Footnotes
Accepted May 5, 2004.
Received March 16, 2004.
DIABETES</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>15277382</pmid><doi>10.2337/diabetes.53.8.2024</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0012-1797 |
| ispartof | Diabetes (New York, N.Y.), 2004-08, Vol.53 (8), p.2024-2033 |
| issn | 0012-1797 1939-327X |
| language | eng |
| recordid | cdi_highwire_diabetes_diabetes_53_8_2024 |
| source | MEDLINE; EZB Electronic Journals Library |
| subjects | Activin Receptors - physiology Activins - antagonists & inhibitors Activins - pharmacology Activins - physiology Animals Biological and medical sciences Cell Differentiation - drug effects Cell Differentiation - physiology Cell Division - drug effects Cell Division - physiology Diabetes. Impaired glucose tolerance Endocrine pancreas Endocrine pancreas. Apud cells (diseases) Endocrinopathies Epithelial Cells - cytology Epithelial Cells - drug effects Follistatin - pharmacology Fundamental and applied biological sciences. Psychology Humans Interferon-gamma - genetics Islets of Langerhans - drug effects Islets of Langerhans - physiology Medical sciences Mice Mice, Inbred NOD Mice, Transgenic Morphology. Functional localizations Pancreas - cytology Pancreatic beta cells Physiological aspects Recombinant Proteins - pharmacology Transforming growth factors Vertebrates: endocrinology |
| title | Inhibition of Activin Signaling Induces Pancreatic Epithelial Cell Expansion and Diminishes Terminal Differentiation of Pancreatic β-Cells |
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