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http://hdl.handle.net/10261/123458
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dc.contributor.author | Álvarez Pérez, Juan Carlos | - |
dc.contributor.author | Ernst, Sara | - |
dc.contributor.author | Demirci, Cem | - |
dc.contributor.author | Casinelli, Gabriella P. | - |
dc.contributor.author | Mellado-Gil, José Manuel | - |
dc.contributor.author | Rausell-Palamos, Francisco | - |
dc.contributor.author | Vasavada, Rupangi C. | - |
dc.contributor.author | García-Ocaña, Adolfo | - |
dc.date.accessioned | 2015-10-16T09:57:32Z | - |
dc.date.available | 2015-10-16T09:57:32Z | - |
dc.date.issued | 2014-01 | - |
dc.identifier | issn: 0012-1797 | - |
dc.identifier | e-issn: 1939-327X | - |
dc.identifier.citation | Diabetes 63(1): 216-223 (2014) | - |
dc.identifier.uri | http://hdl.handle.net/10261/123458 | - |
dc.description.abstract | Hepatocyte growth factor (HGF) is a mitogen required for β-cell replication during pregnancy. To determine whether HGF/c-Met signaling is required for β-cell regeneration, we characterized mice with pancreatic deletion of the HGF receptor, c-Met (PancMet KO mice), in two models of reduced β-cell mass and regeneration: multiple low-dose streptozotocin (MLDS) and partial pancreatectomy (Ppx). We also analyzed whether HGF administration could accelerate β-cell regeneration in wild-type (WT) mice after Ppx. Mouse islets obtained 7 days post-Ppx displayed significantly increased c-Met, suggesting a potential role for HGF/c-Met in β-cell proliferation in situations of reduced β-cell mass. Indeed, adult PancMet KO mice displayed markedly reduced β-cell replication compared with WT mice 7 days post-Ppx. Similarly, β-cell proliferation was decreased in PancMet KO mice in the MLDS mouse model. The decrease in β-cell proliferation post-Ppx correlated with a striking decrease in D-cyclin levels. Importantly, PancMet KO mice showed significantly diminished β-cell mass, decreased glucose tolerance, and impaired insulin secretion compared with WT mice 28 days post-Ppx. Conversely, HGF administration in WT Ppx mice further accelerated β-cell regeneration. These results indicate that HGF/c-Met signaling is critical for β-cell proliferation in situations of diminished β-cell mass and suggest that activation of this pathway can enhance β-cell regeneration. © 2014 by the American Diabetes Association. | - |
dc.description.sponsorship | This work was supported in part by grants from the National Institutes of Health (DK-067351 and DK-077096) and the Juvenile Diabetes Research Foundation (1-2007-3) to A.G.-O. S.E. was the recipient of a postdoctoral fellowship from the National Institutes of Health T32 Research Training grant (T32DK-07052-32). C.D. was the recipient of a research fellowship from the Lawson Wilkins Pediatric Endocrine Society. | - |
dc.publisher | American Diabetes Association | - |
dc.relation.isversionof | Publisher's version | - |
dc.rights | openAccess | - |
dc.title | Hepatocyte growth factor/c-Met signaling is required for β-cell regeneration | - |
dc.type | artículo | - |
dc.identifier.doi | 10.2337/db13-0333 | - |
dc.relation.publisherversion | http://dx.doi.org/10.2337/db13-0333 | - |
dc.date.updated | 2015-10-16T09:57:32Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.rights.license | http://creativecommons.org/licenses/by-nc-nd/3.0/ | - |
dc.contributor.funder | National Institutes of Health (US) | - |
dc.contributor.funder | Juvenile Diabetes Research Foundation International | - |
dc.contributor.funder | Pediatric Endocrine Society (US) | - |
dc.relation.csic | Sí | - |
dc.identifier.funder | http://dx.doi.org/10.13039/100000002 | es_ES |
dc.identifier.funder | http://dx.doi.org/10.13039/100000901 | es_ES |
dc.identifier.pmid | 24089510 | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | With Fulltext | - |
item.cerifentitytype | Publications | - |
item.openairetype | artículo | - |
item.grantfulltext | open | - |
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Hepatocyte_Growth_Factor_AlvarezPerez.pdf | 1,23 MB | Adobe PDF | Visualizar/Abrir |
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