FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2009667997> ?p ?o ?g. }

• W2009667997 endingPage "288" @default.
• W2009667997 startingPage "276" @default.
• W2009667997 abstract "Background/Aims Deficient biliary epithelial cell (BEC) expression of small proline-rich protein (SPRR) 2A in IL-6−/− mice is associated with defective biliary barrier function after bile duct ligation. And numerous gene array expression studies show SPRR2A to commonly be among the most highly up-regulated genes in many non-squamous, stressed and remodeling barrier epithelia. Since the function of SPRR in these circumstances is unknown, we tested the exploratory hypothesis that BEC SPRR2A expression contributes to BEC barrier function and wound repair. Methods The effect of SPRR2A expression was studied in primary mouse BEC cultures; in a BEC cell line after forced overexpression of SPRR2A; and in human livers removed at the time of liver transplantation. Results Forced SPRR2A overexpression showed that it functions as a SH3 domain ligand that increases resistance to oxidative injury and promotes wound restitution by enhancing migration and acquisition of mesenchymal characteristics. Low confluency non-neoplastic mouse BEC cultures show a phenotype similar to the stable transfectants, as did spindle-shaped BEC participating in atypical ductular reactions in primary biliary cirrhosis. Conclusions These observations suggest that SPRR2A-related BEC barrier modifications represent a novel, but widely utilized and evolutionarily conserved, response to stress that is worthy of further study. Deficient biliary epithelial cell (BEC) expression of small proline-rich protein (SPRR) 2A in IL-6−/− mice is associated with defective biliary barrier function after bile duct ligation. And numerous gene array expression studies show SPRR2A to commonly be among the most highly up-regulated genes in many non-squamous, stressed and remodeling barrier epithelia. Since the function of SPRR in these circumstances is unknown, we tested the exploratory hypothesis that BEC SPRR2A expression contributes to BEC barrier function and wound repair. The effect of SPRR2A expression was studied in primary mouse BEC cultures; in a BEC cell line after forced overexpression of SPRR2A; and in human livers removed at the time of liver transplantation. Forced SPRR2A overexpression showed that it functions as a SH3 domain ligand that increases resistance to oxidative injury and promotes wound restitution by enhancing migration and acquisition of mesenchymal characteristics. Low confluency non-neoplastic mouse BEC cultures show a phenotype similar to the stable transfectants, as did spindle-shaped BEC participating in atypical ductular reactions in primary biliary cirrhosis. These observations suggest that SPRR2A-related BEC barrier modifications represent a novel, but widely utilized and evolutionarily conserved, response to stress that is worthy of further study." @default.
• W2009667997 created "2016-06-24" @default.
• W2009667997 creator A5007101138 @default.
• W2009667997 creator A5024874881 @default.
• W2009667997 creator A5049111671 @default.
• W2009667997 creator A5052520143 @default.
• W2009667997 creator A5068464511 @default.
• W2009667997 creator A5082361739 @default.
• W2009667997 creator A5083884798 @default.
• W2009667997 date "2008-02-01" @default.
• W2009667997 modified "2023-09-25" @default.
• W2009667997 title "Small proline-rich proteins (SPRR) function as SH3 domain ligands, increase resistance to injury and are associated with epithelial–mesenchymal transition (EMT) in cholangiocytes" @default.
• W2009667997 cites W137587748 @default.
• W2009667997 cites W1485185791 @default.
• W2009667997 cites W1559370438 @default.
• W2009667997 cites W1689369637 @default.
• W2009667997 cites W1863498511 @default.
• W2009667997 cites W1866441697 @default.
• W2009667997 cites W1892578325 @default.
• W2009667997 cites W1913862483 @default.
• W2009667997 cites W1972305087 @default.
• W2009667997 cites W1972414001 @default.
• W2009667997 cites W1982875532 @default.
• W2009667997 cites W1987408673 @default.
• W2009667997 cites W1989944445 @default.
• W2009667997 cites W1990781807 @default.
• W2009667997 cites W1993672291 @default.
• W2009667997 cites W1994011290 @default.
• W2009667997 cites W1994016440 @default.
• W2009667997 cites W1997902322 @default.
• W2009667997 cites W2003170300 @default.
• W2009667997 cites W2023873999 @default.
• W2009667997 cites W2024161072 @default.
• W2009667997 cites W2028863876 @default.
• W2009667997 cites W2031425131 @default.
• W2009667997 cites W2032221109 @default.
• W2009667997 cites W2032942532 @default.
• W2009667997 cites W2036404794 @default.
• W2009667997 cites W2044212200 @default.
• W2009667997 cites W2049930003 @default.
• W2009667997 cites W2052701545 @default.
• W2009667997 cites W2053796953 @default.
• W2009667997 cites W2060364801 @default.
• W2009667997 cites W207023704 @default.
• W2009667997 cites W2071595908 @default.
• W2009667997 cites W2071601082 @default.
• W2009667997 cites W2084150021 @default.
• W2009667997 cites W2087014116 @default.
• W2009667997 cites W2102265675 @default.
• W2009667997 cites W2104552496 @default.
• W2009667997 cites W2116984018 @default.
• W2009667997 cites W2117383442 @default.
• W2009667997 cites W2120835552 @default.
• W2009667997 cites W2121733174 @default.
• W2009667997 cites W2133782231 @default.
• W2009667997 cites W2140107075 @default.
• W2009667997 cites W2142296051 @default.
• W2009667997 cites W2145042614 @default.
• W2009667997 cites W2147554787 @default.
• W2009667997 cites W2148422863 @default.
• W2009667997 cites W2148798479 @default.
• W2009667997 cites W2149220734 @default.
• W2009667997 cites W2149287054 @default.
• W2009667997 cites W2150050610 @default.
• W2009667997 cites W2155715803 @default.
• W2009667997 cites W2156776995 @default.
• W2009667997 cites W2161155632 @default.
• W2009667997 cites W232119217 @default.
• W2009667997 cites W2417449459 @default.
• W2009667997 cites W2597632520 @default.
• W2009667997 cites W4237918055 @default.
• W2009667997 cites W4250731522 @default.
• W2009667997 doi "https://doi.org/10.1016/j.jhep.2007.09.019" @default.
• W2009667997 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2263141" @default.
• W2009667997 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18155796" @default.
• W2009667997 hasPublicationYear "2008" @default.
• W2009667997 type Work @default.
• W2009667997 sameAs 2009667997 @default.
• W2009667997 citedByCount "38" @default.
• W2009667997 countsByYear W20096679972012 @default.
• W2009667997 countsByYear W20096679972013 @default.
• W2009667997 countsByYear W20096679972014 @default.
• W2009667997 countsByYear W20096679972015 @default.
• W2009667997 countsByYear W20096679972017 @default.
• W2009667997 countsByYear W20096679972018 @default.
• W2009667997 countsByYear W20096679972020 @default.
• W2009667997 countsByYear W20096679972021 @default.
• W2009667997 countsByYear W20096679972022 @default.
• W2009667997 countsByYear W20096679972023 @default.
• W2009667997 crossrefType "journal-article" @default.
• W2009667997 hasAuthorship W2009667997A5007101138 @default.
• W2009667997 hasAuthorship W2009667997A5024874881 @default.
• W2009667997 hasAuthorship W2009667997A5049111671 @default.
• W2009667997 hasAuthorship W2009667997A5052520143 @default.
• W2009667997 hasAuthorship W2009667997A5068464511 @default.
• W2009667997 hasAuthorship W2009667997A5082361739 @default.
• W2009667997 hasAuthorship W2009667997A5083884798 @default.
• W2009667997 hasBestOaLocation W20096679972 @default.

• next