Artículo

Chang, M.-L.; Chen, J.-C.; Alonso, C.R.; Kornblihtt, A.R.; Bissell, D.M. "Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver" (2004) Proceedings of the National Academy of Sciences of the United States of America. 101(52):18093-18098
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Abstract:

Fn containing an extra type III domain (EIIIA in the rat, ED1 or EDA in humans) is commonly termed "fetal" fibronectin, but it is prominent during the injury response of adult tissues and mediates important early events in the response. This form is particularly apparent in acute liver injury, where it has been shown that sinusoidal endothelial cells produce EIIIA-fibronectin. This fibronectin isoform arises by alternative splicing of the primary transcript. In the present experiments, we have studied the regulation of fibronectin splicing in primary sinusoidal endothelial cells by transfecting a minigene containing the EIIIA exon and its flanking introns, driven by various promoters. The results indicate that fibronectin splicing in endothelial cells from normal liver is in part promoter-dependent. However, in cells from injured liver in which expression of both total and EIIIA-fibronectin is strikingly increased, promoter effects disappear. Because fibronectin splicing is known to be regulated in part by TGFβ, we also examined the effect of a soluble inhibitor of the TGFβ type 2 receptor. This agent had no effect on splicing by normal endothelial cells. By contrast, for endothelial cells from the injured liver, the splicing pattern reverted to that of normal cells, i.e., it became promoter-dependent. We conclude that, in the setting of injury in vivo, TGFβ overrides the promoter dependence of fibronectin splicing in normal cells. The data suggest that TGFβ modifies the spliceosome, if not through its known signaling intermediates, then through the products of genes regulated by this cytokine.

Registro:

Documento: Artículo
Título:Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver
Autor:Chang, M.-L.; Chen, J.-C.; Alonso, C.R.; Kornblihtt, A.R.; Bissell, D.M.
Filiación:Liver Ctr. and Dept. of Medicine, University of California, San Francisco, CA 94143, United States
Fetal Treatment Center, Department of Surgery, University of California, San Francisco, CA 94143, United States
Department of Hepatology, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan
Depto. de Fisiol., Biol. Molec./Cel., Fac. de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Department of Zoology, University of Cambridge, Downing Street, Cambridge CB2 3EJ, United Kingdom
Box 0538, University of California, 513 Parnassus Avenue, San Francisco, CA 94143, United States
Palabras clave:Extracellular matrix; Fibrosis; Spliceosome; TGFβ; fibronectin; transforming growth factor beta; transforming growth factor beta receptor; alternative RNA splicing; animal cell; animal experiment; animal model; article; cell growth; controlled study; endothelium cell; extracellular matrix; genetic transfection; HeLa cell; liver histology; liver injury; male; nonhuman; priority journal; promoter region; rat; reporter gene; reverse transcription polymerase chain reaction; spliceosome; Alternative Splicing; Animals; Cell Line; Cell Line, Tumor; Endothelium; Fibronectins; Genes, Reporter; Hela Cells; Humans; Introns; Liver; Male; Mice; Models, Genetic; Plasmids; Promoter Regions (Genetics); Protein Structure, Tertiary; Rats; Rats, Wistar; Receptors, Transforming Growth Factor beta; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Signal Transduction; Spliceosomes; Time Factors; Transfection; Transforming Growth Factor beta; Animalia
Año:2004
Volumen:101
Número:52
Página de inicio:18093
Página de fin:18098
DOI: http://dx.doi.org/10.1073/pnas.0408439102
Handle:http://hdl.handle.net/20.500.12110/paper_00278424_v101_n52_p18093_Chang
Título revista:Proceedings of the National Academy of Sciences of the United States of America
Título revista abreviado:Proc. Natl. Acad. Sci. U. S. A.
ISSN:00278424
CODEN:PNASA
CAS:fibronectin, 86088-83-7; Fibronectins; Receptors, Transforming Growth Factor beta; RNA, Messenger; Transforming Growth Factor beta
PDF:https://bibliotecadigital.exactas.uba.ar/download/paper/paper_00278424_v101_n52_p18093_Chang.pdf
Registro:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00278424_v101_n52_p18093_Chang

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Citas:

---------- APA ----------
Chang, M.-L., Chen, J.-C., Alonso, C.R., Kornblihtt, A.R. & Bissell, D.M. (2004) . Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver. Proceedings of the National Academy of Sciences of the United States of America, 101(52), 18093-18098.
http://dx.doi.org/10.1073/pnas.0408439102
---------- CHICAGO ----------
Chang, M.-L., Chen, J.-C., Alonso, C.R., Kornblihtt, A.R., Bissell, D.M. "Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver" . Proceedings of the National Academy of Sciences of the United States of America 101, no. 52 (2004) : 18093-18098.
http://dx.doi.org/10.1073/pnas.0408439102
---------- MLA ----------
Chang, M.-L., Chen, J.-C., Alonso, C.R., Kornblihtt, A.R., Bissell, D.M. "Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver" . Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 52, 2004, pp. 18093-18098.
http://dx.doi.org/10.1073/pnas.0408439102
---------- VANCOUVER ----------
Chang, M.-L., Chen, J.-C., Alonso, C.R., Kornblihtt, A.R., Bissell, D.M. Regulation of fibronectin splicing in sinusoidal endothelial cells from normal or injured liver. Proc. Natl. Acad. Sci. U. S. A. 2004;101(52):18093-18098.
http://dx.doi.org/10.1073/pnas.0408439102