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Titolo:
Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF beta-receptor null mice
Autore:
Kaminski, WE; Lindahl, P; Lin, NL; Broudy, VC; Crosby, JR; Hellstrom, M; Swolin, B; Bowen-Pope, DF; Martin, PJ; Ross, R; Betsholtz, C; Raines, EW;
Indirizzi:
Univ Washington, Sch Med, Dept Pathol, HMC, Seattle, WA 98104 USA Univ Washington Seattle WA USA 98104 t Pathol, HMC, Seattle, WA 98104 USA Univ Washington, Sch Med, Dept Med, Seattle, WA 98104 USA Univ WashingtonSeattle WA USA 98104 Med, Dept Med, Seattle, WA 98104 USA Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98104 USA Fred Hutchinson Canc Res Ctr Seattle WA USA 98104 , Seattle, WA 98104 USA Univ Gothenburg, Dept Med Biochem, Gothenburg, Sweden Univ Gothenburg Gothenburg Sweden Dept Med Biochem, Gothenburg, Sweden Sahlgrenska Hosp, Dept Clin Chem, Gothenburg, Sweden Sahlgrenska Hosp Gothenburg Sweden , Dept Clin Chem, Gothenburg, Sweden
Titolo Testata:
BLOOD
fascicolo: 7, volume: 97, anno: 2001,
pagine: 1990 - 1998
SICI:
0006-4971(20010401)97:7<1990:BOHDIP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
COLONY-STIMULATING FACTOR; TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE CELLS; DEFICIENT MICE; IN-VITRO; C-MPL; ERYTHROPOIETIN RECEPTOR; MARROW TRANSPLANTATION; ALPHA-RECEPTOR; TGF-BETA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Raines, EW Univ Washington, Sch Med, Dept Pathol, HMC, 325 9th Box 359675,Seattle, WA 98104 USA Univ Washington 325 9th Box 359675 Seattle WA USA 98104 104 USA
Citazione:
W.E. Kaminski et al., "Basis of hematopoietic defects in platelet-derived growth factor (PDGF)-B and PDGF beta-receptor null mice", BLOOD, 97(7), 2001, pp. 1990-1998

Abstract

Platelet-derived growth factor (PDGF)-B and PDGF beta -receptor (PDGFR beta) deficiency in mice is embryonic lethal and results in cardiovascular, renal, placental, and hematologic disorders. The hematologic disorders are described, and a correlation with hepatic hypocellularity is demonstrated. Toexplore possible causes, the colony-forming activity of fetal liver cells in vitro was assessed, and hematopoietic chimeras were demonstrated by the transplantation of mutant fetal liver cells into lethally irradiated recipients. It was found that mutant colony formation is equivalent to that of wild-type controls. Hematopoietic chimeras reconstituted with PDGFB(-/-), PDGFR beta (-/-), or wild-type fetal river cells show complete engraftment (greater than 98%) with donor granulocytes, monocytes, B cells, and T cells and display none of the cardiovascular or hematologic abnormalities seen in mutants. In mouse embryos, PDGF-B is expressed by vascular endothelial cellsand megakaryocytes. After birth, expression is seen in macrophages and neurons. This study demonstrates that hematopoietic PDGF-B or PDGFR beta expression is not required for hematopoiesis or integrity of the cardiovascular system. It is argued that metabolic stress arising from mutant defects in the placenta, heart, or blood vessels may lead to impaired liver growth and decreased production of blood cells. The chimera models in this study will serve as valuable tools to test the role of PDGF in inflammatory and immuneresponses. (Blood. 2001;97:1990-1998) (C) 2001 by The American Society of Hematology.

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Documento generato il 02/12/20 alle ore 16:24:27