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Titolo:
Analysis of SM22 alpha-deficient mice reveals unanticipated insights into smooth muscle cell differentiation and function
Autore:
Zhang, JCL; Kim, S; Helmke, BP; Yu, WW; Du, KL; Lu, MM; Strobeck, M; Yu, QC; Parmacek, MS;
Indirizzi:
Univ Penn, Dept Med, Philadelphia, PA 19104 USA Univ Penn Philadelphia PAUSA 19104 Dept Med, Philadelphia, PA 19104 USA Univ Penn, Dept Bioengn, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 t Bioengn, Philadelphia, PA 19104 USA Univ Penn, Dept Cell & Mol Engn, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Mol Engn, Philadelphia, PA 19104 USA Univ Chicago, Dept Med, Chicago, IL 60637 USA Univ Chicago Chicago IL USA60637 hicago, Dept Med, Chicago, IL 60637 USA
Titolo Testata:
MOLECULAR AND CELLULAR BIOLOGY
fascicolo: 4, volume: 21, anno: 2001,
pagine: 1336 - 1344
SICI:
0270-7306(200102)21:4<1336:AOSAMR>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSGENIC MICE; TRANSCRIPTION FACTOR; EXPRESSION; GENE; PROTEIN; SEQUENCE; PROMOTER; IDENTIFICATION; TRANSFORMATION; PROLIFERATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Parmacek, MS Univ Penn, Dept Med, 91234 Founders Pavil,3400 Spruce St, Philadelphia, PA19104 USA Univ Penn 91234 Founders Pavil,3400 Spruce St Philadelphia PA USA 19104
Citazione:
J.C.L. Zhang et al., "Analysis of SM22 alpha-deficient mice reveals unanticipated insights into smooth muscle cell differentiation and function", MOL CELL B, 21(4), 2001, pp. 1336-1344

Abstract

SM22 alpha is a 22-kDa smooth muscle cell (SMC) lineage-restricted proteinthat physically associates with cytoskeletal actin filament bundles in contractile SMCs. To examine the function of SM22 alpha, gene targeting was used to generate SM22 alpha -deficient (SM22(-/-LacZ)) mice. The gene targeting strategy employed resulted in insertion of the bacterial lacZ reporter gene at the SM22 alpha initiation codon, permitting precise analysis of the temporal and spatial pattern of SM22 alpha transcriptional activation in the developing mouse. Northern and Western blot analyses confirmed that the gene targeting strategy resulted in a null mutation. Histological analysis of SM22(+/-LacZ) embryos revealed detectable beta -galactosidase activity inthe unturned embryonic day 8.0 embryo in the layer of cells surrounding the paired dorsal aortae concomitant with its expression in the primitive heart tube, cephalic mesenchyme, and yolk sac vasculature. Subsequently, during postnatal development, beta -galactosidase activity was observed exclusively in arterial, venous, and visceral SMCs. SM22 alpha -deficient mice are viable and fertile. Their blood pressure and heart rate do not differ significantly front their control SM22 alpha (+/-) and SM22 alpha (+/+) littermates. The vasculature and SMC-containing tissues of SM22 alpha -deficient mice develop normally and appear to be histologically and ultrastructurally similar to those of their control littermates. Taken together, these data demonstrate that SM22 alpha is not required for basal homeostatic functions mediated by vascular and visceral SMCs in the developing mouse. These data also suggest that signaling pathways that regulate SMC specification and differentiation from local mesenchyme are activated earlier in the angiogenic program than previously recognized.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 12:22:33