scholarly journals Chronology of Events Accompanying Follicular Atresia in Hypophysectomized Ewes. Changes in Levels of Steroidogenic Enzymes, Connexin 43, Insulin-Like Growth Factor II/Mannose 6 Phosphate Receptor, Extracellular Matrix Components, and Matrix Metalloproteinases1

1998 ◽  
Vol 58 (1) ◽  
pp. 175-185 ◽  
Author(s):  
Clotilde Huet ◽  
Philippe Monget ◽  
Claudine Pisselet ◽  
Christelle Hennequet ◽  
Alain Locatelli ◽  
...  
2004 ◽  
Vol 24 (10) ◽  
pp. 4448-4464 ◽  
Author(s):  
Thomas V. O. Hansen ◽  
Niels A. Hammer ◽  
Jacob Nielsen ◽  
Mette Madsen ◽  
Charlotte Dalbaeck ◽  
...  

ABSTRACT Insulin-like growth factor II mRNA-binding protein 1 (IMP1) belongs to a family of RNA-binding proteins implicated in mRNA localization, turnover, and translational control. Mouse IMP1 is expressed during early development, and an increase in expression occurs around embryonic day 12.5 (E12.5). To characterize the physiological role of IMP1, we generated IMP1-deficient mice carrying a gene trap insertion in the Imp1 gene. Imp1−/− mice were on average 40% smaller than wild-type and heterozygous sex-matched littermates. Growth retardation was apparent from E17.5 and remained permanent into adult life. Moreover, Imp1−/− mice exhibited high perinatal mortality, and only 50% were alive 3 days after birth. In contrast to most other organs, intestinal epithelial cells continue to express IMP1 postnatally, and Imp1−/− mice exhibited impaired development of the intestine, with small and misshapen villi and twisted colon crypts. Analysis of target mRNAs and global expression profiling at E12.5 indicated that Igf2 translation was downregulated, whereas the postnatal intestine showed reduced expression of transcripts encoding extracellular matrix components, such as galectin- 1, lumican, tenascin-C, procollagen transcripts, and the Hsp47 procollagen chaperone. Taken together, the results demonstrate that IMP1 is essential for normal growth and development. Moreover, IMP1 may facilitate intestinal morphogenesis via regulation of extracellular matrix formation.


1999 ◽  
Vol 274 (38) ◽  
pp. 27076-27082 ◽  
Author(s):  
Catherine A. Yandell ◽  
Andrew J. Dunbar ◽  
John F. Wheldrake ◽  
Zee Upton

2000 ◽  
Vol 275 (25) ◽  
pp. 18647-18656 ◽  
Author(s):  
James C. Byrd ◽  
Jung H. Y. Park ◽  
Beverly S. Schaffer ◽  
Farideh Garmroudi ◽  
Richard G. MacDonald

1995 ◽  
Vol 108 (6) ◽  
pp. 2153-2162 ◽  
Author(s):  
J.F. Talts ◽  
A. Weller ◽  
R. Timpl ◽  
M. Ekblom ◽  
P. Ekblom

We have here studied the composition and regulation of stromal extracellular matrix components in an experimental tumor model. Nude mice were inoculated with WCCS-1 cells, a human Wilms' tumor cell line. In the formed tumors the stroma was found to contain mesenchymal extracellular matrix proteins such as tenascin-C, fibulins-1 and 2 and fibronectin, but no nidogen. Nidogen was confined to basement membranes of tumor blood vessels. Since glucocorticoids have been shown to downregulate tenascin-C expression in vitro, we tested whether dexamethasone can influence biosynthesis of extracellular matrix components during tumor formation in vivo. A downregulation of tenascin-C mRNA and an upregulation of fibronectin mRNA expression by dexamethasone was noted. Transforming growth factor-beta 1 mRNA levels were unaffected by the dexamethasone treatment. Glucocorticoids can thus downregulate tenascin-C synthesis although local stimulatory growth factors are present. The competition between a negative and a positive extrinsic factor on synthesis of stromal extracellular matrix components was studied in a fibroblast/preadipocyte cell line. Transforming growth factor-beta 1 stimulated tenascin-C synthesis but did not affect fibronectin or fibulin-2 synthesis. Dexamethasone at high concentrations could completely suppress the effect of transforming growth factor-beta 1 on tenascin-C mRNA expression. Transforming growth factor-beta 1 could in turn overcome the downregulation of tenascin-C mRNA expression caused by a lower concentration of dexamethasone. We therefore suggest that the limited expression of tenascin-C in part is due to a continuous suppression by physiological levels of glucocorticoids, which can be overcome by local stimulatory growth factors when present in sufficient amounts.


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