| First Author | Tlili A | Year | 2013 |
| Journal | Mol Genet Metab | Volume | 110 |
| Issue | 3 | Pages | 371-7 |
| PubMed ID | 23920041 | Mgi Jnum | J:205302 |
| Mgi Id | MGI:5544539 | Doi | 10.1016/j.ymgme.2013.07.014 |
| Citation | Tlili A, et al. (2013) DYRK1A overexpression decreases plasma lecithin:cholesterol acyltransferase activity and apolipoprotein A-I levels. Mol Genet Metab 110(3):371-7 |
| abstractText | BACKGROUND AND AIMS: Down syndrome is caused by trisomy of all or part of human chromosome 21. Individuals with Down syndrome present some metabolic abnormalities involving lipoproteins, notably lower high-density lipoprotein levels associated with altered lecithin:cholesterol acyltransferase activity and apolipoprotein A-I levels. DYRK1A is a kinase overexpressed in Down syndrome that can activate the STAT3 pathway, which is involved in lecithin:cholesterol acyltransferase expression. Therefore, we characterized the role of DYRK1A overexpression on lecithin:cholesterol acyltransferase activity and expression in mouse models. METHODS: Effects of Dyrk1a overexpression were examined in mice overexpressing Dyrk1a by ELISA, chemical analyses and Western blotting. RESULTS: Overexpression of DYRK1A decreased plasma lecithin:cholesterol acyltransferase activity and hepatic STAT3 activation, which was associated with activation of SHP2, a tyrosine phosphatase. Although hepatic apolipoprotein E and D levels were increased in mice overexpressing DYRK1A, decreased plasma lecithin:cholesterol acyltransferase activity was associated with decreased hepatic and plasma apolipoprotein A-I levels. High-density lipoprotein-cholesterol levels were also decreased in plasma despite similar total cholesterol and non-high-density lipoprotein-cholesterol levels. CONCLUSIONS: We identified the role of DYRK1A overexpression on altered lipoprotein metabolism. |
