| First Author | Li YY | Year | 1998 |
| Journal | Am J Physiol | Volume | 274 |
| Issue | 1 Pt 2 | Pages | H331-41 |
| PubMed ID | 9458884 | Mgi Jnum | J:45819 |
| Mgi Id | MGI:1196158 | Doi | 10.1152/ajpheart.1998.274.1.H331 |
| Citation | Li YY, et al. (1998) IL-1 beta alters the expression of the receptor tyrosine kinase gene r-EphA3 in neonatal rat cardiomyocytes. Am J Physiol 274(1 Pt 2):H331-41 |
| abstractText | To identify proinflammatory cytokine responsive genes in the myocardium, we used differential display to study RNA isolated from neonatal rat cardiac myocytes treated with tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Sequence analysis of differential display products confirmed by reverse Northern blots revealed one clone as the partial sequence of an Eph-related receptor tyrosine kinase (r-EphA3). In cardiac myocytes, 36-h exposure to TNF-alpha and IL-1 beta reduced r-EphA3 transcripts to 59.9% (P < 0.01) of control levels; this effect was largely dependent on IL-1 beta. Western blot analysis showed that changes in r-EphA3 protein levels reflect that seen for transcripts. Cardiac nonmyocytes expressed substantially lower levels of r-EphA3. Full-length r-EphA3 cDNA clone (3,077 base pair) yielded an amino acid sequence with 90-98% homology to the Eph receptor human EphA3, chick EphA3, and mouse EphA3. In the adult rat, r-EphA3 transcripts were most abundant in the heart, brain, and lung. These results suggest that IL-1 beta may exert its effect on cardiac myocytes at least in part by altering r-EphA3 expression. |
