| First Author | Burgess-Beusse BL | Year | 1998 |
| Journal | Mol Cell Biol | Volume | 18 |
| Issue | 12 | Pages | 7269-77 |
| PubMed ID | 9819413 | Mgi Jnum | J:119774 |
| Mgi Id | MGI:3703256 | Doi | 10.1128/mcb.18.12.7269 |
| Citation | Burgess-Beusse BL, et al. (1998) C/EBPalpha is critical for the neonatal acute-phase response to inflammation. Mol Cell Biol 18(12):7269-77 |
| abstractText | Members of the C/EBP (CCAAT/enhancer binding protein) family of transcription factors play important roles in mediating the acute-phase response (APR), an inflammatory process resulting from infection and/or tissue damage. Among the C/EBP family of proteins, C/EBPbeta and -delta were thought to be the primary mediators of the APR. The function of C/EBPalpha in the APR has not been fully characterized to date. Here, we investigate the role of C/EBPalpha in the APR by using neonatal mice that lack C/EBPalpha expression. Northern blot analysis of acute-phase protein gene expression in neonatal mice treated with purified bacterial lipopolysaccharide or recombinant interleukin 1beta as an inflammation stimulus showed a strong APR in wild-type mice, but a response in C/EBPalpha null animals was completely lacking. The C/EBPalpha knockout and wild-type mice demonstrated elevations in C/EBPbeta and -delta mRNA expression and DNA binding as well as increased DNA binding of NF-kappaB, all of which are known to be important in the APR. Null mice, however, failed to activate STAT3 binding in response to lipopolysaccharide. Our results provide the first evidence that C/EBPalpha is absolutely required for the APR in neonatal mice, is involved in STAT3 regulation, and cannot be compensated for by other C/EBP family members. |
