PMID- 10805080 OWN - NLM STAT- MEDLINE DCOM- 20000717 LR - 20231213 IS - 0302-766X (Print) IS - 0302-766X (Linking) VI - 300 IP - 1 DP - 2000 Apr TI - Acute-phase response and circadian expression of connexin26 are not altered in connexin32-deficient mouse liver. PG - 111-7 AB - In mouse hepatocytes, the gap junctional proteins connexin32 (Cx32) and connexin26 (Cx26) are expressed in the same gap junctional plaque. Expression of the major Cx32 protein is downregulated during liver regeneration and cholestasis. Here we have analyzed the acute-phase response (after experimental inflammation) and circadian connexin expression in Cx32-deficient and wild-type mouse liver. Acute-phase response was triggered by intraperitoneal injection of lipopolysaccharide (LPS). Injection of recombinant mouse interleukin-1beta (mIL-1beta), mIL-6 or tumor necrosis factor alpha (mTNF-alpha) had no inflammatory effect. Northern blot analysis of positive and negative acute-phase transcripts following stimulation with cytokine or LPS revealed no difference between Cx32-deficient livers and wild-type controls, suggesting that loss of the Cx32 gene had no effect on experimental liver inflammation. Actin, beta-fibrinogen and Cx26 transcripts were increased after endotoxin stimulation. Under conditions of hepatic acute-phase response, Cx32 transcripts were not detected in LPS-treated livers of wild-type mice. Immunoblot analysis of proteins from inflamed wild-type livers indicated a strongly diminished amount of Cx32 protein, whereas the level of Cx26 protein was increased. Although intraperitoneal injection of mIL-1, mIL-6 as well as mTNF-alpha did not induce an acute-phase response, Cx32 protein expression was diminished, suggesting that post-transcriptional downregulation of Cx32 preceded the acute-phase response. Northern blot hybridization of RNA from wild-type and Cx32-deficient mouse liver revealed a similar circadian regulation of Cx26 and GAPDH transcripts with maximal expression around 2 p.m. and a minimum after midnight. FAU - Temme, A AU - Temme A AD - Abteilung Molekulargenetik, Institut fur Genetik, Universitat Bonn, Germany. FAU - Ott, T AU - Ott T FAU - Haberberger, T AU - Haberberger T FAU - Traub, O AU - Traub O FAU - Willecke, K AU - Willecke K LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Germany TA - Cell Tissue Res JT - Cell and tissue research JID - 0417625 RN - 0 (Actins) RN - 0 (Albumins) RN - 0 (Connexins) RN - 0 (RNA, Messenger) RN - 0 (RNA, Ribosomal, 18S) RN - 127120-53-0 (Connexin 26) RN - 9001-32-5 (Fibrinogen) SB - IM MH - Actins/genetics MH - Acute-Phase Reaction/*metabolism MH - Albumins/genetics MH - Animals MH - Blotting, Northern MH - Circadian Rhythm/*physiology MH - Connexin 26 MH - Connexins/*genetics MH - Fibrinogen/genetics MH - Fluorescent Antibody Technique, Indirect MH - Gap Junctions/metabolism MH - Gene Expression/physiology MH - Liver/*metabolism MH - Mice MH - Mice, Inbred BALB C MH - Mice, Inbred C57BL MH - RNA, Messenger/analysis MH - RNA, Ribosomal, 18S/metabolism MH - Gap Junction beta-1 Protein EDAT- 2000/05/11 09:00 MHDA- 2000/07/25 11:00 CRDT- 2000/05/11 09:00 PHST- 2000/05/11 09:00 [pubmed] PHST- 2000/07/25 11:00 [medline] PHST- 2000/05/11 09:00 [entrez] AID - 10.1007/s004410000177 [doi] PST - ppublish SO - Cell Tissue Res. 2000 Apr;300(1):111-7. doi: 10.1007/s004410000177.