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Nucleic Acids Research, 1985, Vol. 13, No. 6 1953-1963
© 1985

Articles

Induction of liver apolipoprotein A-IV mRNA in porphyric mice

Arthur M. Buchberg and Alan J. Kinniburgh

Department of Human Genetics, Roswell Park Memorial Institute, New York State Department of Health 666 Elm Street, Buffalo, NY 14263, USA

Received December 10, 1984. Revised February 1, 1985. Accepted February 1, 1985.

We have isolated cDNA clones for mRNAS that are Induced by porphyria from a mouse liver library. Of the three inducible clones isolated, we have identified one as being apolipoprotein A-IV (apo A-IV) by its extensive homology with a rat apollpoprotein A-IV cDNA sequence. The level of liver apo A-IV mRNA increases rapidly in response to either of two porphyrogenic drugs. When the ferrochelatase-inhibited drug, 3,5-dicarbethoxy- 1,4,-dihydrocoilidine (DDC) is used, a 6 and 28 fold induction of liver apo A-IV mRNA is observed in male and female mice, respectively, if the heme-destroying porphyrogenic drug, allylisopropylacetamide (AIA) is the inducing agent, liver apo A-IV mRNA levels increase 2–3 fold in both males and females. The level of apo A-IV mRNA reaches a maximum within 6–10 hr. after drug administration. Intestine apo A-IV mRNA levels do not change during either of these drug-induced porphyrias. RNA from acute-phase responsive liver or liver from mice treated with bilirubin, porphobilinogen, or protoporphyrin IX show no increase in apo A-lV mRNA. These results indicate that apo A-IV induction is tied to a disruption in porphyrin-heme biosynthesis but is not directly affected by several heme intermediates nor by the major heme degradation product, bilirubin.


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