Evidence for the macromolecular basis of regulation of heart hypertrophy.
In vivo treatment of rats with triiodothyronine (0.3 micrograms per g body wt for four consecutive days) increases both poly (ADP-ribose) polymerase activity and DNA synthesis in myocardial nuclei obtained from 18-21-days-old rats. The same T3-treatment in 30-33-days-old rats inhibits poly(ADP-ribose) polymerase activity and simultaneously increases RNA syntheses in myocardial nuclei. A correlation was observed between the degree of inhibition of poly(ADP-ribose) polymerase and ventricular enlargement in triiodothyronine treated animals. RNA synthesis in isolated myocardial nuclei was inhibited by in vitro polyADP-ribosylation only when myocardial nuclei were obtained from triiodothyronine treated animals. In vitro poly ADP-ribosylated proteins were isolated from myocardial nuclei by the SDS-phenol extraction. More than 90% of the protein-polyADP-ribose adducts partitioned into the aqueous phase behaving as if they were nucleic acids. Treatment with triiodothyronine significantly, diminished polyADP-ribosylation of three specific groups of polyADP-ribosylated non-histone chromatin proteins corresponding to 130 kDa, 90-80 kDa and 80-65 kDa.
D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism*; D002868:Chromosomal Proteins, Non-Histone / Q000378:metabolism; D004247:DNA / Q000096:biosynthesis*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009244:NAD+ Nucleosidase / Q000378:metabolism*; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism*; D012313:RNA / Q000096:biosynthesis*; D051381:Rats; D014284:Triiodothyronine / Q000633:toxicity
D002868:Chromosomal Proteins, Non-Histone; D000067856:Poly(ADP-ribose) Polymerase Inhibitors; D014284:Triiodothyronine; D012313:RNA; D004247:DNA; D011065:Poly(ADP-ribose) Polymerases; D009244:NAD+ Nucleosidase