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A M Novi

Publications and source records attributed to A M Novi.

At least 19 recordsLinked to original sources
PubMed1980

[Early morphological changes during the development of cardiac hypertrophy (author's transl)].

The development of a cardiac hypertrophy depends on modulation of two parameters, such as the amount of increased work load imposed on the heart and the rapidity with which the work load is applied. A gradual development of cardiac hypertrophy is usually observed in humans; at variance, the induction of cardiac hypertrophy is quite a rapid process in animal experiments. The enlargement of cardiac muscle cells during hypertrophy is due not only to an increased synthesis of contractile proteins but also to an accumulation of other cell constituents parallelly involved in the hypertrophy process. The mechanism whereby new sarcomeres are formed during cardiac hypertrophy is not yet completely clarified. Once the stimulus producing overload is removed, cardiac hypertrophy can regress completely. The possible role of biological regulators in inducing cardiac hypertrophy was also discussed.

Aging↗
PubMed1977

Aurintricarboxylic acid (ATA) and DNA synthesis. I. Inhibition of DNA synthesis by ATA in Go cells stimulated to proliferate.

Aurintricarboxylic acid (ATA) at a concentration which produces 40% inhibition of protein synthesis, inhibits completely isoproterenol-stimulated DNA synthesis in mouse parotid glands. The drug was found to interfere with some essential changes occurring during the prereplicative phase of IPR-stimulated DNA synthesis. It inhibits the increase in ribosonal protein synthesis that takes place by 2 h after stimulation. The peak of ribosonal RNA that occurs 8 h after isoproterenol was also abolished by ATA. Since the drug completely inhibits isoproterenol-stimulated DNA synthesis, these results suggest that the control of ribosome production may be involved in cell growth activation. In view of the finding that ATA first inerferes with the binding of adenylate-rich RNA to polysomes, it was suggested that the drug may act by preferentially inhibiting that fraction of protein synthesis dependent on the newly transcribed messenger RNA.

Animals↗
PubMed1977

Aurintricarboxylic acid (ATA) and DNA synthesis. II. Effect of ATA on structure and function of the crypts of the small intestine.

ATA affects only slightly DNA synthesis of continuously replicating cells. A single injection of the drug reduces the incorporation of (3H)-thymidine into DNA of crypt cells to only 62% of the control. The effect on DNA synthesis is preceded by a slight inhibition of protein synthesis, and by a partial decrease in the number of dividing cells. On the contrary, the incorporation of (3H)-uridine into RNA was enhanced. Electron microscopic studies revealed no cytologic abnormalities in ATA-treated animals. In view of the fact that ATA at the same concentration inhibits DNA synthesis of growth stimulated cells to 100% (Novi, 1976), it was suggested that the drug may become an useful tool in inducing a preferential inhibition of growth stimulation.

Animals↗
PubMed1976

Molecular basis of a control mechanism of DNA synthesis in mammalian cells.

Personal observations made on the model of isoproterenol-stimulated DNA synthesis have pointed out the following: 1) cell hypertrophy precedes constantly the onset of DNA synthesis; 2) the length of the G1 phase is mass-dependent; 3) accumulation of ribosomes is needed for cell progress through G1; 4) ribosomal protein synthesis is involved in cell growth activation. These results together with a consideration of the pertinent literature allow us to formulate a hypothesis on the control of cell division in mammalian cells. DNA synthesis might be the terminal event in a chain of metabolic processes whereby a cell adjusts itself to increased functional demands (Increased Functional Demand Hypothesis). The main points of this model are the following: the interaction of the extracellular effector on the target cells first activates the pre-existent protein-synthesizing apparatus of the cell, which in turn brings about the activation of the "translation-transcription connecting mechanism" whereby the cells adjusts itself to an increased need for protein synthesis. Such a mechanism is characterized by cytoplasmic signals arising from the protein-synthesizing apparatus of the cell which reach the nucleus and call forth a messenger RNA for ribosomal proteins. The latter, once synthesized, protect the nascent ribosomal RNA from nuclease attack, resulting in an accumulation of ribosomes in the cytoplasm. Once the ribosomes have reached a "critical amount", the cell is triggered to enter DNA synthesis. As a link between the enhanced ribosomal RNA synthesis and DNA synthesis a reduction in the capacity of the ribonucleotide pool as source of DNA precursors has been suggested.

Animals↗
PubMed1975

Synthesis of poly(A)-associated RNA in the prereplicative phase of isoproterenol-stimulated DNA synthesis.

Rapidly labelled RNA containing poly(A) sequences has been isolated from polysomes of mouse parotid glands. Filtration on Millipore and binding to poly(u) immobilized on Sepharose-4B, together with significant RNase-resistance (11-16%) indicated that this polysomal fraction contains large tracts of polyadenylate sequences. A single injection of isoproterenol, a procedure that causes, after a lag period of 20 hrs, a marked stimulation of DNA synthesis and cell division in salivary glands of rodents, induces a biphasic increase in the incorporation of (3H)-adenosine into poly(A)-associated polysomal RNA. The incorporation of (3H)-adenosine is already increased within 1 hour after stimulation, decreases at 3 hrs and increases again at 8 hrs, parallelling previously reported changes on chromatin template activity of mouse parotids. However, the percent poly(A) content, and the size of the poly(A)-associated RNA remain constant. Actinomycin D given 30 min prior to isoproterenol, inhibits isoproterenol-Stimulated poly(A)-rich RNA synthesis. These results demonstrate that, as part of the early molecular events of its action, isoproterenol regulates transcription of adenylate-rich RNA in mouse parotid gland.

Animals↗
PubMed1972

Changes in chromatin template activity and their relationship to DNA synthesis in mouse parotid glands stimulated by isoproterenol.

Chromatin template activity of mouse parotid glands increases after a single injection of isoproterenol (IPR), a procedure that causes, after a lag period of 20 hr, a marked stimulation of DNA synthesis and cell division in salivary glands of rodents. The increase in chromatin template activity occurs as early as 1 hr and peaks between 6 and 10 hr after IPR, paralleling previously reported changes in the incorporation of uridine-(3)H into total cellular RNA of mouse parotids. Template activity was measured in vitro in a system in which parotid gland chromatin was incubated with an exogenous RNA polymerase isolated from Escherichia coli. Similar results were obtained when template activity of parotid gland chromatin was assayed using an homologous RNA polymerase from mouse liver. Chromatin template activity in mouse parotids was also studied after the administration of drugs capable of inducing in salivary glands both DNA synthesis and secretion or secretion alone. The results indicate that the increased chromatin template activity occurring 6 hr after IPR is related to the subsequent onset of DNA synthesis. Furthermore, the increased chromatin template activity caused by IPR is inhibited by the previous administration of puromycin, an inhibitor of IPR-stimulated DNA synthesis.

Animals↗