Interaction between sphingomyelin and DNA

Manzoli, Francesco A.; Muchmore, J.H.; Bonora, Bruna; Sabioni, A.; Stefoni, S

doi:10.1016/0005-2787(72)90405-4

Cited by 38 publications

(7 citation statements)

References 15 publications

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“…The presence of lipids inside the nucleus that could be potential substrates for PLA 2 was reported long ago [24,25] but has not received much attention. Initially considered as structural elements [26] these nuclear phospholipids may also be involved in the control of genomic activities as suggested by their higher concentration in active chromatin [27]. Cell cycle‐dependent changes in synthesis rates of the chromatin‐associated pools of phospholipids have been reported [28] and changes in fatty acid composition of nuclear phospholipids have also been described during liver regeneration [29].…”

Section: Resultsmentioning

confidence: 99%

Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level

Specty¹,

Pageaux²,

Dauça³

et al. 2001

FEBS Letters

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Pancreatic phospholipase A 2 (PLA 2 -I) stimulates U III cells proliferation, a rat uterine cell line, after binding to membrane receptors, internalization and translocation. Here, we demonstrate that during these steps of internalization, PLA 2 -I retains its hydrolytic activity and thus could exert its proliferative effect via nuclear phospholipids hydrolysis. Since fatty acids and eicosanoids released by such activity are known to be ligands of PPAR, we study the expression of these nuclear receptors and demonstrate that, in the experimental conditions where PLA 2 -I stimulates U III cells proliferation, PLA 2 -I also regulates PPAR expression indicating a possible mechanism of its proliferative effect. ß

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Section: Resultsmentioning

confidence: 99%

Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level

Specty¹,

Pageaux²,

Dauça³

et al. 2001

FEBS Letters

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“…In fact, an intranuclear complex formed by proteins, RNase-resistant RNA, SM, and phosphatidylcholine (PC), in which the RNA becomes RNase sensitive after hydrolysis of SM by SMase, has been demonstrated (Micheli et al, 1998). Low amount of SM has a stabilising effect during DNA denaturation in vitro (Manzoli et al, 1972).…”

Section: Discussionmentioning

confidence: 99%

Chromatin sphingomyelin changes in cell proliferation and/or apoptosis induced by ciprofibrate

Albi¹,

Pieroni²,

Magni³

et al. 2003

Journal Cellular Physiology

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It has been shown that neutral-sphingomyelinase and sphingomyelin-synthase activities are present in chromatin and they modify the sphingomyelin (SM) content. The activity of the first enzyme is stimulated and the second inhibited, when the hepatocytes enter into the S-phase after partial hepatectomy, thus suggesting that ceramide may have a pivotal role in cell proliferation. An opposite function was attributed to ceramide in hepatocytes which undergo apoptosis after lobular ligature. In order to clarify this point, a model was developed in which the same liver cells undergo proliferation followed by induced apoptosis. To this purpose, the rats were treated for 7 days with ciprofibrate and then left without treatment for 4 days. During the treatment, the peroxisome enzyme markers increase their activity and the number of proliferating cells increases, reaching a maximum after 3 days of treatment, as shown by the number of cells positive for the proliferating cell nuclear antigen. At the same time, the chromatin sphingomyelinase activity reaches the maximum, while a similar increase is not found in the cytoplasm or in the isolated nuclei. On the contrary, SM-synthase activity is depressed in chromatin, but not in the nuclei in which a peak is shown after 3 days of ciprofibrate treatment. After drug withdrawal, the hepatocytes undergo apoptosis as confirmed by the increase of Bax and tissue transglutaminase (tTGase) expression; the chromatin SM increases as a consequence of an increase of SM-synthase activity. It can be hypothesised that chromatin SM may have a role in cell duplication by influencing the chromatin structure stability.

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“…The complex polyU:(A)5 was obtained in 0.01M Tris-HOl pH 7.5 -0.01K KgCl2 (lYmole of pol'y plus 1.5y.mole [3H] (A)5). In experiments with non-radioactive (A)5, its total amount was 6 jAmole. In all the cases the mixtures were supplemented with NaCl to a concentration 0.5K, and the complex polyU:(A)5 puryfied from non-bound (A)5 by gel-filtration on Sephadex G-25.…”

Section: Methodsmentioning

confidence: 99%

Interaction of polynucleotides with natural and model membranes

et al. 1980

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Interaction between sphingomyelin and DNA

Cited by 38 publications

References 15 publications

Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level

Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level

Chromatin sphingomyelin changes in cell proliferation and/or apoptosis induced by ciprofibrate

Interaction of polynucleotides with natural and model membranes

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Interaction between sphingomyelin and DNA

Cited by 38 publications

References 15 publications

Control of cell proliferation via transduction of sPLA2‐I activity and possible PPAR activation at the nuclear level

Control of cell proliferation via transduction of sPLA2‐I activity and possible PPAR activation at the nuclear level

Chromatin sphingomyelin changes in cell proliferation and/or apoptosis induced by ciprofibrate

Interaction of polynucleotides with natural and model membranes

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Product

Resources

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Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level

Control of cell proliferation via transduction of sPLA₂‐I activity and possible PPAR activation at the nuclear level