Biochemical Studies on the Number and the Compostion of Liver Cells in Postnatal Growth of the Rat

Fukuda, Michio; Sibatani, Atuhiro

doi:10.1093/oxfordjournals.jbchem.a126356

Cited by 55 publications

(9 citation statements)

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“…The distribution of total cholesterol label in Kupffer cells compared with whole liver, compared per unit weight of protein, was 1.4 ± 0.11 (SE). Because the Kupffer cells comprise only about 10% of intracellular liver volume (31) it is clear that they were responsible for a relatively small proportion of hepatic cholesterol uptake, which supports the conclusions of Di Luzio and Riggi (27). The in vitro perfused liver is able to take up triglyceride-labeled chylomicrons to the extent of 20-30% (32,33).…”

Section: Resultssupporting

confidence: 65%

Formation of cholesteryl ester-rich particulate lipid during metabolism of chylomicrons

Redgrave¹

1970

J. Clin. Invest.

480

150

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The metabolism of chylomicrons doubly labeled with cholesterol-(3)H and triglyceride-(14)C was studied in unanesthetized rats which were absorbing a fatty test meal. 10 min after intravenous injection, 80% of chylomicron cholesteryl ester, but only 20% of chylomicron triglyceride, was found in the liver. Treatment of recipient rats with puromycin to block hepatic triglyceride release did not increase the proportion of chylomicron triglyceride found in the liver. Rapid partition of chylomicron triglyceride from cholesterol ester also occurred in rats in which the liver had been excluded from the circulation. However, now the cholesteryl ester accumulated in the plasma, whereas triglyceride was cleared by peripheral tissues. Residual labeled cholesterol in the plasma of such rats was shown to be present in particulate form, together with some residual triglyceride. The remnant particles contained about 13% cholesteryl ester. When injected into other rats the remnant particles appeared in the liver more rapidly than did chylomicrons.These observations were consistent with the hypothesis that the first step in chylomicron metabolism occurred in extrahepatic tissues where a large portion of the triglyceride was removed by the action of lipoprotein lipase. The remnant particles so produced contained the chylomicron cholesteryl ester and residual triglyceride, and they were removed from the plasma by the liver.

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Section: Resultssupporting

confidence: 65%

Formation of cholesteryl ester-rich particulate lipid during metabolism of chylomicrons

Redgrave¹

1970

J. Clin. Invest.

480

150

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“…For example, during the cell cycle, mass parallels DNA content (34). In addition, changes in nuclear ploidy in association with cellular hypertrophy have been reported in hypertrophy of salivary glands induced by chronic administration of isoproterenol (26,35), in compensatory renal hypertrophy following unilateral nephrectomy (36,37), in the normal postnatal growth of rat liver (38), and in myocardial hypertrophy (39)(40)(41). In each of these hypertrophic conditions, there is an increase in the average DNA/cell ratio such that a constant ratio of cellular mass to cellular DNA is maintained.…”

Section: Discussionmentioning

confidence: 99%

Smooth muscle cell hypertrophy versus hyperplasia in hypertension.

Owens¹,

Rabinovitch²,

Schwartz³

1981

Proc. Natl. Acad. Sci. U.S.A.

190

107

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Arteries of hypertensive animals have a greater mass of smooth muscle than those of normotensive controls. We examined the contributions ofsmooth muscle cell hypertrophy and hyperplasia to this increase in mass. Cell size measurements obtained by (i) image analysis of enzyme-dispersed cells, (ii) morphometric evaluation of tissue sections, and (iU) biochemical measures of protein/cell and actin/cell ratios on isolated cells showed that average cell size was greater in spontaneously hypertensive rats than in normotensive Wistar-Kyoto and Sprague-Dawley controls. Average DNA/cell ratios were also increased in spontaneously hypertensive rats while protein/DNA ratios were not different. Analysis of nuclear DNA content of individual cells by flow microfluorimetry and Feulgen-DNA microdensitometry measurements showed that >20% of spontaneously hypertensive rat cells were polyploid while <10% of control cells were polyploid. Estimates of cell number per centimeter of aortic length, based on ploidy and DNA content, show no difference between control and hypertensive rats. Thus, smooth muscle hypertrophy alone accounts for the increased mass of smooth muscle in aortas of spontaneously hypertensive rats. Furthermore, this cellular hypertrophy is accompanied by a change in nuclear ploidy. This nuclear response in hypertension may represent a fixed change related to the establishment of a chronic hypertensive state.Folkow and others have implicated thickening ofresistance vessels in the maintenance of increased peripheral resistance in established hypertension (1)(2)(3)(4)(5). This thickening is due, at least in part, to an increase in smooth muscle cell mass (6, 7). It is unclear, however, whether this is due to an increase in cell size-i. e., hypertrophy-or to an increase in cell number-i.e., hyperplasia. Increased cell number has been inferred from increased numbers of vascular smooth muscle cells labeling with [3H]thymidine (8-12) and from an increase in DNA per unit vessel length (11,12) (14), and the endothelium was removed with a piece of Teflon. Media preparations were used for subsequent isolation of smooth muscle cells and for DNA determinations described elsewhere.Smooth muscle cells were isolated by enzyme dispersion as described by . After digestion, cell suspensions were filtered through 250-gm stainless steel wire mesh to remove tissue debris and undigested tissue. The filtrate was centrifuged (200 x g, 5 min), and the cell pellet was suspended in Ca2+-, Mg2e-free Hanks' buffer/0.5 mM ethylene glycol bis(f-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Following incubation for 15-20 min at 370C, cells were fixed (2% glutaraldehyde/1% paraformaldehyde in phosphate buffer, pH 7.0) overnight. Cell viability was >90% as measured by trypan blue exclusion. Cellular yield, determined by DNA assay, was =20% with the greatest loss occurring during the filtration step.For sizing of isolated cells, cell smears of fixed cells were air dried and stained with hematoxylin/eosin. Area measurements (Am2) were ...

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“…Cell size is usually determined by the amount of protein/cell (46,47), which in turn requires an increase in the amount of rRNA (47,48). An increased synthesis of rRNA implies a larger number of ribosomes, hence more protein synthesis and an enlargement of cells (48).…”

Section: Discussionmentioning

confidence: 99%

Nuclear Translocation of Insulin Receptor Substrate-1 by Oncogenes And Igf-I

Batta

Innocent

et al. 2002

Journal of Biological Chemistry

174

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The insulin receptor substrate-1 (IRS-1) is one of the major substrates of both the insulin and IGF-I receptors and is generally localized in the cytosol/membrane fraction of the cell. We show here that a substantial fraction of IRS-1 is translocated to the nucleus in mouse embryo fibroblasts (MEF) expressing the simian virus 40 T antigen. Nuclear translocation of IRS-1 occurs also in MEF stimulated with IGF-I or in MEF expressing the oncogene v-src. Nuclear translocation of IRS-1 can be demonstrated by confocal microscopy, immunohistochemistry, or subcellular fractionation. An antibody to IRS-1 immunoprecipitates from nuclear fractions (but not from cytosolic fractions) the upstream binding factor, which is a key regulator of RNA polymerase I activity and ribosomal RNA (rRNA) synthesis. In agreement with this finding, in 32D murine hemopoietic cells, nuclear translocation of IRS-1 correlates with a markedly increased rRNA synthesis. Our experiments suggest that nuclear IRS-1 may play a specialized role in rRNA synthesis and/or processing.The insulin receptor substrate (IRS) 1 proteins are a family of docking proteins, which include IRS-1-4, Gab-1, and p62 dok (1). IRS-1 was the first to be identified as a docking protein for both the insulin and the IGF-I receptors. It transmits a signal from both receptors by interacting with a number of partners, including phosphatidylinositol 3-kinase, SHP2, Grb2, Crk, and others (2, 3). Tyrosine kinase activity of the receptors and phosphorylation of IRS-1 are essential steps in signal transduction. Of the downstream signals generated by IRS-1, the best studied is the phosphatidylinositol 3-kinase signaling pathway, which plays a major role in a number of biological responses to growth factors (1, 4). IRS-1 interacts directly with both the insulin and the IGF-I receptors, and the domains required for their interaction have also been identified (5). Because of its direct interaction with the receptors, its size, and its downstream signaling, it has been generally assumed that IRS-1 is an exclusively cytosolic (or plasma membrane) protein (6, 7). However, IRS-1 is known to interact with the SV40 T antigen (8, 9) and nucleolin (10). T antigen and nucleolin are predominantly nuclear proteins, although minor fractions of either protein can be found in the cytosol (11-13). It has been therefore tacitly assumed that IRS-1, anchored to the receptor, was interacting with the minor cytosolic fractions of T antigen and nucleolin. There is evidence, however, that signal-transduction molecules can translocate to the nucleus. They include mitogen-activated protein kinase (14), p70 S6K /TOR (15, 16), the STAT proteins (17, 18), Akt (19), ␤-catenin (20), the epidermal growth factor receptor (21), phosphatases (22), IRS-3 (23), and a cleaved ErbB-4 receptor (24). Indeed, Jans and Hassan (25) have summarized in a review the evidence that growth factors and their receptors can accumulate in the nuclei of cells. IGF-I, IGF-IR, and IRS-1 are not mentioned in that review, but insulin is (26).T...

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Biochemical Studies on the Number and the Compostion of Liver Cells in Postnatal Growth of the Rat

Cited by 55 publications

References 0 publications

Formation of cholesteryl ester-rich particulate lipid during metabolism of chylomicrons

Formation of cholesteryl ester-rich particulate lipid during metabolism of chylomicrons

Smooth muscle cell hypertrophy versus hyperplasia in hypertension.

Nuclear Translocation of Insulin Receptor Substrate-1 by Oncogenes And Igf-I

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