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At least 55 records · Page 3Linked to original sources
PubMed2000

Cell-enlargement-related polypeptides are induced via beta(1)-adrenoceptors in mouse parotids.

Induction of cell and gland enlargement (growth-in-size) and induction of a group of secretory polypeptides (polypeptides C-G) seem to occur in close relationship in mouse parotid glands stimulated chronically by the nonselective beta-adrenergic agonist isoproterenol. To determine whether beta(1), beta(2), or both subtypes of beta-adrenergic receptors are involved in those responses, dose-dependency studies were carried out during a 7-day period of daily stimulations to assess the relative abilities of the selective beta-adrenergic agonists dobutamine (beta(1)) and salbutamol (beta(2)) to induce polypeptides C-G and growth-in-size. The relative abilities of the selective beta-adrenoceptor antagonists atenolol (beta(1)) and I.C.I. 118.551 (beta(2)) to interfere with the induction of both responses by chronic treatment with the various beta-adrenergic agonists were also studied. Parotid growth-in-size was assessed by evaluating wet weight, whole protein content, and light microscopy histology. The presence of polypeptides C-G was evaluated after SDS-polyacrylamide gel electrophoresis and Coomassie blue staining. Under these experimental conditions, dobutamine was found to be at least one order of magnitude more potent than salbutamol at inducing growth-in-size. Dobutamine was also found to be clearly stronger than salbutamol as an inducer of polypeptides C-G. On the other hand, atenolol was more effective than I.C.I. 118.551 at preventing the induction of polypeptides C-G and growth-in-size by isoproterenol, dobutamine, or salbutamol. Taken together, these results suggest that in mouse parotid glands, polypeptides C-G and growth-in-size are induced preferentially via adrenergic receptors of the beta(1)-subtype.

Adrenergic beta-Agonists↗
PubMed2002

Cell division and cell enlargement in isolated Cucurbita cotyledons grown in darkness and in light.

The spatial and temporal patterns of post-embryonal cell growth and cell division were characterised in excised cotyledons of vegetable marrow ( Cucurbita pepo L. var. giromontia Alef.) incubated in water. The concurrent roles of these two processes in cotyledon growth were determined using paradermal sections of the first palisade layer of developing cotyledons. Tissue specificity was observed in the pattern of cell division. The daughter cells derived from an initial cell, which had already differentiated before imbibition of the seeds, were tightly packed in a cluster, which enabled us to monitor cell division during early cotyledon development. Heterogeneity of cell size was recognised during the process of cell proliferation in the cluster, suggesting that cell division is uncoupled from control of cell size. There was significantly more cell division in the marginal part of the cotyledons than in other parts, suggesting high activity of the marginal meristem. Light enhanced cell and cotyledon enlargement, but had no effect on the number of divisions. This study elucidated the cellular basis of post-germinative Cucurbita cotyledon morphogenesis and development.

Journal Article↗
PubMed1981

Obesity: can some fat cells enlarge while others are shrinking?

CBA mice were made obese by injection with gold thioglucose (GTG). After receiving transplants of "lean" and "GTG-obese" fat under separate kidney capsules, the host mice were fed a restricted diet for three weeks. Over this period, the fat cells in the lean grafts enlarged whereas the fat cells in the GTG-obese grafts shrank. Concurrent fat loss and fat gain can therefore take place.

Adipose Tissue↗
PubMed1999

Separating growth from elastic deformation during cell enlargement

Plants change size by deforming reversibly (elastically) whenever turgor pressure changes, and by growing. The elastic deformation is independent of growth because it occurs in nongrowing cells. Its occurrence with growth has prevented growth from being observed alone. We investigated whether the two processes could be separated in internode cells of Chara corallina Klien ex Willd., em R.D.W. by injecting or removing cell solution with a pressure probe to change turgor while the cell length was continuously measured. Cell size changed immediately when turgor changed, and growth rates appeared to be altered. Low temperature eliminated growth but did not alter the elastic effects. This allowed elastic deformation measured at low temperature to be subtracted from elongation at warm temperature in the same cell. After the subtraction, growth alone could be observed for the first time. Alterations in turgor caused growth to change rapidly to a new, steady rate with no evidence of rapid adjustments in wall properties. This turgor response, together with the marked sensitivity of growth to temperature, suggested that the growth rate was not controlled by inert polymer extension but rather by biochemical reactions that include a turgor-sensitive step.

Journal Article↗
PubMed2004

Phosphorylation of RNA polymerase II in cardiac hypertrophy: cell enlargement signals converge on cyclin T/Cdk9.

Cardiac myocyte enlargement is the eponymous characteristic of cardiac hypertrophy, regardless of the instigating signal. Such triggers include biomechanical stress (e.g., work load, compensation for ischemic damage), sarcomeric protein mutations, cytoskeletal protein mutations, abnormal energetics, G protein-coupled receptors for ligands (including angiotensin II and endothelin-1), or their signal transducers within cells. In turn, increased myocyte size reflects increased RNA and protein content per cell as responses to these stimuli. In eukaryotic cells, the large subunit of RNA polymerase II (RNAPII) becomes extensively phosphorylated in its serine-rich C-terminal domain (CTD) during the transition from transcript initiation to transcript elongation - that is, "escape" of RNAPII from the promoter-proximal region into the open reading frame. Although this process is believed to be crucial to productive synthesis of mRNA and is known to be governed by two atypical cyclin-dependent kinases, Cdk7 and Cdk9, surprisingly little is understood of how regulatory pathways within cells intersect these RNAPII-directed protein kinases. Investigations of the CTD kinase module in cardiac hypertrophy provide a tentative initial map of a molecular circuit controlling cell size through regulated phosphorylation of RNAPII.

Animals↗
PubMed2005

The transcription factor AP-2beta causes cell enlargement and insulin resistance in 3T3-L1 adipocytes.

We have reported the association of variations in the activating protein-2beta (AP-2beta) transcription factor gene with type 2 diabetes. This gene was preferentially expressed in 3T3-L1 adipocytes in a differentiation stage-dependent manner, and preliminary experiments showed that subjects with the disease-susceptible allele showed stronger expression in adipose tissue than those without the susceptible allele. Thus, we overexpressed the AP-2beta gene in 3T3-L1 adipocytes to clarify whether AP-2beta might play a crucial role in the pathogenesis of type 2 diabetes through dysregulation of adipocyte function. In cells overexpressing AP-2beta, cells increased in size by accumulation of triglycerides accompanied by enhanced glucose uptake. On the contrary, suppression of AP-2beta expression by small interfering RNA inhibited glucose uptake. Enhancement of glucose uptake by AP-2beta overexpression was attenuated by inhibitors of phospholipase C (PLC) and atypical protein kinase Czeta/lambda (PKCzeta/lambda), but not by a phosphatidylinositol 3-kinase (PI3-K) inhibitor. Consistently, we found activation of PLC and atypical PKC, but not PI3-K, by AP-2beta expression. Furthermore, overexpression of PLCgamma enhanced glucose uptake, and this activation was inhibited by an atypical PKC inhibitor, suggesting that the enhanced glucose uptake may be mediated through PLC and atypical PKCzeta/lambda, but not PI3-K. Moreover, we observed the increased tyrosine phosphorylation of Grb2-associated binder-1 (Gab1) and its association with PLCgamma, indicating that Gab1 may be involved in AP-2beta-induced PLCgamma activation. Finally, AP-2beta overexpression was found to relate to the impaired insulin signaling. We propose that AP-2beta is a candidate gene for producing adipocyte hypertrophy and may relate to the abnormal characteristics of adipocytes observed in obesity.

3T3-L1 Cells↗
PubMed1995

Chlorsulfuron blocks 2,4-D-induced cell enlargement and NADH oxidase in excised sections of soybean hypocotyls.

Elongation of soybean hypocotyl sections induced by the auxin herbicide, 2,4-dichlorophenoxyacetic acid (2,4-D), was blocked by micromolar concentrations of the sulfonylurea herbicide chlorsulfuron (2-chloro-N-[[(4-methoxy-6-methyl-1,3,5-trizin-2- yl)amino]carbonyl]benzenesulfonamide). The inhibition at equimolar concentrations of 2,4-D and chlorsulfuron was overcome by a 10- or 100-fold excess of 2,4-D. Stimulation by 2,4-D of an 2,4-D-responsive NADH-oxidase activity of the soybean plasma membrane also was blocked by the presence of concentrations of chlorsulfuron equimolar to the 2,4-D. Chlorsulfuron alone was largely without effect on either cell elongation or the auxin-stimulated NADH-oxidase activity over a range of chlorsulfuron concentrations. The results show a clear correlation between inhibition of auxin-stimulated cell elongation and the inhibition of an auxin-stimulated component of a plasma membrane NADH-oxidase activity.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1955

Cytological studies on the antimetabolite action of 2, 6-diaminopurine in Vicia faba roots.

At a concentration of 9.6 x 10(-5)M, 2,6-diaminopurine (DAP) completely inhibited cell enlargement, cell division, and DNA synthesis (determined by microphotometric measurement of Feulgen dye) in Vicia faba roots. Inhibition of cell enlargement was partially reversed by adenine, guanine, xanthine, adenosine, and desoxyadenosine. Guanine and the nucleosides gave the greatest reversal, suggesting that one point of DAP action upon cell enlargement is a disruption of nucleoside or nucleotide metabolism, possibly during pentosenucleic acid synthesis. DAP inhibited cell division by preventing onset of prophase. At the concentrations used it had no significant effect on the rate or appearance of mitoses in progress. Inhibition of entrance into prophase was not directly due to inhibition of DNA synthesis since approximately half of the inhibited nuclei had the doubled (4C) amount of DNA. Adenine competitively reversed DAP inhibition of cell division, giving an inhibition index of about 0.5. Guanine gave a slight reversal while xanthine, hypoxanthine, adenosine, and desoxyadenosine were inactive. A basic need for free adenine for the onset of mitosis was suggested by this reversal pattern. Meristems treated with DAP contained almost no nuclei with intermediate amounts of DNA, indicating that DAP prevented the onset of DNA synthesis while allowing that underway to reach completion. The inhibition of DNA synthesis was reversed by adenine, adenosine, and desoxyadenosine although synthesis appeared to proceed at a slower rate in reversals than in controls. Inhibition of DNA synthesis by DAP is probably through nucleoside or nucleotide metabolism. A small general depression of DNA content of nuclei in the reversal treatments was observed. This deviation from DNA "constancy" cannot be adequately explained at present although it may be a result of direct incorporation of DAP into DNA. The possible purine precursor, 4-amino-5-imidazolecarboxamide gave no reversal of DAP inhibition of cell elongation and cell division and only a slight possible reversal of inhibition of DNA synthesis.

2-Aminopurine↗
PubMed1989

Turgor and growth at low water potentials.

Turgor affects cell enlargement but has not been measured in enlarging tissue of intact plants when growth is inhibited by inadequate water. Mature or excised tissue can be problematic for these measurements because turgor may not be the same as in intact enlarging cells. Therefore, we measured the average turgor in the elongating region of intact stems of soybean (Glycine max [L.] Merr.) while the seedlings were exposed to low water potentials by transplanting to vermiculite of low water content. Stem growth was completely inhibited by the transplanting, and the average turgor decreased in the mature stem tissue. However, it did not decrease in the elongating region whether measured in intact or excised tissue (total of four methods). At the cellular level, turgor was uniform in the elongating tissue except at transplanting, when turgor decreased in a small number of cortical cells near the xylem. The reduced turgor in these cells, but constant turgor in most of the cells, confirmed that no general turgor loss had occurred but indicated that gradients in water potential extending from the xylem into the enlarging tissue were reduced, thus decreasing the movement of water into the tissue for cell enlargement. A modest growth recovery occurred after 2 days and was preceded by a recovery of the gradient. This suggests that under these conditions, growth initially was inhibited not by turgor loss but by a collapse of the water potential gradient necessary for the growth process.

Journal Article↗