The Two-dimensional polypeptide profile of terminally non-dividing human diploid cells*1

Lincoln, David W.; Braunschweiger, Karen; Braunschweiger, Walter R.; Smith, James R.

doi:10.1016/0014-4827(84)90674-8

Cited by 21 publications

(4 citation statements)

References 24 publications

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“…The possible mechanisms for increased serum FABP4 linking to blunted insulin sensitivity may be as follows: first, overexpression of FABP4 contributes to endoplasmic reticulum stress, inflammatory response and oxidative stress [ 34 ], which in turn may lead to insulin resistance; second, elevated serum FABP4 levels are accompanied visceral adiposity, including ectopic fat deposition in islets of the pancreas, which may induce glucose intolerance, insulin resistance and β-cell dysfunction [ 35 , 36 ]. The mechanisms for increased serum FABP4 linking to insulin secretion are also not well known, but some underlying mechanisms have been indirectly suggested.…”

Section: Discussionmentioning

confidence: 99%

Serum fatty acid-binding protein 4 levels and responses of pancreatic islet β-cells and α-cells in patients with type 2 diabetes

Wang

Cao

et al. 2021

Diabetol Metab Syndr

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Background Serum fatty acid-binding protein 4 (FABP4), as an intracellular lipid chaperone and adipokine, was reported to be related to the incidence of type 2 diabetes (T2D) and diabetic complications, but its association with pancreatic islet β-cell and α-cell functions has not been fully elucidated. So the present study was to investigate the serum FABP4 levels and responses of islet β-cells and α-cells in patients with T2D. Methods 115 patients with T2D and 89 healthy controls (HC), who received serum FABP4 levels test, were recruited to participate in this study. Moreover, 75-g oral glucose tolerance test (OGTT) was performed in T2D patients to evaluate islet β-cell and α-cell functions. Systemic insulin sensitivity and overall insulin secretion of islet β-cell function were assessed by Matsuda index using C peptide (ISIM-cp) and ratio of the area under the C peptide curve to the glucose curve (AUCcp/glu) during OGTT, respectively. Fasting glucagon (Gluca0min) and postchallenge glucagon assessed by the area under the glucagon curve (AUCgluca) were determined during OGTT to evaluate islet α-cell function. And other various clinical variables were also measured in all participants. Skewed variables were natural log-transformed (ln), such as lnFABP4. Results The serum FABP4 levels in T2D patients were significantly higher than those in HC (p < 0.05). And after partially adjusting for fasting plasma glucose, serum lnFABP4 levels were negatively correlated with lnISIM-cp (r = − 0.332, p < 0.001) and positively correlated with lnAUCcp/glu (r = 0.324, p < 0.001), lnGluca0min (r = 0.200, p = 0.040) and lnAUCgluca (r = 0.311, p < 0.001), respectively, in patients with T2D. Furthermore, when multiple linear regression analyses were applied to adjust for other various clinical variables, serum lnFABP4 levels were found to remain associated with lnISIM-cp (β = − 0.296, t = − 2.900, p = 0.005), lnAUCcp/glu (β = 0.223, t = 2.038, p = 0.046), lnGluca0min (β = 0.272, t = 2.330, p = 0.024) and lnAUCgluca (β = 0.341, t = 3.065, p = 0.004), respectively. Conclusion Increased serum FABP4 levels were closely associated with blunted insulin sensitivity, increased insulin secretion, and elevated fasting and postchallenge glucagon levels in patients with T2D.

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Section: Discussionmentioning

confidence: 99%

Serum fatty acid-binding protein 4 levels and responses of pancreatic islet β-cells and α-cells in patients with type 2 diabetes

Wang

Cao

et al. 2021

Diabetol Metab Syndr

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“…The possibility that fibroblasts express senesccncespecific gene products with antiproliferative functions has renewed interest in the identification of polypeptides overexpressed in senescent fibroblasts. Although early studies using two-dimensional polyacrylamide gel electrophoresis identified a few proteins that appeared to be senescent cell-specific, the vast majority of the proteins detected were synthesized by both young and old fibroblasts (Sakagami et al, 1979;Engelhardt et al, 1979;Lincoln et al, 1984). Senescent-specific polypeptides of 57 kDa and 55 kDa have been described by Ching and Wang (1988) and Sottile et al (1987), respectively.…”

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confidence: 99%

Altered regulation of platelet‐derived growth factor A‐chain and c‐fos gene expression in senescent progeria fibroblasts

Winkles

O'connor

Friesel

1990

Journal Cellular Physiology

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The study of human genetic disorders known as premature aging syndromes may provide insight into the mechanisms of cellular senescence. These diseases are clinically characterized by the premature onset and accelerated progression of numerous features normally associated with human aging. Previous studies have indicated that fibroblasts derived from premature aging syndrome patients have in vitro growth properties similar to senescent fibroblasts from normal individuals. As an initial approach to determine whether gene expression is altered in premature aging syndrome fibroblasts, RNA was prepared from various cell strains and used for gel blot hybridization experiments. Although normal fibroblasts only express platelet-derived growth factor (PDGF) A-chain mRNA for a brief period following mitogenic stimulation, one strain of Hutchinson-Gilford (progeria) syndrome fibroblasts, AG3513, constitutively expresses PDGF A-chain mRNA and PDGF-AA homodimers. The PDGF A-chain gene does not appear to be amplified or rearranged in these fibroblasts. AG3513 progeria fibroblasts have properties characteristic of senescent cells, including an altered morphology and a diminished mitogenic response to growth promoters. The diminished response of AG3513 progeria fibroblasts to PDGF stimulation was examined in some detail. Studies using 125I-PDGF-BB, which binds with high affinity to both A- and B-type PDGF receptors, indicate that normal and AG3513 progeria fibroblasts have a similar number of PDGF receptors. Although receptor autophosphorylation occurs normally in PDGF-stimulated AG3513 progeria fibroblasts, c-fos mRNA induction does not. The senescent phenotype of AG3513 fibroblasts is probably unrelated to their constitutive PDGF A-chain gene expression; further studies are necessary in order to directly address this issue. Also, additional analysis of this progeria fibroblast strain may provide information on the control of mitogen-inducible gene expression in normal cells.

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“…It is not known whether increased protein degradation in old cells is caused by an increased proportion of aberrant proteins or an inability to regulate protein turnover in response to growth signals. However, direct attempts to observe abnormal protein on two-dimensional gel electrophoresis and increased error rates have failed to reveal significant general differences between young and old cells (Wilson et al, 1978;Engelhardt et al, 1979;Wojtyk & Goldstein, 1980;Lincoln et al, 1984). Since early-passage cells at confluence have elevated degradation rates, comparable to that of old cells, the increased protein degradation observed during exponential growth of old cells may result from an inability to inhibit protein degradation in response to growth signals.…”

Section: Discussionmentioning

confidence: 99%

Protein Turnover During Aging of Cultured Human Fibroblasts

Harley

Goldstein

1990

Can. J. Aging

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RÉSUMÉLes cellules qui vieillissent in vitro ou bien celles qui sont prélevées de donneurs d'àge avancé ou de sujets manifestant certaines des particularités qui s'apparentent à un vieillissement accéléré (progérie ou le syndrome de Werner), peuvent être qualifiées de 'vieilles'. Celles-ci on des taux de croissance ralentis en milieu de culture si on les compare aux cellules nouvelles ou à mi-passage prélevées de jeunes donneurs normaux. Durant la croissance exponentielle, les taux de constantes pour la synthèse protéique dans les jeunes cellules ne sont pas significativement différents de ceux retrouvés dans les vieilles cellules (0.023 ± 0.002 h1 vs. 0.021 ± 0.002 h1 respectivement) et pourtant les taux de croissance (i.e. accrétion protéique) sont de seulement 0.013±0.003 h1 dans les vieilles cellules comparés à 0.022±0.002 h1 dans les jeunes cellules. Done, le taux ralenti d'accumulation protéique durant la croissance des vieilles cellules comparé aux jeunes cellules est associé à une dégradation protéique accélérée (0.01±0.002h1 vs 0.001 ±0.002 h1; P <0.05) plutôt qu'à des taux ralentis de synthèse protéique. Lorsque les cellules deviennent quiescentes suivant une période d'inhibition de croissance due à la densité, les taux de synthèse protéique diminuent dans les jeunes et les vieilles cellules pour aboutir à des niveaux comparables (0.013±0.002 h1) où les taux de croissance (0.003±0.0003 h1) et de dégradation (0.01±0.003 h1) ne sont significativement pas differents dans les deux groupes. Done, ce n'est qu'en période de croissance exponentielle qu'une différence dans le turn-over protéique entre jeunes et vieilles cellules est observée, alors que la dégradation est accélérée dans les vieilles cellules. La relation causale entre la dégradation protéique accélérée et les taux de croissance ralentis dans les vieilles cellules demeure inconnue.

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The Two-dimensional polypeptide profile of terminally non-dividing human diploid cells*1

Cited by 21 publications

References 24 publications

Serum fatty acid-binding protein 4 levels and responses of pancreatic islet β-cells and α-cells in patients with type 2 diabetes

Serum fatty acid-binding protein 4 levels and responses of pancreatic islet β-cells and α-cells in patients with type 2 diabetes

Altered regulation of platelet‐derived growth factor A‐chain and c‐fos gene expression in senescent progeria fibroblasts

Protein Turnover During Aging of Cultured Human Fibroblasts

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