Age-related changes in membrane lipid composition, fluidity and respiratory burst in rat peritoneal neutrophils

Alvarez, Eloísa; Ruı́z-Gutı́errez, Valentina; Sobrino, Francisco; Santa-María, Consuelo

doi:10.1046/j.1365-2249.2001.01490.x

Cited by 62 publications

(38 citation statements)

References 57 publications

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“…These data are in accordance with those obtained in cultured cells and tissues (1,5,16,29). The increase of membrane fluidity can also be explained by a change in fatty acid lipid composition that causes an increase in free volume between the lipid chains, due to the presence of double bounds in fatty acids (18:2 and 20:4), leading to a bend in the lipid chain itself.…”

Section: Discussionsupporting

confidence: 90%

Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema

Palestini

Calvi

Conforti

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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. Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema. Am J Physiol Lung Cell Mol Physiol 282: L1382-L1390, 2002. First published February 1, 2002 10.1152/ajplung.00447.2001.-We evaluated the changes in plasma membrane composition, biophysical properties, and morphology of pulmonary endothelial cells in anesthetized rabbits receiving 0.5 ml ⅐ kg Ϫ1 ⅐ min Ϫ1 saline infusion for 180 min, causing mild interstitial edema. Plasma membrane fractions were obtained from lung homogenates with gradient centrifugation, allowing a sixfold enrichment in caveolin-1. In edematous lungs, cholesterol content and phospholipidic phosphorus increased by 15 and 40%, respectively. These data correlated with morphometric analysis of lungs fixed in situ by vascular perfusion with 2.5% glutaraldehyde, suggesting a relative increase in surface of luminal to interstitial front of the capillary endothelial cells, due to a convoluted luminal profile. In edematous lungs, the fraction of double-bound fatty acids increased in membrane lipids; moreover, the phosphatidylcholine/phosphatidylethanolamine and the cholesterol/phospholipid ratios decreased. These changes were consistent with the increase in fluorescence anisotropy of plasma membrane, indicating an increase in its fluidity. Data suggest that mechanical stimuli elicited by a modest (ϳ4%) increase in extravascular water cause marked changes in plasma membranes that may be of relevance in signal transduction and endothelial cell activation. rabbit; air-blood barrier; endothelial cells; membrane composition and fluidity THE ALVEOLAR AND CAPILLARY walls delimit the pulmonary interstitium, a thin compartment made of a fiber system, serving as a scaffold, and other macromolecules forming the capillary and the alveolar basement membranes. Extravascular water is distributed within the interstitial compartment of the air-blood barrier and is physiologically kept at a minimum volume to optimize gas diffusion. Recent work, based on an experimental model causing a mild form of pulmonary interstitial edema, allowed us to describe the mechanisms contributing to a tight control of extravascular lung volume in the air-blood barrier (6,20). These studies also showed that, despite a remarkable resistance of the pulmonary tissue to edema formation, the increase in interstitial fluid volume occurs as a consequence of fragmentation of proteoglycans, important macromolecules of the extracellular matrix (24,25,31,32) controlling microvascular permeability and tissue mechanical resistance. We wished to further investigate the condition of mild interstitial edema because it represents a critical equilibrium between matrix degradation and deposition provided by cellular activation. We focused on cellular involvement in mild interstitial edema, particularly on the composition and fluidity of plasma membranes that are known to be sensitive to alterations in chemical and physical stimuli of the environment surrounding the cells (34, 36). MATERIALS AND METHODS C...

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Section: Discussionsupporting

confidence: 90%

Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema

Palestini

Calvi

Conforti

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…8). Similar changes were seen in hepatocytes from old rats (46), although other studies using various types of tissues have shown enzyme activities to increase (32), decrease (2), and stay the same (6). Glutathione peroxidase has been shown to be essential for the survival of HUVECs after treatment with peroxides (22).…”

Section: Discussionsupporting

confidence: 69%

“…We observed a very small percentage of large cells in our young cultures (Ͻ20 CPD), and these cells tended to stain positive for senescence-associated ␤-galactosidase and were often multinucleated (data not shown). Similarly, multinucleated cells (2)(3)(4)(5)(6)(7)(8)(9)(10) were observed in cultures established from vessels (50). As our cultures increased in CPD, all the cells were seen to increase in size.…”

Section: Discussionmentioning

confidence: 89%

Endothelial cells maintain a reduced redox environment even as mitochondrial function declines

Carlisle

Rhoads

et al. 2002

American Journal of Physiology-Cell Physiology

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. Endothelial cells maintain a reduced redox environment even as mitochondrial function declines. Am J Physiol Cell Physiol 283: C1675-C1686, 2002. First published August 22, 2002 10.1152/ajpcell.00092.2002 are an endothelial model of replicative senescence. Oxidative stress, possibly due to dysfunctional mitochondria, is believed to play a key role in replicative senescence and atherosclerosis, an age-related vascular disease. In this study, we determined the effect of cell division on genomic instability, mitochondrial function, and redox status in HUVECs that were able to replicate for ϳ60 cumulative population doublings (CPD). After 20 CPD, the nuclear genome deteriorated and the protein content of the cell population increased. This indicated an increase in cell size, which was accompanied by an increase in oxygen consumption, ATP production, and mitochondrial genome copy number and ϳ10% increase in mitochondrial mass. The antioxidant capacity increased, as seen by an increase in reduced glutathione, glutathione peroxidase, GSSG reductase, and glucose-6-phosphate dehydrogenase. However, by CPD 52, the latter two enzymes decreased, as well as the ratio of mitochondrial-to-nuclear genome copies, the mitochondrial mass, and the oxygen consumption per milligram of protein. Our results signify that HUVECs maintain a highly reducing (GSH) environment as they replicate despite genomic instability and loss of mitochondrial function. replicative senescence; glutathione; cell size changes; genomic instability; human umbilical vein endothelial cells HUMAN UMBILICAL VEIN ENDOTHELIAL CELLS (HUVECs) replicate a finite number of times in culture and are an endothelial model of replicative senescence. Reactive oxygen species (ROS) and oxidative damage to DNA (24), protein (7), and lipid (45) increase with age and have been implicated in aging and replicative senescence (19,48). Oxidative stress has also been implicated in atherosclerosis, an age-related vascular disease, and homocysteine, a contributing factor to atherosclerosis that induces oxidative stress, accelerates endothelial senescence in culture (52). Atherosclerosis is hypothesized to be the result of a "response to injury" of the endothelium. The endothelium must constantly respond to changes in the vascular environment and experiences frequent insults from mechanical, hemodynamic, and inflammatory stresses, all of which enhance oxygen free radical production. In response to injury, endothelial cells must replicate to repair blood vessels. Telomere length is shorter in endothelial cells derived from vessels where there is greater hemodynamic stress, and presumably more endothelial cell replication to repair injury, than in cells isolated from areas of lower stress (10). Injury induced by balloon catheter denudation of rabbit carotid arteries has been shown to result in the accumulation of senescent endothelial cells (18). Studies of the endothelium at atherosclerotic lesions (9, 50) and in vessels from elderly people (30, 50) have detected multinucleated cells ...

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“…Decline in priming and activation of neutrophils in response to LPS, granulocyte CSF (G-CSF), FMLP, and ligation of triggering receptor expressed on myeloid cell 1 has also been reported in elderly humans (101,112,158). Recent studies have implicated defective recruitment of signaling intermediaries into lipid rafts as a potential unifying defect in the signals generated at the membrane (9,343). Future studies will likely establish whether these defects are attributable to altered membrane fluidity, cytoskeletal changes, or altered protein domains.…”

Section: Immune Senescence and Interventionsmentioning

confidence: 99%

Aging and Immune Function: Molecular Mechanisms to Interventions

Ponnappan

2011

Antioxidants & Redox Signaling

290

266

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The immune system of an organism is an essential component of the defense mechanism aimed at combating pathogenic stress. Age-associated immune dysfunction, also dubbed ''immune senescence,'' manifests as increased susceptibility to infections, increased onset and progression of autoimmune diseases, and onset of neoplasia. Over the years, extensive research has generated consensus in terms of the phenotypic and functional defects within the immune system in various organisms, including humans. Indeed, age-associated alterations such as thymic involution, T cell repertoire skewing, decreased ability to activate naïve T cells and to generate robust memory responses, have been shown to have a causative role in immune decline. Further, understanding the molecular mechanisms underlying the generation of proteotoxic stress, DNA damage response, modulation of ubiquitin proteasome pathway, and regulation of transcription factor NFkB activation, in immune decline, have paved the way to delineating signaling pathways that cross-talk and impact immune senescence. Given the role of the immune system in combating infections, its effectiveness with age may well be a marker of health and a predictor of longevity. It is therefore believed that a better understanding of the mechanisms underlying immune senescence will lead to an effective interventional strategy aimed at improving the health span of individuals. Antioxid. Redox Signal. 14, 1551-1585.

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Age-related changes in membrane lipid composition, fluidity and respiratory burst in rat peritoneal neutrophils

Cited by 62 publications

References 57 publications

Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema

Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema

Endothelial cells maintain a reduced redox environment even as mitochondrial function declines

Aging and Immune Function: Molecular Mechanisms to Interventions

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