The Experts below are selected from a list of 25743 Experts worldwide ranked by ideXlab platform
Clifford D. Wright - One of the best experts on this subject based on the ideXlab platform.
-
regulation of polymorphonuclear leukocyte Membrane Fluidity effect of cytoskeletal modification
Journal of Leukocyte Biology, 1994Co-Authors: Marc E Wiles, Clifford D. Wright, James A. DykensAbstract:We previously demonstrated that the f-actin cytoskeleton modulates oxygen radical production as- sociated with polymorphonuclear leukocyte (PMN) ox- idative burst activity. Given the close association of the actin and microtubule cytoskeletons with the plasma Membrane and the transMembrane location of the PMN NADPH oxidase, it is likely cytoskeletal change may affect PMN Membrane responses, such as cellular anisotropy. Changes in PMN Membrane Fluidity were therefore examined after PMN activation by the chemo- attractant N-formyl-1-methionyl-1-leucyl-1-phenylalanine (fMLP) in the presence or absence of phalloidin or cytochalasin B (CB), agents that stabilize and disrupt f- actin, or taxol and vincristine, which stabilize and dis- rupt microtubules, respectively. Phalloidin and taxol treatment of PMN signifIcantly decreased whereas CB and vincristine significantly increased Membrane Fluidity. Activation of PMN by fMLP (106 M) resulted in a significant increase in Membrane Fluidity that was at- tenuated by PMN pretreatment with phalloidin or taxol. CB and vincristine pretreatment of PMN did not alter the fMLP response. These data suggest that stabilization of the f-actin or microtubule cytoskeleton may prevent in- creases in cellular Membrane Fluidity associated with PMN activation.- J. Leukoc. Biol. 56: 192-199; 1994.
Lo R Presti - One of the best experts on this subject based on the ideXlab platform.
-
polymorphonuclear leukocyte Membrane Fluidity before and after activation in subjects with insulin resistance
Acta Diabetologica, 2000Co-Authors: Gregorio Caimi, D Sinagra, A M Scarpitta, V Bonaventura, Mario Montana, Baldassare Canino, Lo R PrestiAbstract:The aim of this research was the evaluation of polymorphonuclear leukocyte (PMN) Membrane Fluidity in subjects with insulin resistance. Insulin sensitivity, in fact, may be influenced by plasma Membrane Fluidity. We enrolled 19 subjects with insulin resistance previously demonstrated during an euglycemic hyperinsulinemic clamp. PMN Membrane Fluidity was studied by labeling intact cells with the fluorescent probe 1-[4-(trimethyl-amino)phenyl]-6-phenyl-1,3,5-hexatriene and calculating the fluorescence polarization degree. The measurement was made before and after incubation of PMNs with two activating agents: 4-phorbol 12-myristate 13-acetate (PMN) and N-formyl-methionyl-leucyl-phenylalanine (fMLP). The baseline data showed a reduction of PMN memebrane Fluidity in subjects wit insulin resistance. After PMN activation with PMA and fMLP, no significant variation in Membrane Fluidity was present in PMNs from normals, while in those from subjects with insulin resistance a slight decrease in PMN Membrane Fluidity was found only after activation with fMLP. The behavior of PMN Membrane Fluidity, before and after activation, distinguishes insulin-resistant subjects from normal controls, although the effect cannot be directly correlated with the degree of insulin resistance.
-
polymorphonuclear leukocyte Membrane Fluidity and cytosolic ca2 concentration in diabetes mellitus
Acta Diabetologica, 1998Co-Authors: Gregorio Caimi, Antonio Catania, Mario Montana, Giorgio Ventimiglia, Baldassare Canino, Lo R PrestiAbstract:We evaluated polymorphonuclear Membrane (PMN) Fluidity in 32 subjects with type 1 diabetes mellitus, 38 subjects with type 2 diabetes mellitus and 38 normal control subjects, by marking intact and unstimulated PMN cells with the fluorescent probe 1-[4-(trimethylamino)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). We also evaluated PMN cytosolic Ca2+ content by marking intact and unstimulated PMN cells with the fluorescent probe Fura 2-AM. PMN Membrane Fluidity differentiated normal subjects from type 1 and 2 diabetic subjects. The PMN cytosolic Ca2+ concentration did not discriminate type 1 and 2 diabetic subjects from normal control subjects. No statistical correlation was found between PMN Membrane Fluidity and PMN cytosolic Ca2+ concentration in any of the groups of subjects, nor were significant correlations found between PMN Membrane Fluidity and cytosolic Ca2+ concentration in several plasma parameters (serum glucose, cholesterol and triglycerides). In conclusion, in type 1 and 2 diabetic patients we found a decrease in PMN Membrane Fluidity and this decrease, which was greater in type 2 diabetic patients, may be a marker of PMN dysfunction.
Cedric Govaerts - One of the best experts on this subject based on the ideXlab platform.
-
phosphatidylethanolamine is a key regulator of Membrane Fluidity in eukaryotic cells
Journal of Biological Chemistry, 2016Co-Authors: Rosie Dawaliby, Cataldo Trubbia, Cedric Delporte, Caroline Noyon, Pierre Van Antwerpen, Jean Marie Ruysschaert, Cedric GovaertsAbstract:Abstract Adequate Membrane Fluidity is required for a variety of key cellular processes and in particular for proper function of Membrane proteins. In most eukaryotic cells Membrane Fluidity is known to be regulated by fatty acids desaturation and cholesterol although some cells, such insect cells, are almost devoid of sterols synthesis. We show here that insect and mammalian cells present similar microviscosity at their respective physiological temperature. In order to investigate how both sterols and phospholipids control Fluidity homeostasis we quantified the lipidic composition of insect SF9b and mammalian HEK 293T cells under normal or sterol-modified condition. As expected, insect cells show minimal sterols compared to mammalian cells. A major difference is also observed in phospholipid content as the ratio of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) is inverted (four times higher in SF9 cells). In vitro studies in liposomes confirm that both cholesterol and PE can increase rigidity of the bilayer, suggesting that both can be used by cells to maintain Membrane Fluidity. We then show that exogenously increasing the cholesterol amount in SF9 Membranes leads to a significant decrease in PE/PC ratio while decreasing cholesterol in HEK 293T cells using statin treatment leads to an increase in the PE/PC ratio. In all cases the Membrane Fluidity is maintained, indicating that both cell types combine regulation by sterols and phospholipids to control proper Membrane Fluidity.
-
phosphatidylethanolamine is a key regulator of Membrane Fluidity in eukaryotic cells
Journal of Biological Chemistry, 2016Co-Authors: Rosie Dawaliby, Cataldo Trubbia, Cedric Delporte, Caroline Noyon, Pierre Van Antwerpen, Jean Marie Ruysschaert, Cedric GovaertsAbstract:Abstract Adequate Membrane Fluidity is required for a variety of key cellular processes and in particular for proper function of Membrane proteins. In most eukaryotic cells Membrane Fluidity is known to be regulated by fatty acids desaturation and cholesterol although some cells, such insect cells, are almost devoid of sterols synthesis. We show here that insect and mammalian cells present similar microviscosity at their respective physiological temperature. In order to investigate how both sterols and phospholipids control Fluidity homeostasis we quantified the lipidic composition of insect SF9b and mammalian HEK 293T cells under normal or sterol-modified condition. As expected, insect cells show minimal sterols compared to mammalian cells. A major difference is also observed in phospholipid content as the ratio of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) is inverted (four times higher in SF9 cells). In vitro studies in liposomes confirm that both cholesterol and PE can increase rigidity of the bilayer, suggesting that both can be used by cells to maintain Membrane Fluidity. We then show that exogenously increasing the cholesterol amount in SF9 Membranes leads to a significant decrease in PE/PC ratio while decreasing cholesterol in HEK 293T cells using statin treatment leads to an increase in the PE/PC ratio. In all cases the Membrane Fluidity is maintained, indicating that both cell types combine regulation by sterols and phospholipids to control proper Membrane Fluidity.
Abigail Savietto - One of the best experts on this subject based on the ideXlab platform.
-
flotillin mediated Membrane Fluidity controls peptidoglycan synthesis and mreb movement
eLife, 2020Co-Authors: Aleksandra Zielinska, Abigail Savietto, Anabela De Sousa Borges, Denis Martinez, Melanie Berbon, Joel R Roelofsen, Alwin M Hartman, Rinse De BoerAbstract:The bacterial plasma Membrane is an important cellular compartment. In recent years it has become obvious that protein complexes and lipids are not uniformly distributed within Membranes. Current hypotheses suggest that flotillin proteins are required for the formation of complexes of Membrane proteins including cell-wall synthetic proteins. We show here that bacterial flotillins are important factors for Membrane Fluidity homeostasis. Loss of flotillins leads to a decrease in Membrane Fluidity that in turn leads to alterations in MreB dynamics and, as a consequence, in peptidoglycan synthesis. These alterations are reverted when Membrane Fluidity is restored by a chemical fluidizer. In vitro, the addition of a flotillin increases Membrane Fluidity of liposomes. Our data support a model in which flotillins are required for direct control of Membrane Fluidity rather than for the formation of protein complexes via direct protein-protein interactions.
-
Membrane Fluidity controls peptidoglycan synthesis and mreb movement
bioRxiv, 2019Co-Authors: Aleksandra Zielinska, Abigail Savietto, Anabela De Sousa Borges, Joel R Roelofsen, Alwin M Hartman, Rinse De Boer, Ida J Van Der Klei, Anna K H HirschAbstract:Abstract The bacterial plasma Membrane is an important cellular compartment. In recent years it has become obvious that protein complexes and lipids are not uniformly distributed within Membranes. Current hypotheses suggest that flotillin proteins are required for the formation of complexes of Membrane proteins including cell-wall synthetic proteins. We show here that bacterial flotillins are important factors for Membrane Fluidity homeostasis. Loss of flotillins leads to changes in Membrane Fluidity that in turn lead to alterations in MreB dynamics and, as a consequence, in peptidoglycan synthesis. Our data support a model in which flotillins are required for growth-rate dependent control of Membrane Fluidity rather than for the formation of protein complexes via direct protein-protein interactions.
Alwin M Hartman - One of the best experts on this subject based on the ideXlab platform.
-
flotillin mediated Membrane Fluidity controls peptidoglycan synthesis and mreb movement
eLife, 2020Co-Authors: Aleksandra Zielinska, Abigail Savietto, Anabela De Sousa Borges, Denis Martinez, Melanie Berbon, Joel R Roelofsen, Alwin M Hartman, Rinse De BoerAbstract:The bacterial plasma Membrane is an important cellular compartment. In recent years it has become obvious that protein complexes and lipids are not uniformly distributed within Membranes. Current hypotheses suggest that flotillin proteins are required for the formation of complexes of Membrane proteins including cell-wall synthetic proteins. We show here that bacterial flotillins are important factors for Membrane Fluidity homeostasis. Loss of flotillins leads to a decrease in Membrane Fluidity that in turn leads to alterations in MreB dynamics and, as a consequence, in peptidoglycan synthesis. These alterations are reverted when Membrane Fluidity is restored by a chemical fluidizer. In vitro, the addition of a flotillin increases Membrane Fluidity of liposomes. Our data support a model in which flotillins are required for direct control of Membrane Fluidity rather than for the formation of protein complexes via direct protein-protein interactions.
-
Membrane Fluidity controls peptidoglycan synthesis and mreb movement
bioRxiv, 2019Co-Authors: Aleksandra Zielinska, Abigail Savietto, Anabela De Sousa Borges, Joel R Roelofsen, Alwin M Hartman, Rinse De Boer, Ida J Van Der Klei, Anna K H HirschAbstract:Abstract The bacterial plasma Membrane is an important cellular compartment. In recent years it has become obvious that protein complexes and lipids are not uniformly distributed within Membranes. Current hypotheses suggest that flotillin proteins are required for the formation of complexes of Membrane proteins including cell-wall synthetic proteins. We show here that bacterial flotillins are important factors for Membrane Fluidity homeostasis. Loss of flotillins leads to changes in Membrane Fluidity that in turn lead to alterations in MreB dynamics and, as a consequence, in peptidoglycan synthesis. Our data support a model in which flotillins are required for growth-rate dependent control of Membrane Fluidity rather than for the formation of protein complexes via direct protein-protein interactions.