Interaction of vaginal Lactobacillus strains with HeLa cells plasma membrane

2017 ◽  
Vol 8 (4) ◽  
pp. 625-633 ◽  
Author(s):  
N. Calonghi ◽  
C. Parolin ◽  
G. Sartor ◽  
L. Verardi ◽  
B. Giordani ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Physical Properties ◽  
Hela Cells ◽  
Protective Role ◽  
Vaginal Infections ◽  
Vaginal Lactobacilli ◽  
Cell Line Hela ◽  
Cervical Cells ◽  
Host Epithelium

Vaginal lactobacilli offer protection against recurrent urinary and vaginal infections. The precise mechanisms underlying the interaction between lactobacilli and the host epithelium remain poorly understood at the molecular level. Deciphering such events can provide valuable information on the mode of action of commensal and probiotic bacteria in the vaginal environment. We investigated the effects exerted by five Lactobacillus strains of vaginal origin (Lactobacillus crispatus BC1 and BC2, Lactobacillus gasseri BC9 and BC11 and Lactobacillus vaginalis BC15) on the physical properties of the plasma membrane in a cervical cell line (HeLa). The interaction of the vaginal lactobacilli with the cervical cells determined two kinds of effects on plasma membrane: (1) modification of the membrane polar lipid organisation and the physical properties (L. crispatus BC1 and L. gasseri BC9); (2) modification of α5β1 integrin organisation (L. crispatus BC2, L. gasseri BC11 and L. vaginalis BC15). These two mechanisms can be at the basis of the protective role of lactobacilli against Candida albicans adhesion. Upon stimulation with all Lactobacillus strains, we observed a reduction of the basal oxidative stress in HeLa cells that could be related to modifications in physical properties and organisation of the plasma membrane. These results confirm the strictly strain-specific peculiarities of Lactobacillus and deepen the understanding of the mechanisms underlying the health-promoting role of this genus within the vaginal ecosystem.

Lipid order and molecular assemblies in the plasma membrane of eukaryotic cells

2009 ◽  
Vol 37 (5) ◽  
pp. 1056-1060 ◽  
Author(s):  
Marek Cebecauer ◽  
Dylan M. Owen ◽  
Anna Markiewicz ◽  
Anthony I. Magee
Keyword(s):  
Plasma Membrane ◽  
Physical Properties ◽  
Live Cell Imaging ◽  
Cell Imaging ◽  
Live Cell ◽  
Eukaryotic Cells ◽  
Dynamic Nature ◽  
Membrane Components ◽  
Technological Improvements

Multimolecular assemblies on the plasma membrane exhibit dynamic nature and are often generated during the activation of eukaryotic cells. The role of lipids and their physical properties in helping to control the existence of these structures is discussed. Technological improvements for live cell imaging of membrane components are also reviewed.

scholarly journals Quantitative FRET Microscopy Reveals a Crucial Role of Cytoskeleton in Promoting PI(4,5)P2 Confinement

2021 ◽  
Vol 22 (21) ◽  
pp. 11727
Author(s):  
Maria J. Sarmento ◽  
Luís Borges-Araújo ◽  
Sandra N. Pinto ◽  
Nuno Bernardes ◽  
Joana C. Ricardo ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Hela Cells ◽  
Membrane Trafficking ◽  
Actin Polymerization ◽  
Fluorescent Proteins ◽  
Resonance Energy Transfer ◽  
Resonance Energy ◽  
Cellular Functions ◽  
Cytoskeleton Organization

Phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) is an essential plasma membrane component involved in several cellular functions, including membrane trafficking and cytoskeleton organization. This function multiplicity is partially achieved through a dynamic spatiotemporal organization of PI(4,5)P2 within the membrane. Here, we use a Förster resonance energy transfer (FRET) approach to quantitatively assess the extent of PI(4,5)P2 confinement within the plasma membrane. This methodology relies on the rigorous evaluation of the dependence of absolute FRET efficiencies between pleckstrin homology domains (PHPLCδ) fused with fluorescent proteins and their average fluorescence intensity at the membrane. PI(4,5)P2 is found to be significantly compartmentalized at the plasma membrane of HeLa cells, and these clusters are not cholesterol-dependent, suggesting that membrane rafts are not involved in the formation of these nanodomains. On the other hand, upon inhibition of actin polymerization, compartmentalization of PI(4,5)P2 is almost entirely eliminated, showing that the cytoskeleton network is the critical component responsible for the formation of nanoscale PI(4,5)P2 domains in HeLa cells.

scholarly journals Metallothionein isoform 2A expression is inducible and protects against ROS-mediated cell death in rotenone-treated HeLa cells

2006 ◽  
Vol 395 (2) ◽  
pp. 405-415 ◽  
Author(s):  
Fimmie Reinecke ◽  
Oksana Levanets ◽  
Yolanda Olivier ◽  
Roan Louw ◽  
Boitumelo Semete ◽  
...  
Keyword(s):  
Hela Cells ◽  
Complex I ◽  
Protective Role ◽  
Nadh:Ubiquinone Oxidoreductase ◽  
Ros Production ◽  
Complex I Deficiency ◽  
Overexpressing Cell ◽  
Dose Dependent Decrease ◽  
Complex I Activity

The role of MT (metallothionein) gene expression was investigated in rotenone-treated HeLa cells to induce a deficiency of NADH:ubiquinone oxidoreductase (complex I). Complex I deficiency leads to a diversity of cellular consequences, including production of ROS (reactive oxygen species) and apoptosis. HeLa cells were titrated with rotenone, resulting in dose-dependent decrease in complex I activity and elevated ROS production at activities lower than 33%. Expression of MT2A (MT isoform 2A), but not MT1A or MT1B RNA, was significantly inducible by rotenone (up to 7-fold), t-BHP (t-butyl hydroperoxide; 5-fold) and CdCl2 (50-fold), but not ZnCl2. Myxothiazol treatment did not elevate either ROS or MT2A levels, which supports a ROS-related mechanism for rotenone-induced MT2A expression. To evaluate the role of MT2A expression, MT2A and MT1B were overexpressed in HeLa cells and treated with rotenone. Compared with control and MT1B-overexpressing cells, ROS production was significantly lower and cell viability higher in MT2A-overexpressing HeLa cells when ROS production was enhanced by treatment with t-BHP. Mitochondrial membrane potential was noticeably less reduced in both MT-overexpressing cell lines. MT2A overexpression in rotenone-treated cells also significantly reduced or delayed apoptosis induction, as measured by caspase 3/7 activity and cytosolic nucleosome enrichment. We conclude that MT2A offers significant protection against the main death-causing consequences of rotenone-induced complex I deficiency in HeLa cells. Our results are in support of the protective role against oxidative stress ascribed to MTs and provide evidence that MT2A expression may be a beneficial downstream adaptive response in complex I-deficient cells.

Possible Influence of Glycocalyx on Physical Properties of the Platelet Plasma Membrane.

1979 ◽  
Author(s):  
Gwendolyn J. Stewart ◽  
Kundagallore G. Varma ◽  
Pamela Sandler ◽  
Thomas Morinelli ◽  
Stefan Niewiarowski
Keyword(s):  
Plasma Membrane ◽  
Physical Properties ◽  
Shape Change ◽  
Blood Platelets ◽  
Lipid Layer ◽  
Major Band ◽  
Membrane Invagination ◽  
Pas Staining ◽  
Surface Glycoproteins

In blood platelets the role of surface glycoproteins as receptors for secretogogs, and enzymes is widely accepted. The possibility that these might also influence physical properties of the platelet plasma membrane and its attachment to the submembranous microfilament cortex apparently has not been considered. Studies with platelets exposed to pronase and chymotrypsin suggested this possibility. Pronase greatly reduced the PAS staining material (2 major bands in SDS disc gels). Chymotrypsin reduced the major band, but did not affect minor bands. Pronase treatment caused characteristic, massive invagination of platelet plasma membrane but limited shape change even when secretion was extensive. PGE1 inhibited secretion but not the membrane response. Chymotrypsin caused few membrane invagination (and no secretion) but did cause extensive shape change. Microtubules were present in platelets from both treatments. These observations could be explained if: (1) carbohydrate residues were bulky and attached to a peptide that transversed the lipid layer to attach to micorfilaments and (2) pronase but no chymotrypsin cleaved the peptide connecting surface glycoproteins and microfilaments, thereby releasing glycoprotein from the membrane outside and microfilaments from their connection to the membrans inside. The fluid lipid layer would then be free to flow into the cytoplasms through gaps in the uncoupled microfilament cortex.

scholarly journals Lactobacillus rhamnosus reduces the cytotoxic effects of Group B Streptococcus on HeLa cells

2021 ◽  
Author(s):  
Jan Mikhale B Cajulao ◽  
Lily Chen
Keyword(s):  
Hela Cell ◽  
Hela Cells ◽  
Group B Streptococcus ◽  
Lactobacillus Rhamnosus ◽  
Protective Role ◽  
Lactobacillus Species ◽  
Sem Images ◽  
Vaginal Tract ◽  
Group B

Group B Streptococcus (GBS) is an opportunistic pathogen found in the vaginal tract and is a leading cause of preterm birth and neonatal illness. Aside from GBS, the vaginal tract is predominantly colonized by commensal Lactobacillus species that are thought to protect the vaginal tract from pathogens, including GBS. Studies that examined if, and how Lactobacilli modulate GBS pathogenicity remain limited. This study sought to investigate the potential protective role of Lactobacillus rhamnosus against GBS, using an in vitro model system. Immunofluorescence microscopy and Scanning Electron Microscopy (SEM) captured images of infected HeLa cells and were analyzed using the image analysis program ImageJ. Results indicate that GBS causes HeLa cell detachment unless L. rhamnosus is present. SEM images show that GBS reduces length and number of microvilli on HeLa cell surface, as well as size of secreted vesicles. L. rhamnosus partially inhibits GBS-dependent microvilli and vesicle disruption. GBS also disrupts HeLa cell F-actin fibers unless L. rhamnosus is present. These results reveal effects of GBS infection on the host cell cytoskeleton and implies a protective role of L. rhamnosus against GBS colonization.

scholarly journals Orai1α, but not Orai1β, co-localizes with TRPC1 and is required for its plasma membrane location and activation in HeLa cells

2022 ◽  
Vol 79 (1) ◽  
Author(s):  
Jose Sanchez-Collado ◽  
Jose J. Lopez ◽  
Isaac Jardin ◽  
Alejandro Berna-Erro ◽  
Pedro J. Camello ◽  
...  
Keyword(s):  
Amino Acids ◽  
Plasma Membrane ◽  
Hela Cells ◽  
Mammalian Cells ◽  
Store Depletion ◽  
Agonist Stimulation ◽  
Dependent Inactivation ◽  
Crac Channel ◽  
Membrane Location

AbstractThe identification of two variants of the canonical pore-forming subunit of the Ca2+ release-activated Ca2+ (CRAC) channel Orai1, Orai1α and Orai1β, in mammalian cells arises the question whether they exhibit different functional characteristics. Orai1α and Orai1β differ in the N-terminal 63 amino acids, exclusive of Orai1α, and show different sensitivities to Ca2+-dependent inactivation, as well as distinct ability to form arachidonate-regulated channels. We have evaluated the role of both Orai1 variants in the activation of TRPC1 in HeLa cells. We found that Orai1α and Orai1β are required for the maintenance of regenerative Ca2+ oscillations, while TRPC1 plays a role in agonist-induced Ca2+ influx but is not essential for Ca2+ oscillations. Using APEX2 proximity labeling, co-immunoprecipitation and the fluorescence of G-GECO1.2 fused to Orai1α our results indicate that agonist stimulation and Ca2+ store depletion enhance Orai1α–TRPC1 interaction. Orai1α is essential for TRPC1 plasma membrane location and activation. Thus, TRPC1 function in HeLa cells depends on Ca2+ influx through Orai1α exclusively.

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

Parenting Behaviors and Anxiety in Young Adults

2015 ◽  
Vol 36 (3) ◽  
pp. 170-176 ◽  
Author(s):  
Erin N. Stevens ◽  
Joseph R. Bardeen ◽  
Kyle W. Murdock
Keyword(s):  
Effortful Control ◽  
Parenting Behaviors ◽  
Protective Role ◽  
Anxiety Symptoms ◽  
Interactive Effects ◽  
Parental Overprotection ◽  
High Control ◽  
Development Of Anxiety ◽  
The Relationship

Parenting behaviors – specifically behaviors characterized by high control, intrusiveness, rejection, and overprotection – and effortful control have each been implicated in the development of anxiety pathology. However, little research has examined the protective role of effortful control in the relation between parenting and anxiety symptoms, specifically among adults. Thus, we sought to explore the unique and interactive effects of parenting and effortful control on anxiety among adults (N = 162). Results suggest that effortful control uniquely contributes to anxiety symptoms above and beyond that of any parenting behavior. Furthermore, effortful control acted as a moderator of the relationship between parental overprotection and anxiety, such that overprotection is associated with anxiety only in individuals with lower levels of effortful control. Implications for potential prevention and intervention efforts which specifically target effortful control are discussed. These findings underscore the importance of considering individual differences in self-regulatory abilities when examining associations between putative early-life risk factors, such as parenting, and anxiety symptoms.

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