Publications by authors named "Effie Bastounis"

16 Publications

  • Page 1 of 1

Volume measurement and biophysical characterization of mounds in epithelial monolayers after intracellular bacterial infection.

STAR Protoc 2021 Jun 21;2(2):100551. Epub 2021 May 21.

Department of Biology and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.

Mechanical forces are important in (patho)physiological processes, including how host epithelial cells interact with intracellular bacterial pathogens. As these pathogens disseminate within host epithelial monolayers, large mounds of infected cells are formed due to the forceful action of surrounding uninfected cells, limiting bacterial spread across the basal cell monolayer. Here, we present a protocol for mound volume measurement and biophysical characterization of mound formation. Modifications to this protocol may be necessary for studying different host cell types or pathogenic organisms. For complete details on the use and execution of this protocol, please refer to Bastounis et al. (2021).
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http://dx.doi.org/10.1016/j.xpro.2021.100551DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8165451PMC
June 2021

Mechanical competition triggered by innate immune signaling drives the collective extrusion of bacterially infected epithelial cells.

Dev Cell 2021 Feb;56(4):443-460.e11

Department of Biology and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA. Electronic address:

Intracellular pathogens alter their host cells' mechanics to promote dissemination through tissues. Conversely, host cells may respond to the presence of pathogens by altering their mechanics to limit infection. Here, we monitored epithelial cell monolayers infected with intracellular bacterial pathogens, Listeria monocytogenes or Rickettsia parkeri, over days. Under conditions in which these pathogens trigger innate immune signaling through NF-κB and use actin-based motility to spread non-lytically intercellularly, we found that infected cell domains formed three-dimensional mounds. These mounds resulted from uninfected cells moving toward the infection site, collectively squeezing the softer and less contractile infected cells upward and ejecting them from the monolayer. Bacteria in mounds were less able to spread laterally in the monolayer, limiting the growth of the infection focus, while extruded infected cells underwent cell death. Thus, the coordinated forceful action of uninfected cells actively eliminates large domains of infected cells, consistent with this collective cell response representing an innate immunity-driven process.
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http://dx.doi.org/10.1016/j.devcel.2021.01.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7982222PMC
February 2021

Subendothelial stiffness alters endothelial cell traction force generation while exerting a minimal effect on the transcriptome.

Sci Rep 2019 12 3;9(1):18209. Epub 2019 Dec 3.

Department of Biology and Howard Hughes Medical Institute, University of Washington, Seattle, WA, 98195-1800, USA.

Endothelial cells respond to changes in subendothelial stiffness by altering their migration and mechanics, but whether those responses are due to transcriptional reprogramming remains largely unknown. We measured traction force generation and also performed gene expression profiling for two endothelial cell types grown in monolayers on soft or stiff matrices: primary human umbilical vein endothelial cells (HUVEC) and immortalized human microvascular endothelial cells (HMEC-1). Both cell types respond to changes in subendothelial stiffness by increasing the traction stresses they exert on stiffer as compared to softer matrices, and exhibit a range of altered protein phosphorylation or protein conformational changes previously implicated in mechanotransduction. However, the transcriptome has only a minimal role in this conserved biomechanical response. Only few genes were differentially expressed in each cell type in a stiffness-dependent manner, and none were shared between them. In contrast, thousands of genes were differentially regulated in HUVEC as compared to HMEC-1. HUVEC (but not HMEC-1) upregulate expression of TGF-β2 on stiffer matrices, and also respond to application of exogenous TGF-β2 by enhancing their endogenous TGF-β2 expression and their cell-matrix traction stresses. Altogether, these findings provide insights into the relationship between subendothelial stiffness, endothelial mechanics and variation of the endothelial cell transcriptome, and reveal that subendothelial stiffness, while critically altering endothelial cells' mechanical behavior, minimally affects their transcriptome.
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http://dx.doi.org/10.1038/s41598-019-54336-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6890669PMC
December 2019

A Multi-well Format Polyacrylamide-based Assay for Studying the Effect of Extracellular Matrix Stiffness on the Bacterial Infection of Adherent Cells.

J Vis Exp 2018 07 5(137). Epub 2018 Jul 5.

Departments of Biochemistry, Microbiology and Immunology and Howard Hughes Medical Institute, Stanford University School of Medicine.

Extracellular matrix stiffness comprises one of the multiple environmental mechanical stimuli that are well known to influence cellular behavior, function, and fate in general. Although increasingly more adherent cell types' responses to matrix stiffness have been characterized, how adherent cells' susceptibility to bacterial infection depends on matrix stiffness is largely unknown, as is the effect of bacterial infection on the biomechanics of host cells. We hypothesize that the susceptibility of host endothelial cells to a bacterial infection depends on the stiffness of the matrix on which these cells reside, and that the infection of the host cells with bacteria will change their biomechanics. To test these two hypotheses, endothelial cells were used as model hosts and Listeria monocytogenes as a model pathogen. By developing a novel multi-well format assay, we show that the effect of matrix stiffness on infection of endothelial cells by L. monocytogenes can be quantitatively assessed through flow cytometry and immunostaining followed by microscopy. In addition, using traction force microscopy, the effect of L. monocytogenes infection on host endothelial cell biomechanics can be studied. The proposed method allows for the analysis of the effect of tissue-relevant mechanics on bacterial infection of adherent cells, which is a critical step towards understanding the biomechanical interactions between cells, their extracellular matrix, and pathogenic bacteria. This method is also applicable to a wide variety of other types of studies on cell biomechanics and response to substrate stiffness where it is important to be able to perform many replicates in parallel in each experiment.
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http://dx.doi.org/10.3791/57361DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6124605PMC
July 2018

Listeria monocytogenes InlP interacts with afadin and facilitates basement membrane crossing.

PLoS Pathog 2018 05 30;14(5):e1007094. Epub 2018 May 30.

Benioff Children's Hospital, University of California, San Francisco, San Francisco, California, United States of America.

During pregnancy, the placenta protects the fetus against the maternal immune response, as well as bacterial and viral pathogens. Bacterial pathogens that have evolved specific mechanisms of breaching this barrier, such as Listeria monocytogenes, present a unique opportunity for learning how the placenta carries out its protective function. We previously identified the L. monocytogenes protein Internalin P (InlP) as a secreted virulence factor critical for placental infection. Here, we show that InlP, but not the highly similar L. monocytogenes internalin Lmo2027, binds to human afadin (encoded by AF-6), a protein associated with cell-cell junctions. A crystal structure of InlP reveals several unique features, including an extended leucine-rich repeat (LRR) domain with a distinctive Ca2+-binding site. Despite afadin's involvement in the formation of cell-cell junctions, MDCK epithelial cells expressing InlP displayed a decrease in the magnitude of the traction stresses they could exert on deformable substrates, similar to the decrease in traction exhibited by AF-6 knock-out MDCK cells. L. monocytogenes ΔinlP mutants were deficient in their ability to form actin-rich protrusions from the basal face of polarized epithelial monolayers, a necessary step in the crossing of such monolayers (transcytosis). A similar phenotype was observed for bacteria expressing an internal in-frame deletion in inlP (inlP ΔLRR5) that specifically disrupts its interaction with afadin. However, afadin deletion in the host cells did not rescue the transcytosis defect. We conclude that secreted InlP targets cytosolic afadin to specifically promote L. monocytogenes transcytosis across the basal face of epithelial monolayers, which may contribute to the crossing of the basement membrane during placental infection.
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http://dx.doi.org/10.1371/journal.ppat.1007094DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6044554PMC
May 2018

Matrix stiffness modulates infection of endothelial cells by Listeria monocytogenes via expression of cell surface vimentin.

Mol Biol Cell 2018 07 2;29(13):1571-1589. Epub 2018 May 2.

Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305.

Extracellular matrix stiffness (ECM) is one of the many mechanical forces acting on mammalian adherent cells and an important determinant of cellular function. While the effect of ECM stiffness on many aspects of cellular behavior has been studied previously, how ECM stiffness might mediate susceptibility of host cells to infection by bacterial pathogens is hitherto unexplored. To address this open question, we manufactured hydrogels of varying physiologically relevant stiffness and seeded human microvascular endothelial cells (HMEC-1) on them. We then infected HMEC-1 with the bacterial pathogen Listeria monocytogenes (Lm) and found that adhesion of Lm to host cells increases monotonically with increasing matrix stiffness, an effect that requires the activity of focal adhesion kinase (FAK). We identified cell surface vimentin as a candidate surface receptor mediating stiffness-dependent adhesion of Lm to HMEC-1 and found that bacterial infection of these host cells is decreased when the amount of surface vimentin is reduced. Our results provide the first evidence that ECM stiffness can mediate the susceptibility of mammalian host cells to infection by a bacterial pathogen.
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http://dx.doi.org/10.1091/mbc.E18-04-0228DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6080647PMC
July 2018

Mechanosensitive Adhesion Explains Stepping Motility in Amoeboid Cells.

Biophys J 2017 Jun;112(12):2672-2682

Department of Mathematics, University of California Davis, Davis, California.

Cells employing amoeboid motility exhibit repetitive cycles of rapid expansion and contraction and apply coordinated traction forces to their environment. Although aspects of this process are well studied, it is unclear how the cell controls the coordination of cell length changes with adhesion to the surface. Here, we develop a simple model to mechanistically explain the emergence of periodic changes in length and spatiotemporal dynamics of traction forces measured in chemotaxing unicellular amoeba, Dictyostelium discoideum. In contrast to the biochemical mechanisms that have been implicated in the coordination of some cellular processes, we show that many features of amoeboid locomotion emerge from a simple mechanochemical model. The mechanism for interaction with the environment in Dictyostelium is unknown and thus, we explore different cell-environment interaction models to reveal that mechanosensitive adhesions are necessary to reproduce the spatiotemporal adhesion patterns. In this modeling framework, we find that the other motility modes, such as smooth gliding, arise naturally with variations in the physical properties of the surface. Thus, our work highlights the prominent role of biomechanics in determining the emergent features of amoeboid locomotion.
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http://dx.doi.org/10.1016/j.bpj.2017.04.033DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5478966PMC
June 2017

Rickettsia Sca4 Reduces Vinculin-Mediated Intercellular Tension to Promote Spread.

Cell 2016 Oct;167(3):670-683.e10

Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address:

Spotted fever group (SFG) rickettsiae are human pathogens that infect cells in the vasculature. They disseminate through host tissues by a process of cell-to-cell spread that involves protrusion formation, engulfment, and vacuolar escape. Other bacterial pathogens rely on actin-based motility to provide a physical force for spread. Here, we show that SFG species Rickettsia parkeri typically lack actin tails during spread and instead manipulate host intercellular tension and mechanotransduction to promote spread. Using transposon mutagenesis, we identified surface cell antigen 4 (Sca4) as a secreted effector of spread that specifically promotes protrusion engulfment. Sca4 interacts with the cell-adhesion protein vinculin and blocks association with vinculin's binding partner, α-catenin. Using traction and monolayer stress microscopy, we show that Sca4 reduces vinculin-dependent mechanotransduction at cell-cell junctions. Our results suggest that Sca4 relieves intercellular tension to promote protrusion engulfment, which represents a distinctive strategy for manipulating cytoskeletal force generation to enable spread.
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http://dx.doi.org/10.1016/j.cell.2016.09.023DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5097866PMC
October 2016

Cooperative cell motility during tandem locomotion of amoeboid cells.

Mol Biol Cell 2016 Apr 24;27(8):1262-71. Epub 2016 Feb 24.

Section of Cell and Developmental Biology, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0380

Streams of migratory cells are initiated by the formation of tandem pairs of cells connected head to tail to which other cells subsequently adhere. The mechanisms regulating the transition from single to streaming cell migration remain elusive, although several molecules have been suggested to be involved. In this work, we investigate the mechanics of the locomotion ofDictyosteliumtandem pairs by analyzing the spatiotemporal evolution of their traction adhesions (TAs). We find that in migrating wild-type tandem pairs, each cell exerts traction forces on stationary sites (∼80% of the time), and the trailing cell reuses the location of the TAs of the leading cell. Both leading and trailing cells form contractile dipoles and synchronize the formation of new frontal TAs with ∼54-s time delay. Cells not expressing the lectin discoidin I or moving on discoidin I-coated substrata form fewer tandems, but the trailing cell still reuses the locations of the TAs of the leading cell, suggesting that discoidin I is not responsible for a possible chemically driven synchronization process. The migration dynamics of the tandems indicate that their TAs' reuse results from the mechanical synchronization of the leading and trailing cells' protrusions and retractions (motility cycles) aided by the cell-cell adhesions.
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http://dx.doi.org/10.1091/mbc.E15-12-0836DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4831880PMC
April 2016

Three-dimensional balance of cortical tension and axial contractility enables fast amoeboid migration.

Biophys J 2015 Feb;108(4):821-832

Department of Mechanical and Aerospace Engineering, University of California at San Diego, San Diego, California; Institute for Engineering in Medicine, University of California at San Diego, San Diego, California. Electronic address:

Fast amoeboid migration requires cells to apply mechanical forces on their surroundings via transient adhesions. However, the role these forces play in controlling cell migration speed remains largely unknown. We used three-dimensional force microscopy to measure the three-dimensional forces exerted by chemotaxing Dictyostelium cells, and examined wild-type cells as well as mutants with defects in contractility, internal F-actin crosslinking, and cortical integrity. We showed that cells pull on their substrate adhesions using two distinct, yet interconnected mechanisms: axial actomyosin contractility and cortical tension. We found that the migration speed increases when axial contractility overcomes cortical tension to produce the cell shape changes needed for locomotion. We demonstrated that the three-dimensional pulling forces generated by both mechanisms are internally balanced by an increase in cytoplasmic pressure that allows cells to push on their substrate without adhering to it, and which may be relevant for amoeboid migration in complex three-dimensional environments.
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http://dx.doi.org/10.1016/j.bpj.2014.11.3478DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4336364PMC
February 2015

Cytoskeletal Mechanics Regulating Amoeboid Cell Locomotion.

Appl Mech Rev 2014 Jun;66(5)

Mechanical and Aerospace Engineering Department, Institute for Engineering in Medicine, Bioengineering Department, University of California, San Diego, La Jolla, CA.

Migrating cells exert traction forces when moving. Amoeboid cell migration is a common type of cell migration that appears in many physiological and pathological processes and is performed by a wide variety of cell types. Understanding the coupling of the biochemistry and mechanics underlying the process of migration has the potential to guide the development of pharmacological treatment or genetic manipulations to treat a wide range of diseases. The measurement of the spatiotemporal evolution of the traction forces that produce the movement is an important aspect for the characterization of the locomotion mechanics. There are several methods to calculate the traction forces exerted by the cells. Currently the most commonly used ones are traction force microscopy methods based on the measurement of the deformation induced by the cells on elastic substrate on which they are moving. Amoeboid cells migrate by implementing a motility cycle based on the sequential repetition of four phases. In this paper we review the role that specific cytoskeletal components play in the regulation of the cell migration mechanics. We investigate the role of specific cytoskeletal components regarding the ability of the cells to perform the motility cycle effectively and the generation of traction forces. The actin nucleation in the leading edge of the cell, carried by the ARP2/3 complex activated through the SCAR/WAVE complex, has shown to be fundamental to the execution of the cyclic movement and to the generation of the traction forces. The protein PIR121, a member of the SCAR/WAVE complex, is essential to the proper regulation of the periodic movement and the protein SCAR, also included in the SCAR/WAVE complex, is necessary for the generation of the traction forces during migration. The protein Myosin II, an important F-actin cross-linker and motor protein, is essential to cytoskeletal contractility and to the generation and proper organization of the traction forces during migration.
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http://dx.doi.org/10.1115/1.4026249DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4201387PMC
June 2014

Both contractile axial and lateral traction force dynamics drive amoeboid cell motility.

J Cell Biol 2014 Mar;204(6):1045-61

Department of Mechanical and Aerospace Engineering and 2 Department of Bioengineering, Jacobs School of Engineering; 3 Section of Cell and Developmental Biology, Division of Biological Sciences; and 4 Institute for Engineering in Medicine, University of California, San Diego, La Jolla, CA 92093.

Chemotaxing Dictyostelium discoideum cells adapt their morphology and migration speed in response to intrinsic and extrinsic cues. Using Fourier traction force microscopy, we measured the spatiotemporal evolution of shape and traction stresses and constructed traction tension kymographs to analyze cell motility as a function of the dynamics of the cell's mechanically active traction adhesions. We show that wild-type cells migrate in a step-wise fashion, mainly forming stationary traction adhesions along their anterior-posterior axes and exerting strong contractile axial forces. We demonstrate that lateral forces are also important for motility, especially for migration on highly adhesive substrates. Analysis of two mutant strains lacking distinct actin cross-linkers (mhcA(-) and abp120(-) cells) on normal and highly adhesive substrates supports a key role for lateral contractions in amoeboid cell motility, whereas the differences in their traction adhesion dynamics suggest that these two strains use distinct mechanisms to achieve migration. Finally, we provide evidence that the above patterns of migration may be conserved in mammalian amoeboid cells.
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http://dx.doi.org/10.1083/jcb.201307106DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998796PMC
March 2014

Three-dimensional quantification of cellular traction forces and mechanosensing of thin substrata by fourier traction force microscopy.

PLoS One 2013 4;8(9):e69850. Epub 2013 Sep 4.

Mechanical and Aerospace Engineering Department, University of California San Diego, La Jolla, California, United States of America ; Institute for Engineering in Medicine, University of California San Diego, La Jolla, California, United States of America.

We introduce a novel three-dimensional (3D) traction force microscopy (TFM) method motivated by the recent discovery that cells adhering on plane surfaces exert both in-plane and out-of-plane traction stresses. We measure the 3D deformation of the substratum on a thin layer near its surface, and input this information into an exact analytical solution of the elastic equilibrium equation. These operations are performed in the Fourier domain with high computational efficiency, allowing to obtain the 3D traction stresses from raw microscopy images virtually in real time. We also characterize the error of previous two-dimensional (2D) TFM methods that neglect the out-of-plane component of the traction stresses. This analysis reveals that, under certain combinations of experimental parameters (cell size, substratums' thickness and Poisson's ratio), the accuracy of 2D TFM methods is minimally affected by neglecting the out-of-plane component of the traction stresses. Finally, we consider the cell's mechanosensing of substratum thickness by 3D traction stresses, finding that, when cells adhere on thin substrata, their out-of-plane traction stresses can reach four times deeper into the substratum than their in-plane traction stresses. It is also found that the substratum stiffness sensed by applying out-of-plane traction stresses may be up to 10 times larger than the stiffness sensed by applying in-plane traction stresses.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069850PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3762859PMC
April 2014

Alterations of baroreflex sensitivity after carotid endarterectomy according to the preoperative carotid plaque echogenicity.

J Vasc Surg 2012 Dec 23;56(6):1591-7. Epub 2012 Oct 23.

Jobst Vascular Institute, Promedica Toledo Hospital, Toledo, Ohio, USA.

Objective: Baroreflex sensitivity is lower in patients with echogenic carotid plaques compared with patients with echolucent ones. The purpose of our study was to compare the baroreflex function after carotid endarterectomy (CEA) between patients with different plaque echogenicity.

Method: Spontaneous baroreflex sensitivity (sBRS), heart rate, and systolic and diastolic arterial pressure were calculated in 51 patients with a severe carotid stenosis (70%-99%) 24 hours before CEA, as well as 24 and 48 hours after CEA. Carotid plaque echogenicity was graded from 1 to 4 according to Gray-Weale classification, after duplex examination, and the patients were divided into two groups: the echolucent (grade 1 or 2) and the echogenic (grade 3 or 4).

Results: The postoperative mean systolic arterial pressure values in all 51 patients at 24 and 48 hours (143.2 and 135.5 mm Hg, respectively) were found to be significantly increased compared with the preoperative value (132.5 mm Hg; x2=32, P<.001). Mean sBRS value, in all patients, was significantly reduced postoperatively to 2.1 ms mm Hg(-1), from the mean preoperative value, 3.7 ms mm Hg(-1), independently of plaque echogenicity. Twenty patients (39%) were included in the echolucent group and 31 (61%) in the echogenic. The two groups had significant differences in two parameters: the rate of diabetes mellitus and the rate of symptomatic plaques. After adjusting the two groups for these differences, we found that the preoperative difference in sBRS between the two groups (F[1,51]=11, P<.003) was eliminated 24 and 48 hours after CEA (F[1,51]=.007, P<.9 and F[1,51]=.4, P<.5 for 24 and 48 hours, respectively).

Conclusions: Before the removal of carotid atheroma, baroreflex sensitivity, which is a well established cardiovascular risk factor, seems to be affected by carotid plaque echogenicity. However, CEA has as a result a similar baroreflex response in all patients, regardless of plaque echogenicity, implying no association of plaque morphology and postoperative baroreflex sensitivity.
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http://dx.doi.org/10.1016/j.jvs.2012.05.103DOI Listing
December 2012

The SCAR/WAVE complex is necessary for proper regulation of traction stresses during amoeboid motility.

Mol Biol Cell 2011 Nov 7;22(21):3995-4003. Epub 2011 Sep 7.

Department of Bioengineering, Jacobs School of Engineering, University of California, San Diego, La Jolla, CA 92093, USA.

Cell migration requires a tightly regulated, spatiotemporal coordination of underlying biochemical pathways. Crucial to cell migration is SCAR/WAVE-mediated dendritic F-actin polymerization at the cell's leading edge. Our goal is to understand the role the SCAR/WAVE complex plays in the mechanics of amoeboid migration. To this aim, we measured and compared the traction stresses exerted by Dictyostelium cells lacking the SCAR/WAVE complex proteins PIR121 (pirA(-)) and SCAR (scrA(-)) with those of wild-type cells while they were migrating on flat, elastic substrates. We found that, compared to wild type, both mutant strains exert traction stresses of different strengths that correlate with their F-actin levels. In agreement with previous studies, we found that wild-type cells migrate by repeating a motility cycle in which the cell length and strain energy exerted by the cells on their substrate vary periodically. Our analysis also revealed that scrA(-) cells display an altered motility cycle with a longer period and a lower migration velocity, whereas pirA(-) cells migrate in a random manner without implementing a periodic cycle. We present detailed characterization of the traction-stress phenotypes of the various cell lines, providing new insights into the role of F-actin polymerization in regulating cell-substratum interactions and stresses required for motility.
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http://dx.doi.org/10.1091/mbc.E11-03-0278DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3204062PMC
November 2011

The role of carotid plaque echogenicity in baroreflex sensitivity.

J Vasc Surg 2011 Jul 31;54(1):93-9. Epub 2011 Mar 31.

Laiko General Hospital, First Surgical Department, Vascular Division, University of Athens Medical School, Athens, Greece.

Objective: The baroreflex sensitivity is impaired in patients with carotid atherosclerosis. The purpose of our study was to assess the impact of carotid plaque echogenicity on the baroreflex function in patients with significant carotid atherosclerosis, who have not undergone carotid surgery.

Method: Spontaneous baroreflex sensitivity (sBRS) was estimated in 45 patients with at least a severe carotid stenosis (70%-99%). sBRS calculation was performed noninvasively, with the spontaneous sequence method, based on indirectly estimated central blood pressures from radial recordings. This method failed in three patients due to poor-quality recordings, and eventually 42 patients were evaluated. After carotid duplex examination, carotid plaque echogenicity was graded from 1 to 4 according to Gray-Weale classification and the patients were divided into two groups: the echolucent group (grades 1 and 2) and the echogenic group (grades 3 and 4).

Results: Sixteen patients (38%) and 26 patients (62%) were included in the echolucent and echogenic group, respectively. Diabetes mellitus was observed more frequently among echolucent plaques (χ(2) = 8.0; P < .004), while those plaques were also more commonly symptomatic compared with echogenic atheromas (χ(2) = 8.5; P < .003). Systolic arterial pressure, diastolic arterial pressure, and heart rate were similar in the two groups. Nevertheless, the mean value of baroreflex sensitivity was found to be significantly lower in the echogenic group (2.96 ms/mm Hg) compared with the echolucent one (5.0 ms/mm Hg), (F [1, 42] = 10.1; P < .003).

Conclusions: These findings suggest that echogenic plaques are associated with reduced baroreflex function compared with echolucent ones. Further investigation is warranted to define whether such an sBRS impairment could be responsible for cardiovascular morbidity associated with echogenic plaques.
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http://dx.doi.org/10.1016/j.jvs.2010.11.121DOI Listing
July 2011
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