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Journal articles on the topic 'Instabilités de type Weibel'

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Published: 8 June 2024

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Lazar, M., R. Schlickeiser, R. Wielebinski, and S. Poedts. "COSMOLOGICAL EFFECTS OF WEIBEL-TYPE INSTABILITIES." Astrophysical Journal 693, no. 2 (2009): 1133–41. http://dx.doi.org/10.1088/0004-637x/693/2/1133.

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Mirón-Granese, Nahuel, Esteban Calzetta, and Alejandra Kandus. "Primordial Weibel instability." Journal of Cosmology and Astroparticle Physics 2022, no. 01 (2022): 028. http://dx.doi.org/10.1088/1475-7516/2022/01/028.

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Abstract We study the onset of vector instabilities in the post-inflationary epoch of the Universe as a mechanism for primordial magnetic fields amplification. We assume the presence of a charged spectator scalar field arbitrarily coupled to gravity during Inflation in its vacuum de Sitter state. Gravitational particle creation takes place at the transition from Inflation to the subsequent Reheating stage and thus the vacuum field state becomes an excited many particles one. Consequently this state can be described as a real fluid, and we build out the hydrodynamic framework using second order theories for relativistic fluids with a relaxation time prescription for the collision integral. Given the high-temperature regime and the vanishing scalar curvature of the Universe during Reheating (radiation-dominated-type era), the fluid can be regarded as a conformal one. The large quantum fluctuations induced by the rapid transition from inflationary to effectively radiation dominated expansion become statistical fluctuations whereby both a charge excess and anisotropic pressures are produced in any finite domain. The precise magnitude of the effect for each scale is determined by the size of the averaging domain and the coupling to curvature. We look at domains which are larger than the horizon at the beginning of Reheating, but much smaller than our own horizon, and show that in a finite fraction of them the anisotropy and charge excess provide suitable conditions for a Weibel instability. If moreover the duration of reheating is shorter than the relaxation time of the fluid, then this instability can compensate or even overcome the conformal dilution of a primordial magnetic field. We show that the non-trivial topology of the magnetic field encoded in its magnetic helicity is also amplified if present.

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OKADA, T., I. SAJIKI, and K. SATOU. "Weibel instability by ultraintense laser pulses." Laser and Particle Beams 17, no. 3 (1999): 515–18. http://dx.doi.org/10.1017/s0263034699173191.

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Particle-in-cell (PIC) simulations show that an anisotropic electron velocity distribution is demonstrated by ultraintense laser pulses in underdense plasmas. Recently, it is reported that the anisotropy has been experimentally demonstrated in laser-produced plasmas. It is also pointed out that gigagauss magnetic fields are generated by ultraintense laser pulses. We have already published that the Weibel-type electromagnetic instabilities can be theoretically excited by electrons in a velocity distribution with anisotropic temperature. If these electromagnetic waves are excited, the target may have a possibility not only to give rise to a new type of energy loss mechanism but also to influence the implosion characteristics. In this work, we present PIC simulation of the interaction of ultraintense laser pulses with plasmas. Intense self-generated magnetic fields is produced by the mechanism of Weibel instability in underdense plasmas.

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Baumjohann, W., R. Nakamura, and R. A. Treumann. "Magnetic guide field generation in collisionless current sheets." Annales Geophysicae 28, no. 3 (2010): 789–93. http://dx.doi.org/10.5194/angeo-28-789-2010.

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Abstract. In thin (Δ< few λi) collisionless current sheets in a space plasma like the magnetospheric tail or magnetopause current layer, magnetic fields can grow from thermal fluctuation level by the action of the non-magnetic Weibel instability (Weibel, 1959). The instability is driven by the counter-streaming electron inflow from the "ion diffusion" (ion inertial Hall) region into the inner current (electron inertial) region after thermalisation by the two-stream instability. Under magnetospheric tail conditions it takes ~50 e-folding times (~100 s) for the Weibel field to reach observable amplitudes |bW|~1 nT. In counter-streaming inflows these fields are of guide field type.

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SUGIE, M., K. OGAWA, and T. OKADA. "DEVELOPMENT OF ELECTROMAGNETIC WEIBEL-TYPE INSTABILITIES IN ANISOTROPIC PLASMAS." International Journal of Modern Physics B 21, no. 03n04 (2007): 637–41. http://dx.doi.org/10.1142/s0217979207042458.

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LAZAR, M., A. SMOLYAKOV, R. SCHLICKEISER, and P. K. SHUKLA. "A comparative study of the filamentation and Weibel instabilities and their cumulative effect. I. Non-relativistic theory." Journal of Plasma Physics 75, no. 1 (2009): 19–33. http://dx.doi.org/10.1017/s0022377807007015.

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AbstractA comparative study of the electromagnetic instabilities in anisotropic unmagnetized plasmas is undertaken. The instabilities considered are the filamentation and Weibel instability, and their cumulative effect. Dispersion relations are derived and the growth rates are plotted systematically for the representative cases of non-relativistic counterstreaming plasmas with isotropic or anisotropic velocity distributions functions of Maxwellian type. The pure filamentation mode is attenuated by including an isotropic Maxwellian distribution function. Moreover, it is observed that counterstreaming plasmas can be fully stabilized by including bi-Maxellian distributions with a negative thermal anisotropy. This effect is relevant for fusion plasma experiments. Otherwise, for plasma streams with a positive anisotropy the filamentation and Weibel instabilities cumulate leading to a growth rate by orders of magnitude larger than that of a simple filamentation mode. This is noticeable for the quasistatic magnetic field generated in astrophysical sources, and which is expected to saturate at higher values and explain the non-thermal emission observed.

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Lazar, M., R. Schlickeiser, and T. Skoda. "Cosmological magnetic field seeds produced by the Weibel instabilities." Proceedings of the International Astronomical Union 6, S271 (2010): 387–88. http://dx.doi.org/10.1017/s1743921311017923.

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AbstractThe source of the cosmological magnetic field is still unknown because the widely invoked dynamo processes are only able to regenerate and amplify some initial magnetic field seeds. In the hot and highly ionized intergalactic matter such magnetic field seeds can easily be produced by the (electro-)magnetic instabilities of Weibel type. Here we discuss suplementary mechanisms that can make these Weibel created fields to evolve at large scales presently observed in galaxies and clusters and can also enhance these magnetic field seeds after the dissipation.

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Inglebert, A., A. Ghizzo, T. Reveille, D. Del Sarto, P. Bertrand, and F. Califano. "A multi-stream Vlasov modeling unifying relativistic Weibel-type instabilities." EPL (Europhysics Letters) 95, no. 4 (2011): 45002. http://dx.doi.org/10.1209/0295-5075/95/45002.

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Skoutnev, V., A. Hakim, J. Juno, and J. M. TenBarge. "Temperature-dependent Saturation of Weibel-type Instabilities in Counter-streaming Plasmas." Astrophysical Journal 872, no. 2 (2019): L28. http://dx.doi.org/10.3847/2041-8213/ab0556.

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Sarrat, M., D. Del Sarto, and A. Ghizzo. "Fluid description of Weibel-type instabilities via full pressure tensor dynamics." EPL (Europhysics Letters) 115, no. 4 (2016): 45001. http://dx.doi.org/10.1209/0295-5075/115/45001.

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Doğan, Mustafa, and Kazım Yavuz Ekşi. "Stimulated emission–based model of fast radio bursts." Monthly Notices of the Royal Astronomical Society 494, no. 1 (2020): 876–84. http://dx.doi.org/10.1093/mnras/staa708.

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ABSTRACT Fast radio bursts (FRBs) are bright, short-duration radio transients with very high brightness temperatures implying highly coherent emission. We suggest that the FRBs are caused by the self-focusing of an electron beam interacting with an ambient plasma right beyond the light cylinder radius of a neutron star. The magnetic field at the light cylinder radius is relatively high that can accommodate both young Crab-like systems and old millisecond pulsars addressing the diverse environments of FRBs. At the first stage, the intense pulsed-beam passing through the background plasma causes instabilities such that the trapped particles in local Buneman-type cavitons saturate the local field. The beam is then radially self-focused due to the circular electric field developed by the two-stream instability that leads to Weibel instability in the transverse direction. Finally, the non-linear saturation of the Weibel instability results in the self-modulational formation of solitons due to plasmoid instability. The resonant solitary waves are the breather-type solitons hosting relativistic particles with self-excited oscillations. The analytical solutions obtained for non-linear dispersion and solitons suggest that, near the current sheets, the relativistic bunches are accelerated/amplified by klystron-like structures due to self-excited oscillations by the induced local electric field. Boosted coherent radio emission propagates through a narrow cone with strong focusing due to radial electric field and magnetic pinching. The non-linear evolution of solitons and the stimulated emission are associated with the Buneman instability and the possibility of the presence of nanosecond shots in FRBs are investigated.

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Inglebert, A., A. Ghizzo, T. Reveille, D. Del Sarto, P. Bertrand, and F. Califano. "Multi-stream Vlasov model for the study of relativistic Weibel-type instabilities." Plasma Physics and Controlled Fusion 54, no. 8 (2012): 085004. http://dx.doi.org/10.1088/0741-3335/54/8/085004.

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Okada, T., T. Shimojo, and K. Niu. "Weibel-type instability of intense ion beam propagation in a reactor chamber." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 278, no. 1 (1989): 97–98. http://dx.doi.org/10.1016/0168-9002(89)91139-x.

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Struck, Curtis. "The role of wind driving in OB star bow nebulae." Monthly Notices of the Royal Astronomical Society 494, no. 2 (2020): 1838–47. http://dx.doi.org/10.1093/mnras/staa838.

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ABSTRACT Bow-shaped mid-infrared (mid-IR) emission regions have been discovered in satellite observations of numerous late-type O and early-type B stars with moderate velocities relative to the ambient interstellar medium. Previously, hydrodynamical bow shock models have been used to study this emission. It appears that such models are incomplete in that they neglect kinetic effects associated with long mean free paths of stellar wind particles, and the complexity of Weibel instability fronts. Wind ions are scattered in the Weibel instability and mix with the interstellar gas. However, they do not lose their momentum and most ultimately diffuse further into the ambient gas like cosmic rays, and share their energy and momentum. Lacking other coolants, the heated gas transfers energy into interstellar dust grains, which radiate it. This process, in addition to grain photoheating, provides the energy for the emission. A weak R-type ionization front, formed well outside the IR emission region, generally moderates the interstellar gas flow into the emission region. The theory suggests that the IR emission process is limited to cases of moderate stellar peculiar velocities, evidently in accord with the observations.

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Emelyanov, N. A., and V. V. Kocharovsky. "Collisional Mechanism of Expanding Wavenumbers Range of Weibel-Type Instability in Magnetoactive Plasma." Plasma Physics Reports 50, no. 2 (2024): 199–205. http://dx.doi.org/10.1134/s1063780x23602067.

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STOCKEM, A., M. LAZAR, P. K. SHUKLA, and A. SMOLYAKOV. "A comparative study of the filamentation and Weibel instabilities and their cumulative effect. II. Weakly relativistic beams." Journal of Plasma Physics 75, no. 4 (2009): 529–43. http://dx.doi.org/10.1017/s002237780800768x.

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AbstractCounterstreaming plasma systems with intrinsic temperature anisotropies are unstable against the excitation of Weibel-type instabilities, namely, filamentation and Weibel instabilities, and their cumulative effect. Here, the analysis is extended to counterstreaming plasmas with weakly relativistic bulk velocities, while the thermal velocities are still considered to be non-relativistic. Such plasma systems are relevant for fusion plasma experiments and the more violent astrophysical phenomena, such as jets in gamma-ray burst sources. Simple analytical forms of the dispersion relations are derived in the limit of a small transverse temperature or a large temperature anisotropy of the beams. The aperiodic growing solutions are plotted systematically for the representative cases chosen in Paper I (Lazar et al. 2009 J. Plasma Phys. 75, in press). In the limit of slow non-relativistic plasma flows, the numerical solutions fit well with those obtained in Paper I, but for weakly relativistic streams an important deviation is found.

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Lazar, M., R. Schlickeiser, and P. K. Shukla. "Cumulative effect of the Weibel-type instabilities in symmetric counterstreaming plasmas with kappa anisotropies." Physics of Plasmas 15, no. 4 (2008): 042103. http://dx.doi.org/10.1063/1.2896232.

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Ghizzo, A. "On the multistream approach of relativistic Weibel instability. II. Bernstein-Greene-Kruskal-type waves in magnetic trapping." Physics of Plasmas 20, no. 8 (2013): 082110. http://dx.doi.org/10.1063/1.4817751.

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Garasev, M. A., Vl V. Kocharovsky, A. A. Nechaev, A. N. Stepanov, and V. V. Kocharovsky. "The Coexistence of Orthogonal Current Structures and the Development of Different-Type Weibel Instabilities in Adjacent Regions of a Plasma Transition Layer with a Hot Electron Flow." Геомагнетизм и аэрономия 63, no. 1 (2023): 12–27. http://dx.doi.org/10.31857/s0016794022060050.

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Abstract—By means of particle-in-cell numerical simulations, we find the possibility of the formation andlong-term coexistence of orthogonal current structures in adjacent layers of an inhomogeneous cold plasmapenetrated by a hot electron flow. The formationof these structures is shown to occur in a wide range ofparameters specifying collisionless expansion of high-energy electrons out of a dense plasma into a rarefiedplasma. These structures originate due to the development of Weibel instabilities of two different types thatare associated with qualitatively different anisotropic electron velocity distributions. Experiments with a laserplasma produced in the course of target ablation by means of quasi-cylindrical focusing of a high-power femtosecond-laser radiation beam are proposed in order to observe the predicted phenomenon

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Lazar, M., R. Schlickeiser, and P. K. Shukla. "Erratum: “Cumulative effect of the Weibel-type instabilities in symmetric counterstreaming plasmas with kappa anisotropies” [Phys. Plasmas 15, 042103 (2008)]." Physics of Plasmas 15, no. 7 (2008): 079901. http://dx.doi.org/10.1063/1.2953799.

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Garasev, M. A., Vl V. Kocharovsky, A. A. Nechaev, A. N. Stepanov, and V. V. Kocharovsky. "The Coexistence of Orthogonal Current Structures and the Development of Different-Type Weibel Instabilities in Adjacent Regions of a Plasma Transition Layer with a Hot Electron Flow." Geomagnetism and Aeronomy 62, S1 (2022): S10—S24. http://dx.doi.org/10.1134/s0016793222600436.

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Duţan, Ioana, Ken-Ichi Nishikawa, Yosuke Mizuno, et al. "Particle-in-cell Simulations of Global Relativistic Jets with Helical Magnetic Fields." Proceedings of the International Astronomical Union 12, S324 (2016): 199–202. http://dx.doi.org/10.1017/s1743921316012722.

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AbstractWe study the interaction of relativistic jets with their environment, using 3-dimen- sional relativistic particle-in-cell simulations for two cases of jet composition: (i) electron-proton (e− − p+) and (ii) electron-positron (e±) plasmas containing helical magnetic fields. We have performed simulations of “global” jets containing helical magnetic fields in order to examine how helical magnetic fields affect kinetic instabilities such as the Weibel instability, the kinetic Kelvin-Helmholtz instability and the Mushroom instability. We have found that these kinetic instabilities are suppressed and new types of instabilities can grow. For the e− − p+ jet, a recollimation-like instability occurs and jet electrons are strongly perturbed, whereas for the e± jet, a recollimation-like instability occurs at early times followed by kinetic instability and the general structure is similar to a simulation without a helical magnetic field. We plan to perform further simulations using much larger systems to confirm these new findings.

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Tautz, R. C., and I. Lerche. "Nonlinear Weibel-type soliton modes." Journal of Physics A: Mathematical and Theoretical 44, no. 4 (2010): 045501. http://dx.doi.org/10.1088/1751-8113/44/4/045501.

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Tautz, R. C., and I. Lerche. "Nonlinear Weibel-type soliton modes." Journal of Physics A: Mathematical and Theoretical 44, no. 16 (2011): 169602. http://dx.doi.org/10.1088/1751-8121/44/16/169602.

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Haberichter, Sandra L., Elizabeth P. Merricks, Scot A. Fahs, Pamela A. Christopherson, Timothy C. Nichols, and Robert R. Montgomery. "Re-establishment of VWF-dependent Weibel-Palade bodies in VWD endothelial cells." Blood 105, no. 1 (2005): 145–52. http://dx.doi.org/10.1182/blood-2004-02-0464.

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Abstract Type 3 von Willebrand disease (VWD) is a severe hemorrhagic defect in humans. We now identify the homozygous mutation in the Chapel Hill strain of canine type 3 VWD that results in premature termination of von Willebrand factor (VWF) protein synthesis. We cultured endothelium from VWD and normal dogs to study intracellular VWF trafficking and Weibel-Palade body formation. Weibel-Palade bodies could not be identified in the canine VWD aortic endothelial cells (VWD-AECs) by P-selectin, VWFpp, or VWF immunostaining and confocal microscopy. We demonstrate the reestablishment of Weibel-Palade bodies that recruit endogenous P-selectin by expressing wild-type VWF in VWD-AECs. Expression of mutant VWF proteins confirmed that VWF multimerization is not necessary for Weibel-Palade body creation. Although the VWF propeptide is required for the formation of Weibel-Palade bodies, it cannot independently induce the formation of the granule. These VWF-null endothelial cells provide a unique opportunity to examine the biogenesis of Weibel-Palade bodies in endothelium from a canine model of type 3 VWD.

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Kobayashi, Toshihide, Ulrich M. Vischer, Corinne Rosnoblet, et al. "The Tetraspanin CD63/lamp3 Cycles between Endocytic and Secretory Compartments in Human Endothelial Cells." Molecular Biology of the Cell 11, no. 5 (2000): 1829–43. http://dx.doi.org/10.1091/mbc.11.5.1829.

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In the present study, we show that in human endothelial cells the tetraspanin CD63/lamp3 distributes predominantly to the internal membranes of multivesicular–multilamellar late endosomes, which contain the unique lipid lysobisphosphatidic acid. Some CD63/lamp3 is also present in Weibel–Palade bodies, the characteristic secretory organelle of these cells. We find that CD63/lamp3 molecules can be transported from late endosomes to Weibel–Palade bodies and thus that CD63/lamp3 cycles between endocytic and biosynthetic compartments; however, movement of CD63/lamp3 is much slower than that of P-selectin, which is known to cycle between plasma membrane and Weibel–Palade bodies. When cells are treated with U18666A, a drug that mimics the Niemann-Pick type C syndrome, both proteins accumulate in late endosomes and fail to reach Weibel–Palade bodies efficiently, suggesting that P-selectin, like CD63/lamp3, cycles via late endosomes. Our data suggest that CD63/lamp3 partitions preferentially within late endosome internal membranes, thus causing its accumulation, and that this mechanism contributes to CD63/lamp3 retention in late endosomes; however, our data also indicate that the protein can eventually escape from these internal membranes and recycle toward Weibel–Palade bodies to be reused. Our observations thus uncover the existence of a selective trafficking route from late endosomes to Weibel–Palade bodies.

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Chauhan, Anil K., Janka Kisucka, Colin B. Lamb, Wofgang Bergmeier, and Denisa D. Wagner. "von Willebrand Factor and Factor VIII Are Independently Required To Form Stable Occlusive Thrombi in Injured Veins." Blood 108, no. 11 (2006): 1789. http://dx.doi.org/10.1182/blood.v108.11.1789.1789.

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Abstract von Willebrand factor (VWF) is a large adhesive glycoprotein synthesized in megakaryocytes and endothelial cells and stored in platelet a-granules and Weibel-Palade bodies respectively. It protects Factor VIII (FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall thus playing an important role in hemostasis and thrombosis. VWF is crucial for the formation of occlusive thrombi at arterial shear rates. However, with only a few conflicting studies published, the role of VWF in venous thrombosis is still unclear. Therefore in order to understand the in vivo role of VWF and FVIII in experimental thrombosis under venous flow conditions, we decided to evaluate thrombosis in VWF−/−, FVIII−/− and transgenic mice lacking the GPIbα extracellular domain which was replaced by human Interleukin-4 receptor (IL4Rα/GPIbα-tg). In ferric chloride-injured veins, platelet adhesion to subendothelium is decreased and thrombus growth is impaired in the VWF−/− mice when compared to wild-type (WT). In the WT mice, thrombi grew to occlusive size with a mean time of 18 min and all injured venules occluded, whereas in VWF−/− mice none of the vessels occluded by 40 min after injury, when observation was terminated. Venules of mice deficient in FVIII treated similarly also did not occlude because of embolization. The infusion of recombinant human-FVIII (r-hu-FVIII) in FVIII−/− mice normalized the occlusion time to WT values. We also observed thrombus instability in the VWF−/− mice, which was due to lower FVIII levels in these mice since r-huFVIII restored thrombus stability i.e. prevented breaking of the thrombi with large platelet aggregates moving downstream. Despite normalization of blood clotting time and thrombus stability after r-FVIII infusion, the VWF−/− thrombi grew at a slower rate than WT and the venules did not occlude. In transgenic mice lacking the GPIbα extracellular domain, all injured venules occluded. Thus, VWF uses other adhesion receptors besides GPIbα in thrombus growth under venous shear conditions. Our studies document crucial independent roles for VWF and FVIII in experimental thrombosis under venous flow conditions in vivo.

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Hüller, S., and A. Porzio. "Weibull-type speckle distributions as a result of saturation in stimulated scattering processes." Laser and Particle Beams 33, no. 4 (2015): 667–78. http://dx.doi.org/10.1017/s0263034615000713.

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AbstractDuring the propagation of an optically smoothed laser beam through a warm plasma the speckle field pattern and the corresponding speckle intensity distribution are modified in time and along the laser propagation direction. It is shown here that the laser–plasma interaction can change the character of speckle statistics from an initially exponential-type limit law to a Weibull-type law. The Weibull distribution is characterized by a power-law-type behavior in a limited interval of the random variable, which is, in the present case, the speckle intensity. The properties of the speckle distributions are studied using methods of extremal and order statistics. The scattering instability process (here stimulated Brillouin forward scattering) causing the change in speckle statistics has an onset behavior associated with a “critical gain” value, as pointed out in work by Rose and DuBois (1993b). The saturation of the instability process as a function of intensity explains the limited interval of the Weibull-type speckle distribution. The differences in the type of the speckle statistics are analyzed by using “excess over threshold” methods relying on the generalized Pareto distribution, which clearly brings to evidence the transition from an exponential type distribution to the Weibull-type distribution as a function of the instability gain value, that is, from the regime below critical gain to values above the critical gain.

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Emeis, J. J., Y. van den Eijnden-Schrauwen, C. M. van den Hoogen, W. de Priester, A. Westmuckett, and F. Lupu. "An Endothelial Storage Granule for Tissue-Type Plasminogen Activator." Journal of Cell Biology 139, no. 1 (1997): 245–56. http://dx.doi.org/10.1083/jcb.139.1.245.

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In previous studies we have shown that, after stimulation by a receptor ligand such as thrombin, tissue-type plasminogen activator (tPA) and von Willebrand factor (vWf) will be acutely released from human umbilical vein endothelial cells (HUVEC). However, the mechanisms involved in the secretion of these two proteins differ in some respects, suggesting that the two proteins may be stored in different secretory granules. By density gradient centrifugation of rat lung homogenates, a particle was identified that contained nearly all tPA activity and antigen. This particle had an average density of 1.11–1.12 g/ml, both in Nycodenz density gradients and in sucrose density gradients. A similar density distribution of tPA was found for a rat endothelial cell line and for HUVEC. After thrombin stimulation of HUVEC to induce tPA secretion, the amount of tPA present in high-density fractions decreased, concomitant with the release of tPA into the culture medium and a shift in the density distribution of P-selectin. vWf, known to be stored in Weibel-Palade bodies, showed an identical distribution to tPA in Nycodenz gradients. In contrast, the distribution in sucrose gradients of vWf from both rat and human lung was very different from that of tPA, suggesting that tPA and vWf were not present in the same particle. Using double-immunofluorescence staining of HUVEC, tPA- and vWf-containing particles showed a different distribution by confocal microscopy. The distribution of tPA also differed from the distribution of tissue factor pathway inhibitor, endothelin-1, and caveolin. By immunoelectronmicroscopy, immunoreactive tPA could be demonstrated in small vesicles morphologically different from the larger Weibel-Palade bodies. It is concluded that tPA in endothelial cells is stored in a not-previously-described, small and dense (d = 1.11– 1.12 g/ml) vesicle, which is different from a Weibel-Palade body.

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Chauhan, Anil K., Janka Kisucka, Alexander Brill, Meghan T. Walsh, Friedrich Scheiflinger, and Denisa D. Wagner. "ADAMTS13: a new link between thrombosis and inflammation." Journal of Experimental Medicine 205, no. 9 (2008): 2065–74. http://dx.doi.org/10.1084/jem.20080130.

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von Willebrand factor (VWF) levels are elevated and a disintegrin-like and metalloprotease with thrombospondin type I repeats–13 (ADAMTS13) activity is decreased in both acute and chronic inflammation. We hypothesized that by cleaving hyperactive ultralarge VWF (ULVWF) multimers, ADAMTS13 down-regulates both thrombosis and inflammation. Using intravital microscopy, we show that ADAMTS13 deficiency results in increased leukocyte rolling on unstimulated veins and increased leukocyte adhesion in inflamed veins. Both processes were dependent on the presence of VWF. Depletion of platelets in Adamts13−/− mice reduced leukocyte rolling, suggesting that platelet interaction with ULVWF contributes to this process. Increased levels of endothelial P-selectin and plasma VWF in Adamts13−/− compared with wild-type (WT) mice indicated an elevated release of Weibel-Palade bodies. ULVWF multimers released upon stimulation with histamine, a secretagogue of Weibel-Palade bodies, slowed down leukocyte rolling in Adamts13−/− but not in WT mice. Furthermore, in inflammatory models, ADAMTS13 deficiency resulted in enhanced extravasation of neutrophils, and this process was also dependent on VWF. Our findings reveal an important role for ADAMTS13 in preventing excessive spontaneous Weibel-Palade body secretion, and in the regulation of leukocyte adhesion and extravasation during inflammation.

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Castaman, Giancarlo, Sofia Helene Giacomelli, Paula M. Jacobi, Tobias Obser, Reinhard Schneppenheim, and Sandra L. Haberichter. "Reduced Von Willebrand Factor Secretion Is Associated with Loss of Weibel-Palade Formation." Blood 116, no. 21 (2010): 541. http://dx.doi.org/10.1182/blood.v116.21.541.541.

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Abstract Abstract 541 Background. Von Willebrand Disease (VWD) is caused by mutations in von Willebrand factor (VWF) that have different pathophysiologic effect in causing low plasma VWF levels. Type 1 VWD includes patients with quantitative plasma VWF deficiency with normal VWF structure and function. Aim of the study. We report three different novel type 1 VWF mutations (A1716P, C2190Y and R2663C) which although located in different VWF domains are associated with reduced secretion and lack of formation of Weibel-Palade body-like granules. Methods. Transient expression of recombinant mutant full-length VWF in 293 EBNA cells was performed and secretion, collagen binding, and GpIb binding assessed in comparison to wild-type VWF. Furthermore, expression was also examined in HEK293 cells that form Weibel-Palade body (WPB)-like granules when transfected with wt VWF. Results. The multimer analysis of plasma VWF was compatible with type 1 VWD. The results of 3 different expression experiments showed a slightly reduced VWF synthesis and drastically impaired secretion into the medium with homozygous expression. In HEK293 cells, homozygous A1716P and C2190Y VWF variants failed to form WPB-like granules, while R2663C was capable of forming granules, but had fewer cells with granules and more with ER-localized VWF. Heterozygous expression of A1716P and C2160Y VWF variants had a negative impact on wild-type VWF and WPB-like granules were observed in transfected cells. Conclusions. Our results demonstrate that homozygous and heterozygous quantitative VWF deficiency caused by missense VWF mutations can be associated with inability to form endothelial Weibel-Palade-like granules and mutations in different VWF domains can affect the formation of these organelles. Disclosures: No relevant conflicts of interest to declare.

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Dieckmann, M. E. "The formation of relativistic plasma structures and their potential role in the generation of cosmic ray electrons." Nonlinear Processes in Geophysics 15, no. 6 (2008): 831–46. http://dx.doi.org/10.5194/npg-15-831-2008.

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Abstract. Recent particle-in-cell (PIC) simulation studies have addressed particle acceleration and magnetic field generation in relativistic astrophysical flows by plasma phase space structures. We discuss the astrophysical environments such as the jets of compact objects, and we give an overview of the global PIC simulations of shocks. These reveal several types of phase space structures, which are relevant for the energy dissipation. These structures are typically coupled in shocks, but we choose to consider them here in an isolated form. Three structures are reviewed. (1) Simulations of interpenetrating or colliding plasma clouds can trigger filamentation instabilities, while simulations of thermally anisotropic plasmas observe the Weibel instability. Both transform a spatially uniform plasma into current filaments. These filament structures cause the growth of the magnetic fields. (2) The development of a modified two-stream instability is discussed. It saturates first by the formation of electron phase space holes. The relativistic electron clouds modulate the ion beam and a secondary, spatially localized electrostatic instability grows, which saturates by forming a relativistic ion phase space hole. It accelerates electrons to ultra-relativistic speeds. (3) A simulation is also revised, in which two clouds of an electron-ion plasma collide at the speed 0.9c. The inequal densities of both clouds and a magnetic field that is oblique to the collision velocity vector result in waves with a mixed electrostatic and electromagnetic polarity. The waves give rise to growing corkscrew distributions in the electrons and ions that establish an equipartition between the electron, the ion and the magnetic energy. The filament-, phase space hole- and corkscrew structures are discussed with respect to electron acceleration and magnetic field generation.

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Mohamed, Yazidi, Eloutassi Noureddine, Nabih Khadija, Hammi Abdel Hadi, Yazidi Abdelaziz, and Benziane Fouad. "Gestion Des Risques Majeurs Au Maroc: Les Instabilités De Terrain." European Scientific Journal, ESJ 13, no. 12 (2017): 46. http://dx.doi.org/10.19044/esj.2017.v13n12p46.

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Instabilities of the ground is regarded as one of the most serious problems that affect many areas in Morocco. The study is important and beneficial because it concerns various sections of the Rif area. Indeed, certain zones which came at the top have been seriously affected. Disorders are numerous: destruction of homes, loss of agricultural land, and deterioration of infrastructure (roads, railways, and bridges). The aim of this study is focused on the zones where the road network generally is much damaged. This, however, causes a disturbance and even an interruption of the road traffic during stormy periods. The detailed study of lithology, climatology, geomorphology, hydrology, and the slope of the studied zones allows us to highlight the characteristics of the unstable grounds. It also helped us to figure out that the rheological nature of the ground plays a significant role in the characterization of the type of movement.The analysis of various movements which was found enables us to conclude that an instability of the ground depends on the conjunction on many factors, whether they are of provision or release. The most important factors causing the instabilities of the ground are: The alternation of rocks of nature; permeability and plasticity were well contrasted. The rugged relief and steep slopes. Geotechnical properties. Seismicity. Irregular rainfall. Geomorphology and land use. Anthropogenic action. Spatial distribution of the risk zones shows that the majority of the studied sections experience strong risks and medium risks levels.

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Iafrati, Mark D., Olga Vitseva, Kahraman Tanriverdi, et al. "Compensatory mechanisms influence hemostasis in setting of eNOS deficiency." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (2005): H1627—H1632. http://dx.doi.org/10.1152/ajpheart.00819.2004.

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The balance between thrombosis and hemorrhage is carefully regulated. Nitric oxide (NO) is an important mediator of these processes, as it prevents platelet adhesion to the endothelium and inhibits platelet recruitment. Although endothelial NO synthase (eNOS)-deficient mice have decreased vascular reactivity and mild hypertension, enhanced thrombosis in vivo has not been demonstrated. To determine the role of endogenous NO in hemostasis, a model of carotid arterial injury and thrombosis was performed using eNOS-deficient and wild-type mice. Paradoxically, the eNOS-deficient animals had a prolongation of time to occlusion compared with the wild-type mice ( P < 0.001). Consistent with this finding, plasma markers suggesting enhanced fibrinolysis [tissue plasminogen activator (t-PA) activity and antigen and D-dimer levels] were significantly elevated in eNOS-deficient animals. Vascular tissue expression of t-PA and platelet activity levels were not altered. In endothelial cells, t-PA is stored in Weibel-Palade bodies, and exocytosis of these storage granules is inhibited by NO. Thus in the absence of NO, release of Weibel-Palade body contents (and t-PA) could be enhanced; this observation is also supported by increased von Willebrand factor levels observed in eNOS-deficient animals. In summary, although eNOS deficiency attenuates vascular reactivity and increases platelet recruitment, it is also associated with enhanced fibrinolysis due to lack of NO-dependent inhibition of Weibel-Palade body release. These processes highlight the complexity of NO-dependent regulation of vascular homeostasis. Such compensatory mechanisms may partially explain the lack of spontaneous thrombosis, minimally elevated baseline blood pressure, and normal life span that are seen in animals deficient in a pivotal regulator of vascular patency.

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Groot, Evelyn, Rob Fynheer, Silvie AE Sebastian, Peter J. Lenting, and Philip G. De Groot. "Transition from Non-Platelet-Binding to Platelet-Binding Conformation of Von Willebrand Factor Occurs upon Exocytosis." Blood 112, no. 11 (2008): 3917. http://dx.doi.org/10.1182/blood.v112.11.3917.3917.

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Abstract Introduction Von Willebrand factor (VWF) is a large multimeric glycoprotein that contributes to platelet recruitment at sites of vascular injury. VWF is mainly produced in endothelial cells from where it is secreted directly into the circulation or stored in the rod-shaped organelles called Weibel-Palade bodies. VWF present in the circulation does not bind to platelets. Stimulated endothelial cells secrete VWF that has the capacity to spontaneously interact with platelets. Conversion of the platelet-binding conformation of secreted VWF into the non-binding conformation of plasma VWF involves proteolytic processing by the metalloprotease ADAMTS13. At sites of vascular injury, binding of VWF to the exposed subendothelial collagen induces a conformational change in VWF allowing a strong interaction with the platelet receptor glycoprotein (Gp)Ibα. Undesired secretion of active VWF may also occur in several pathological conditions. One example is von Willebrand disease type 2B (VWD2B), where a gain of function mutation in the VWF/A1 domain induces a permanent platelet-binding state in the VWF molecule. As a consequence, VWF can spontaneously interact with platelets in the circulation, leading to thrombocytopenia, a hallmark of VWD2B. Objective The aim of this study was to investigate whether VWF present in the Weibel-Palade bodies of endothelial cells is stored in a platelet-binding conformation. Methods Immunofluorescence experiments were performed on wildtype and VWD2B endothelial cells. Monoclonal antibody AU/VWF-a11 is directed against the VWF/A1 domain and recognizes VWF only when it is in its GpIb-binding conformation. Monoclonal antibody AU/VWF-C37H is directed against the VWF/A3 domain and recognizes both the platelet-binding and the non-platelet- binding conformation. Experiments were performed on cultured endothelial cells to study the conformation of VWF in the Weibel-Palade bodies. To study the conformation of secreted VWF, stimulated endothelial cells were perfused with washed platelets. Results AU/VWF-C37H fluorescence was observed in the Weibel-Palade bodies of both wildtype and VWD2B endothelial cells, whereas AU/VWF-a11 fluorescence was only detected in the Weibel-Palade bodies of the VWD2B cells. Perfusion of washed platelets over wildtype and VWD2B endothelial cells resulted in adhesion of platelets to thin strings of secreted VWF. These strings stained positive for both AU/VWF-C37H and AU/VWF-a11. Of note, significantly more platelets adhered to VWF secreted from VWD2B than from wildtype endothelial cells. This hyperactive VWD2B-like platelet adhesion pattern could be mimicked by wildtype endothelial cells upon perfusion with platelets that were mixed with ristocetin. Conclusions VWF stored within the Weibel-Palade bodies of endothelial cells does not possess platelet-binding capacities. Upon secretion, VWF undergoes a conformational change that allows the adhesion of platelets. The presence of ADAMTS13 is necessary to prevent the release of platelet-binding VWF in the circulation. In the absence of ADAMTS13, secreted VWF does not expose all its GpIb-binding sites as more platelets adhere to ristocetin activated VWF-strings or strings released from VWD2B endothelial cells.

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Rosnoblet, Corinne, Ulrich M. Vischer, Robert D. Gerard, Jean-Claude Irminger, Philippe A. Halban, and Egbert K. O. Kruithof. "Storage of Tissue-Type Plasminogen Activator in Weibel-Palade Bodies of Human Endothelial Cells." Arteriosclerosis, Thrombosis, and Vascular Biology 19, no. 7 (1999): 1796–803. http://dx.doi.org/10.1161/01.atv.19.7.1796.

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Zeghloul, A., M. Mliha-Touati, and S. Bakir. "Étude des domaines d'existence des instabilités plastiques du type Portevin-Le Chatelier dans l'alliage d'aluminium-magnesium AG3." Journal de Physique III 6, no. 11 (1996): 1467–78. http://dx.doi.org/10.1051/jp3:1996196.

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Dieckmann, M. E., J. D. Riordan, and A. Pe'er. "Change of a Weibel-type to an Alfvénic shock in pair plasma by upstream waves." Physics of Plasmas 27, no. 6 (2020): 062107. http://dx.doi.org/10.1063/5.0003596.

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Barkalow, FJ, MJ Goodman, ME Gerritsen, and TN Mayadas. "Brain endothelium lack one of two pathways of P-selectin-mediated neutrophil adhesion." Blood 88, no. 12 (1996): 4585–93. http://dx.doi.org/10.1182/blood.v88.12.4585.bloodjournal88124585.

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P-selectin, an endothelial leukocyte adhesion receptor, is rapidly translocated to the cell surface upon release from storage granules called Weibel-Palade bodies and is also transcriptionally upregulated upon cytokine stimulation of endothelial cells (ECs). These two pathways of surface expression are coincident with the rapid and cytokine-inducible pathway of neutrophil adhesion to ECs. Constitutive P-selectin expression is largely absent in cultured murine brain microvascular EC (BMEC) monolayers, but interleukin-1beta and tumor necrosis factor-alpha stimulation for 4 hours leads to dramatic P-selectin upregulation. The functional relevance of differential P-selectin expression in these cells was examined by studying BMECs derived from wild-type mice and P-selectin-deficient mice. We show that P-selectin deficiency does not affect Weibel-Palade body formation or their release in response to short-acting agonists. However, in the absence of P-selectin, the brain endothelium is unable to support neutrophil adhesion after stimulation with these agonists, which may contribute to the immune privilege status of the brain. We show that P- selectin does play a major role in supporting neutrophil adhesion in the cytokine-induced pathway in BMECs in the context of other cytokine- inducible endothelial-leukocyte adhesion receptors, E-selectin, ICAM-1, and VCAM-1.

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Dekker, Rob J., Reinier A. Boon, Mariska G. Rondaij, et al. "KLF2 provokes a gene expression pattern that establishes functional quiescent differentiation of the endothelium." Blood 107, no. 11 (2006): 4354–63. http://dx.doi.org/10.1182/blood-2005-08-3465.

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Abstract The flow-responsive transcription factor KLF2 is acquiring a leading role in the regulation of endothelial cell gene expression. A genome-wide microarray expression profiling is described employing lentivirus-mediated, 7-day overexpression of human KLF2 at levels observed under prolonged flow. KLF2 is not involved in lineage typing, as 42 endothelial-specific markers were unaffected. Rather, KLF2 generates a gene transcription profile (> 1000 genes) affecting key functional pathways such as cell migration, vasomotor function, inflammation, and hemostasis and induces a morphology change typical for shear exposure including stress fiber formation. Protein levels for thrombomodulin, endothelial nitric oxide synthase, and plasminogen activator inhibitor type-1 are altered to atheroprotective levels, even in the presence of the inflammatory cytokine TNF-α. KLF2 attenuates cell migration by affecting multiple genes including VEGFR2 and the potent antimigratory SEMA3F. The distribution of Weibel-Palade bodies in cultured cell populations is normalized at the single-cell level without interfering with their regulated, RalA-dependent release. In contrast, thrombin-induced release of Weibel-Palade bodies is significantly attenuated, consistent with the proposed role of VWF release at low–shear stress regions of the vasculature in atherosclerosis. These results establish that KLF2 acts as a central transcriptional switch point between the quiescent and activated states of the adult endothelial cell.

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Dadkhahi, Sara, Julia Gansler, Mona Saffarzadeh, et al. "Expression and localisation of vascular ribonucleases in endothelial cells." Thrombosis and Haemostasis 105, no. 02 (2011): 345–55. http://dx.doi.org/10.1160/th10-06-0345.

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SummaryThe functions of extracellular RNA in the vascular system as new procoagulatory and permeability-increasing factor in vivoand in vitrowere shown to be counteracted by pancreatic type RNase1. Based on the identification of RNase1 in plasma and serum, it is proposed that the enzyme is expressed by vascular cells to contribute in the regulation of extracellular RNA. It is demonstrated that RNase1 and RNase5 (also termed angiogenin) were differentially expressed in various types of endothelial cells, whereby human umbilical vein endothelial cells (HUVEC) expressed and released the highest concentration of active RNase1. Expression and release of RNase5 were similar in all types of endothelial cells tested. Both RNases were constitutively produced and secreted, whereby a portion of RNase1, but not RNase5, was stored in Weibel-Palade bodies, co-localising with von Willlebrand factor and P-selectin. Accordingly, immediate release of RNase1 from these granules was demonstrated in vitroand in vivousing Weibel-Palade body exocytosis-inducing agents. Additionally, extracellular RNA or poly:IC (but not DNA) induced this short-term release of RNase1. Our results indicate that vascular RNase1 and RNase5 are mainly produced by vascular endothelial cells and can serve, depending on the vascular bed, different functions in vascular homeostasis and endothelial cell responses.

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Fiedler, Ulrike, Marion Scharpfenecker, Stefanie Koidl, et al. "The Tie-2 ligand Angiopoietin-2 is stored in and rapidly released upon stimulation from endothelial cell Weibel-Palade bodies." Blood 103, no. 11 (2004): 4150–56. http://dx.doi.org/10.1182/blood-2003-10-3685.

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Abstract The angiopoietins Ang-1 and Ang-2 have been identified as ligands with opposing functions of the receptor tyrosine kinase Tie-2 regulating endothelial cell survival and vascular maturation. Ang-1 acts in a paracrine agonistic manner, whereas Ang-2 appears to act primarily as an autocrine antagonistic regulator. To shed further light on the complexity of autocrine/paracrine agonistic/antagonistic functions of the angiopoietin/Tie-2 system, we have studied Ang-2 synthesis and secretion in different populations of wild-type and retrovirally Ang-2–transduced endothelial cells. Endogenous and overexpressed endothelial cell Ang-2 is expressed in a characteristic granular pattern indicative of a cytoplasmic storage granule. Light and electron microscopic double staining revealed Ang-2 colocalization with von Willebrand factor, identifying Ang-2 as a Weibel-Palade body molecule. Costaining with P-selectin showed that storage of Ang-2 and P-selectin in Weibel-Palade bodies is mutually exclusive. Stored Ang-2 has a long half-life of more than 18 hours and can be secreted within minutes of stimulation (eg, by phorbol 12-myristate 13-acetate [PMA], thrombin, and histamine). Collectively, the identification of Ang-2 as a stored, rapidly available molecule in endothelial cells strongly suggests functions of the angiopoietin/Tie-2 system beyond the established roles during angiogenesis likely to be involved in rapid vascular homeostatic reactions such as inflammation and coagulation.

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Haberichter, Sandra L., Paula Jacobi, and Robert R. Montgomery. "Critical independent regions in the VWF propeptide and mature VWF that enable normal VWF storage." Blood 101, no. 4 (2003): 1384–91. http://dx.doi.org/10.1182/blood-2002-07-2281.

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Von Willebrand factor (VWF) is synthesized in endothelial cells, where it is stored in Weibel-Palade bodies. Administration of 1-desamino-8-D-arginine-vasopressin (DDAVP) to patients with type 1 von Willebrand disease and to healthy individuals causes a rapid increase in plasma VWF levels. This increase is the result of stimulated release of VWF from Weibel-Palade bodies in certain beds of endothelial cells. The VWF propeptide (VWFpp) targets VWF to storage granules through a noncovalent association. The nature of the VWFpp/VWF interaction was investigated by using cross-species differences in VWF storage. While canine VWFpp traffics to storage granules and facilitates the multimerization of human VWF, it does not direct human VWF to storage granules. Since storage takes place after furin cleavage, this defect appears to be due to the defective interaction of canine VWFpp and human VWF. To determine the regions within VWFpp and VWF important for this VWFpp/VWF association and costorage, a series of human-canine chimeric VWFpp and propeptide-deleted VWF (Δpro) constructs were produced and expressed in AtT-20 cells. The intracellular localization of coexpressed proteins was examined by confocal microscopy. Two amino acids, 416 in VWFpp and 869 in the mature VWF molecule, were identified as being critical for the association and granular storage of VWF.

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Chauhan, Anil K., Janka Kiucka, Alexander Brill, Meghan T. Walsh, and Denisa D. Wagner. "Deficiency of the VWF-Cleaving Protease ADAMTS13 Results in Increased Leukocyte Rolling and Adhesion in Mice." Blood 110, no. 11 (2007): 290. http://dx.doi.org/10.1182/blood.v110.11.290.290.

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Abstract von Willebrand factor (VWF) is synthesized in megakaryocytes and endothelial cells and stored in a-granules and Weibel-Palade bodies, respectively. VWF levels are elevated in both chronic and acute inflammation. ADAMTS13 (A D isintegrin-like A nd M etalloprotease with T hrombo s pondin type I repeats-13) is a metalloprotease that cleaves ultra large von Willebrand factor (ULVWF) multimers quickly after its release from endothelium. Recent studies have found that VWF promotes leukocyte adhesion in vitro and that ADAMTS13 activity is reduced in inflammation and sepsis. We hypothesized that by cleaving ULVWF multimers, ADAMTS13 not only inhibits thrombosis, but also attenuates leukocyte rolling and adhesion. Using intravital microscopy, we found more leukocyte rolling/min on the unstimulated veins in Adamts13-/- mice (Mean ± SE: 98 ± 16) compared to WT (Mean ± SE: 35 ± 6, P<0.001), n=18–20 from 10–11 mice per group. This process was dependent on VWF because the number of leukocytes rolling in Adamts13-/-/Vwf-/- veins was similar to that in Vwf-/-. Significantly increased soluble P-selectin and VWF concentrations were found in the plasma of Adamts13-/- compared to WT mice as quantitated by ELISA. In addition, endothelial P-selectin surface expression was increased in Adamts13-/- mice compared to WT. These results suggest elevated release of Weibel-Palade bodies in Adamts13-/- mice. Notably, circulating platelets were not activated in the absence of ADAMTS13. Upon stimulation of the mesentery with histamine, leukocyte rolling was slower in Adamts13-/- veins compared to WT. Furthermore, upon stimulation with the inflammatory cytokine TNF-alpha (i.v) 3.5 h prior to surgery, the number of leukocytes adhering/250 um was significantly increased in microvenules (diameter of 25–30 um) of Adamts13-/- mice (Mean ± SD: 21 ± 6) compared to WT (Mean ± SD: 12 ± 5, P<0.001), n=10–11 mice per group. This firm adhesion was also dependent on VWF because the number of adherent leukocytes in veins of Adamts13-/-/Vwf-/- was similar to Vwf-/-. Our studies indicate a crucial role for ADAMTS13 in preventing excessive spontaneous Weibel-Palade secretion and in attenuating leukocyte rolling and adhesion to ultra large VWF presented by endothelial cells during inflammation.

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André, Patrick, Cécile V. Denis, Jerry Ware, et al. "Platelets adhere to and translocate on von Willebrand factor presented by endothelium in stimulated veins." Blood 96, no. 10 (2000): 3322–28. http://dx.doi.org/10.1182/blood.v96.10.3322.

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Abstract With the use of intravital microscopy, a new type of platelet–endothelial interaction in mouse mesenteric venules at low shear (80-100 seconds−1) is described. Stimulation of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation without the formation of aggregates. This stop-and-go process reached a maximum in approximately 1 minute, when approximately 25 000 platelets adhered/mm2·s, and then adhesion progressively decreased. This adhesion process was dependent on von Willebrand factor (vWF) and independent of P-selectin. Immunohistologic analysis showed that the venules were not denuded withA23187 treatment, suggesting that platelets adhered to vWF secreted on the luminal face of the endothelial cells. Histamine treatment induced a similar adhesion phenomenon. Platelet adhesion was not abolished in β3-deficient mice or when the platelets were treated with inhibitory antibodies to PECAM-1 or PSGL-1, indicating that these molecules are not required for platelet–endothelium interaction at low shear. The adhesion was mediated by platelet glycoprotein Ibα (GPIbα) because the adhesion of murine platelets expressing exclusively the human GPIbα could be prevented by a pretreatment with mocarhagin, a snake venom protease that cleaves human GPIbα. The results indicate that vWF released from Weibel-Palade bodies can dramatically increase the concentration of platelets along the vessel wall through an interaction with GPIbα. It is proposed that this process may rapidly recruit platelets to sites of injury or inflammation in veins.

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With the use of intravital microscopy, a new type of platelet–endothelial interaction in mouse mesenteric venules at low shear (80-100 seconds−1) is described. Stimulation of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation without the formation of aggregates. This stop-and-go process reached a maximum in approximately 1 minute, when approximately 25 000 platelets adhered/mm2·s, and then adhesion progressively decreased. This adhesion process was dependent on von Willebrand factor (vWF) and independent of P-selectin. Immunohistologic analysis showed that the venules were not denuded withA23187 treatment, suggesting that platelets adhered to vWF secreted on the luminal face of the endothelial cells. Histamine treatment induced a similar adhesion phenomenon. Platelet adhesion was not abolished in β3-deficient mice or when the platelets were treated with inhibitory antibodies to PECAM-1 or PSGL-1, indicating that these molecules are not required for platelet–endothelium interaction at low shear. The adhesion was mediated by platelet glycoprotein Ibα (GPIbα) because the adhesion of murine platelets expressing exclusively the human GPIbα could be prevented by a pretreatment with mocarhagin, a snake venom protease that cleaves human GPIbα. The results indicate that vWF released from Weibel-Palade bodies can dramatically increase the concentration of platelets along the vessel wall through an interaction with GPIbα. It is proposed that this process may rapidly recruit platelets to sites of injury or inflammation in veins.

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Ewenstein, BM, A. Inbal, JS Pober, and RI Handin. "Molecular studies of von Willebrand disease: reduced von Willebrand factor biosynthesis, storage, and release in endothelial cells derived from patients with type I von Willebrand disease [published erratum appears in Blood 1990 Nov 1;76(9):1901]." Blood 75, no. 7 (1990): 1466–72. http://dx.doi.org/10.1182/blood.v75.7.1466.1466.

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Abstract Endothelial cells were cultured from the umbilical veins of two neonates with type I von Willebrand disease (vWD) and compared with cells cultured in parallel from normal control umbilical veins. In both cases, cultured vWD endothelial cells contained less messenger RNA (mRNA) encoding von Willebrand factor (vWF), and constitutively secreted two- to fourfold less vWF protein than their matched controls. Regulated secretion of stored vWF induced by thrombin or phorbol-12- myristate-13-acetate (PMA) was also diminished in vWD cells. Both the mRNA and protein produced by each of these type I vWD cells appeared to be of normal size. However, despite the diminished size of the vWF storage pool, electron microscopy of endothelial cells in situ showed normal appearing vWF storage organelles (Weibel-Palade bodies). These studies show that cultured umbilical vein endothelial cells can be used to explore the molecular defects in type I and perhaps other forms of vWD, and suggest that at least some forms of type I vWD are caused by diminished mRNA transcription or subsequent translation due to a defective vWF allele.

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Endothelial cells were cultured from the umbilical veins of two neonates with type I von Willebrand disease (vWD) and compared with cells cultured in parallel from normal control umbilical veins. In both cases, cultured vWD endothelial cells contained less messenger RNA (mRNA) encoding von Willebrand factor (vWF), and constitutively secreted two- to fourfold less vWF protein than their matched controls. Regulated secretion of stored vWF induced by thrombin or phorbol-12- myristate-13-acetate (PMA) was also diminished in vWD cells. Both the mRNA and protein produced by each of these type I vWD cells appeared to be of normal size. However, despite the diminished size of the vWF storage pool, electron microscopy of endothelial cells in situ showed normal appearing vWF storage organelles (Weibel-Palade bodies). These studies show that cultured umbilical vein endothelial cells can be used to explore the molecular defects in type I and perhaps other forms of vWD, and suggest that at least some forms of type I vWD are caused by diminished mRNA transcription or subsequent translation due to a defective vWF allele.

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Daidone, Viviana, Giovanni Barbon, Elena Pontara, et al. "Loss of cysteine 584 impairs the storage and release, but not the synthesis of von Willebrand factor." Thrombosis and Haemostasis 112, no. 12 (2014): 1159–66. http://dx.doi.org/10.1160/th14-04-0391.

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SummaryCysteines play a key part in von Willebrand factor (VWF) dimerisation and polymerisation, and their loss may severely affect VWF structure and function. We report on three patients with type 3 von Willebrand disease carrying the new c.1751G>T missense mutation that induces the substitution of cysteine 584 by phenylalanine (C584F), and the deletion of seven nucleotides in exon 7 (c.729_735del), producing a premature stop codon at position 454 (E244Lfs*211). VWF was almost undetectable in the patients’ plasma and platelets, while a single, poorly represented, oligomer emerged on plasma VWF multimer analysis. No post-DDAVP increase in VWF and factor VIII was observed. Expressing human recombinant C584F-VWF in HEK293T cells showed that C584F-VWF was synthesised and multimerised but not secreted – apart from the first oligomer, which was slightly represented in the conditioned medium, with a pattern similar to the patients’ plasma VWF. The in vitro expression of the E244Lfs*211–VWF revealed a defective synthesis of the mutated VWF, with a behavior typical of loss of function mutations. Cellular trafficking, investigated in HEK293 cells, indicated a normal C584F-VWF content in the endoplasmic reticulum and Golgi apparatus, confirming the synthesis and multimerisation of C584F-VWF. No pseudo-Weibel Palade bodies were demonstrable, however, suggesting that C584F mutation impairs the storage of C584F-VWF. These findings point to cysteine 584 having a role in the release of VWF and its targeting to pseudo-Weibel Palade bodies in vitro, as well as in its storage and release by endothelial cells in vivo.

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Lopes da Silva, Mafalda, Marie N. O'Connor, Janos Kriston-Vizi, et al. "Type II PI4-kinases control Weibel-Palade body biogenesis and von Willebrand factor structure in human endothelial cells." Journal of Cell Science 129, no. 10 (2016): 2096–105. http://dx.doi.org/10.1242/jcs.187864.

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