-
1
-
-
34250788226
-
In vivo thrombus formation
-
Furie B, Furie BC. In vivo thrombus formation. J Thromb Haemost 2007; 5 (Suppl 1):12-17.
-
(2007)
J Thromb Haemost
, vol.5
, Issue.SUPPL. 1
, pp. 12-17
-
-
Furie, B.1
Furie, B.C.2
-
2
-
-
34247176342
-
In vivo thrombus formation in murine models
-
Sachs UJ, Nieswandt B. In vivo thrombus formation in murine models. Circ Res 2007; 100:979-991.
-
(2007)
Circ Res
, vol.100
, pp. 979-991
-
-
Sachs, U.J.1
Nieswandt, B.2
-
4
-
-
8644222225
-
Hematopoietic cell-derived microparticle tissue factor contributes to fibrin formation during thrombus propagation
-
DOI 10.1182/blood-2004-03-0935
-
Chou J, Mackman N, Merrill-Skoloff G, et al. Hematopoietic cell-derived microparticle tissue factor contributes to fibrin formation during thrombus propagation. Blood 2004; 104:3190-3197. (Pubitemid 39507134)
-
(2004)
Blood
, vol.104
, Issue.10
, pp. 3190-3197
-
-
Chou, J.1
Mackman, N.2
Merrill-Skoloff, G.3
Pedersen, B.4
Furie, B.C.5
Furie, B.6
-
5
-
-
11144248088
-
Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wall
-
DOI 10.1182/blood-2004-06-2225
-
Day SM, Reeve JL, Pedersen B, et al. Macrovascular thrombosis is driven by tissue factor derived primarily from the blood vessel wall. Blood 2005; 105:192-198. (Pubitemid 40053082)
-
(2005)
Blood
, vol.105
, Issue.1
, pp. 192-198
-
-
Day, S.M.1
Reeve, J.L.2
Pedersen, B.3
Farris, D.M.4
Myers, D.D.5
Im, M.6
Wakefield, T.W.7
Mackman, N.8
Fay, W.P.9
-
6
-
-
23744471627
-
Up against the wall
-
author reply 1506-1507
-
Hathcock JJ, Nemerson Y. Up against the wall. Blood 2005; 106:1505. [author reply 1506-1507]
-
(2005)
Blood
, vol.106
, pp. 1505
-
-
Hathcock, J.J.1
Nemerson, Y.2
-
7
-
-
60249092962
-
Vascular smooth muscle-derived tissue factor is critical for arterial thrombosis after ferric chloride-induced injury
-
This study uses a cre-lox strategy to demonstrate the importance of vascular smooth muscle cell derived TF on murine carotid arterial thrombosis. This elegant model of tissue specific TF deletion will likely be used for many vascular studies in the future
-
Wang L, Miller C, Swarthout RF, et al. Vascular smooth muscle-derived tissue factor is critical for arterial thrombosis after ferric chloride-induced injury. Blood 2009; 113:705-713. This study uses a cre-lox strategy to demonstrate the importance of vascular smooth muscle cell derived TF on murine carotid arterial thrombosis. This elegant model of tissue specific TF deletion will likely be used for many vascular studies in the future.
-
(2009)
Blood
, vol.113
, pp. 705-713
-
-
Wang, L.1
Miller, C.2
Swarthout, R.F.3
-
8
-
-
46149092753
-
Key role of platelet procoagulant activity in tissue factor and collagen-dependent thrombus formation in arterioles and venules in vivo differential sensitivity to thrombin inhibition
-
This study demonstrates marked differences in the response to FeCl injury between murine mesenteric venules and arterioles. The experiments compare and contrast (via pharmacologic and genetic models) the relative roles of inhibition of thrombin, TF, platelet phosphatidylserine, and collagen in venule versus arteriole thrombus formation
-
Kuijpers MJ, Munnix IC, Cosemans JM, et al. Key role of platelet procoagulant activity in tissue factor and collagen-dependent thrombus formation in arterioles and venules in vivo differential sensitivity to thrombin inhibition. Microcirculation 2008; 15:269-282. This study demonstrates marked differences in the response to FeCl injury between murine mesenteric venules and arterioles. The experiments compare and contrast (via pharmacologic and genetic models) the relative roles of inhibition of thrombin, TF, platelet phosphatidylserine, and collagen in venule versus arteriole thrombus formation.
-
(2008)
Microcirculation
, vol.15
, pp. 269-282
-
-
Kuijpers, M.J.1
Munnix, I.C.2
Cosemans, J.M.3
-
9
-
-
46149124084
-
Critical role of FcR gamma-chain, LAT, PLCgamma2 and thrombin in arteriolar thrombus formation upon mild, laser-induced endothelial injury in vivo
-
DOI 10.1080/10739680701728822, PII 790730918
-
Kalia N, Auger JM, Atkinson B, Watson SP. Critical role of FcR gamma-chain, LAT, PLCgamma2 and thrombin in arteriolar thrombus formation upon mild, laser-induced endothelial injury in vivo. Microcirculation 2008; 15:325-335. This study provides a comparison of genetic mouse knock-out models and demonstrates the importance of GPVI, FcR gamma-chain (which complexes with GPVI), and the adapter protein LAT (linker for activation of T-cells) in laser-induced thrombus formation. (Pubitemid 351903347)
-
(2008)
Microcirculation
, vol.15
, Issue.4
, pp. 325-335
-
-
Kalia, N.1
Auger, J.2
Atkinson, B.3
Watson, S.4
-
10
-
-
34249852075
-
Acute ischemic stroke: Overview of major experimental rodent models, pathophysiology, and therapy of focal cerebral ischemia
-
DOI 10.1016/j.pbb.2007.04.015, PII S0091305707001372
-
Durukan A, Tatlisumak T. Acute ischemic stroke: overview of major experimental rodent models, pathophysiology, and therapy of focal cerebral ischemia. Pharmacol Biochem Behav 2007; 87:179-197. (Pubitemid 46860315)
-
(2007)
Pharmacology Biochemistry and Behavior
, vol.87
, Issue.1
, pp. 179-197
-
-
Durukan, A.1
Tatlisumak, T.2
-
11
-
-
58149357102
-
Extension of the thrombolytic time window with minocycline in experimental stroke
-
This study provides evidence that an MMP inhibitor, minocycline, exerts protective effects in a rat model of embolic stroke. The authors demonstrate that minocyline delivered at 4 h prior to tPA at 6 h could provide a reduced infarct volume and reduced hemorrhage compared to only the tPA at 6 h postinfarct
-
Murata Y, Rosell A, Scannevin RH, et al. Extension of the thrombolytic time window with minocycline in experimental stroke. Stroke 2008; 39:3372-3377. This study provides evidence that an MMP inhibitor, minocycline, exerts protective effects in a rat model of embolic stroke. The authors demonstrate that minocyline delivered at 4 h prior to tPA at 6 h could provide a reduced infarct volume and reduced hemorrhage compared to only the tPA at 6 h postinfarct.
-
(2008)
Stroke
, vol.39
, pp. 3372-3377
-
-
Murata, Y.1
Rosell, A.2
Scannevin, R.H.3
-
12
-
-
54049120640
-
Synergistic effect of an endothelin type a receptor antagonist, S-0139, with rtPA on the neuroprotection after embolic stroke
-
This study demonstrates that a specific endothelin type A receptor antagonist (provided at 2 h) can exert protective effects in an embolic stroke model
-
Zhang RL, Zhang C, Zhang L, et al. Synergistic effect of an endothelin type A receptor antagonist, S-0139, with rtPA on the neuroprotection after embolic stroke. Stroke 2008; 39:2830-2836. This study demonstrates that a specific endothelin type A receptor antagonist (provided at 2 h) can exert protective effects in an embolic stroke model.
-
(2008)
Stroke
, vol.39
, pp. 2830-2836
-
-
Zhang, R.L.1
Zhang, C.2
Zhang, L.3
-
13
-
-
54049147394
-
Cerebrovascular thromboprophylaxis in mice by erythrocyte-coupled tissue-type plasminogen activator
-
This study provides evidence that the coupling of tPA to erythrocytes elicits an effective strategy for the prevention of cerebrovascular thrombosis. The authors provide evidence that RBC/tPA has robust efficacy compared with vehicle and tPA alone in response to cerebral thromboemboli. This strategy appeared to have no influence on bleeding tendency but unfortunately the data presented in this study is describing delivery prior to injury rather than in response to injury, reducing the likely clinical utility of the strategy
-
Danielyan K, Ganguly K, Ding BS, et al. Cerebrovascular thromboprophylaxis in mice by erythrocyte-coupled tissue-type plasminogen activator. Circulation 2008; 118:1442-1449. This study provides evidence that the coupling of tPA to erythrocytes elicits an effective strategy for the prevention of cerebrovascular thrombosis. The authors provide evidence that RBC/tPA has robust efficacy compared with vehicle and tPA alone in response to cerebral thromboemboli. This strategy appeared to have no influence on bleeding tendency but unfortunately the data presented in this study is describing delivery prior to injury rather than in response to injury, reducing the likely clinical utility of the strategy.
-
(2008)
Circulation
, vol.118
, pp. 1442-1449
-
-
Danielyan, K.1
Ganguly, K.2
Ding, B.S.3
-
14
-
-
46749118298
-
Activation of PDGF-CC by tissue plasminogen activator impairs blood-brain barrier integrity during ischemic stroke
-
This exciting study demonstrates that PDGF-CC is activated by tPA and may lead to increased vascular permeability. In addition, an inhibitor (imatinib) to the PDGF-CC receptor, PDGFR-alpha, delivered 1 h after injury reduced cerebrovascular permeability providing evidence that inhibiting the PDGF-CC/ PDGFR-alpha pathway may attenuate stroke severity via reducing vascular permeability
-
Su EJ, Fredriksson L, Geyer M, et al. Activation of PDGF-CC by tissue plasminogen activator impairs blood-brain barrier integrity during ischemic stroke. Nat Med 2008; 14:731-737. This exciting study demonstrates that PDGF-CC is activated by tPA and may lead to increased vascular permeability. In addition, an inhibitor (imatinib) to the PDGF-CC receptor, PDGFR-alpha, delivered 1 h after injury reduced cerebrovascular permeability providing evidence that inhibiting the PDGF-CC/ PDGFR-alpha pathway may attenuate stroke severity via reducing vascular permeability.
-
(2008)
Nat Med
, vol.14
, pp. 731-737
-
-
Su, E.J.1
Fredriksson, L.2
Geyer, M.3
-
15
-
-
39049145302
-
Real-time measurement of non-lethal platelet thromboembolic responses in the anaesthetized mouse
-
Tymvios C, Jones S, Moore C, et al. Real-time measurement of nonlethal platelet thromboembolic responses in the anaesthetized mouse. Thromb Haemost 2008; 99:435-440. This study outlines an interesting and novel method for examining platelet activation in vivo without invasive procedures. The authors confirm a loss of agonistinduced platelet activation following aspirin treatment. (Pubitemid 351244039)
-
(2008)
Thrombosis and Haemostasis
, vol.99
, Issue.2
, pp. 435-440
-
-
Tymvios, C.1
Jones, S.2
Moore, C.3
Pitchford, S.C.4
Page, C.P.5
Emerson, M.6
-
16
-
-
40549083384
-
Development of an experimental hemolytic uremic syndrome in rats
-
Berlin, Germany This study provided evidence that the injection of rats with shiga toxin (Stx2) elicits features similar to hemolytic uremic syndrome. Features of treated rats included thrombocytopenia (60% lower than controls), anemia (32% lower hemoglobin), leukocytosis (53% higher), and microangiopathic thrombosis
-
Zotta E, Lago N, Ochoa F, et al. Development of an experimental hemolytic uremic syndrome in rats. Pediatr Nephrol (Berlin, Germany) 2008; 23:559-567. This study provided evidence that the injection of rats with shiga toxin (Stx2) elicits features similar to hemolytic uremic syndrome. Features of treated rats included thrombocytopenia (60% lower than controls), anemia (32% lower hemoglobin), leukocytosis (53% higher), and microangiopathic thrombosis.
-
(2008)
Pediatr Nephrol
, vol.23
, pp. 559-567
-
-
Zotta, E.1
Lago, N.2
Ochoa, F.3
-
17
-
-
0032985071
-
Protein disulphide isomerase mediates platelet aggregation and secretion
-
Essex DW, Li M. Protein disulphide isomerase mediates platelet aggregation and secretion. Br J Haematol 1999; 104:448-454. (Pubitemid 29119264)
-
(1999)
British Journal of Haematology
, vol.104
, Issue.3
, pp. 448-454
-
-
Essex, D.W.1
Li, M.2
-
18
-
-
0034737776
-
Physical proximity and functional association of glycoprotein 1balpha and protein-disulfide isomerase on the platelet plasma membrane
-
DOI 10.1074/jbc.275.13.9758
-
Burgess JK, Hotchkiss KA, Suter C, et al. Physical proximity and functional association of glycoprotein 1balpha and protein-disulfide isomerase on the platelet plasma membrane. J Biol Chem 2000; 275:9758-9766. (Pubitemid 30185210)
-
(2000)
Journal of Biological Chemistry
, vol.275
, Issue.13
, pp. 9758-9766
-
-
Burgess, J.K.1
Hotchkiss, K.A.2
Suter, C.3
Dudman, N.P.B.4
Szollosi, J.5
Chesterman, C.N.6
Chong, B.H.7
Hogg, P.J.8
-
19
-
-
40549084318
-
A critical role for extracellular protein disulfide isomerase during thrombus formation in mice
-
This study provided in-vivo evidence that laser-induced injury to arterioles results in a rapid activation of extracellular PDI and demonstrated that antibodies to PDI or a PDI inhibitor both effectively block fibrin generation and platelet deposition. A dose-dependent effect was evident for the PDI inhibitor; however, the highest dose also caused a significant increase in bleeding tendency
-
Cho J, Furie BC, Coughlin SR, Furie B. A critical role for extracellular protein disulfide isomerase during thrombus formation in mice. J Clin Invest 2008; 118:1123-1131. This study provided in-vivo evidence that laser-induced injury to arterioles results in a rapid activation of extracellular PDI and demonstrated that antibodies to PDI or a PDI inhibitor both effectively block fibrin generation and platelet deposition. A dose-dependent effect was evident for the PDI inhibitor; however, the highest dose also caused a significant increase in bleeding tendency.
-
(2008)
J Clin Invest
, vol.118
, pp. 1123-1131
-
-
Cho, J.1
Furie, B.C.2
Coughlin, S.R.3
Furie, B.4
-
20
-
-
40549121595
-
Protein disulfide isomerase acts as an injury response signal that enhances fibrin generation via tissue factor activation
-
This study demonstrated an important role of PDI in thrombus formation following vascular injury and demonstrated an important role for PDI in activation of TF via disulfide bond formation. The authors suggest that PDI inhibition will benefit several prothrombotic conditions but that additional studies are needed to further characterize the thrombotic and hemostatic effects of PDI inhibition
-
Reinhardt C, von Bruhl ML, Manukyan D, et al. Protein disulfide isomerase acts as an injury response signal that enhances fibrin generation via tissue factor activation. J Clin Invest 2008; 118:1110-1122. This study demonstrated an important role of PDI in thrombus formation following vascular injury and demonstrated an important role for PDI in activation of TF via disulfide bond formation. The authors suggest that PDI inhibition will benefit several prothrombotic conditions but that additional studies are needed to further characterize the thrombotic and hemostatic effects of PDI inhibition.
-
(2008)
J Clin Invest
, vol.118
, pp. 1110-1122
-
-
Reinhardt, C.1
Von Bruhl, M.L.2
Manukyan, D.3
-
21
-
-
47249124947
-
Identification of a fibrin-independent platelet contractile mechanism regulating primary hemostasis and thrombus growth
-
This studydemonstratedtheimportanceof plateletcontraction for themaintenanceof a stable platelet thrombus. The authors provide in-vivo evidence using intravital microscopythat thrombus surface area normally contractsbut is inhibited by amyosin IIa inhibitor and a rho kinase inhibitor. They demonstrate that this effect on thrombus contractionis evidentevenintheabsenceofthrombinactivationofplateletsvia studies of PAR4-deficient mice and using thrombin inhibition with lepirudin
-
Ono A, Westein E, Hsiao S, et al. Identification of a fibrin-independent platelet contractile mechanism regulating primary hemostasis and thrombus growth. Blood 2008; 112:90-99. This studydemonstratedtheimportanceof plateletcontraction for themaintenanceof a stable platelet thrombus. The authors provide in-vivo evidence using intravital microscopythat thrombus surface area normally contractsbut is inhibited by amyosin IIa inhibitor and a rho kinase inhibitor. They demonstrate that this effect on thrombus contractionis evidentevenintheabsenceofthrombinactivationofplateletsvia studies of PAR4-deficient mice and using thrombin inhibition with lepirudin.
-
(2008)
Blood
, vol.112
, pp. 90-99
-
-
Ono, A.1
Westein, E.2
Hsiao, S.3
-
22
-
-
36148955807
-
Megakaryocyte-restricted MYH9 inactivation dramatically affects hemostasis while preserving platelet aggregation and secretion
-
DOI 10.1182/blood-2007-03-080184
-
Leon C, Eckly A, Hechler B, et al. Megakaryocyte-restricted MYH9 inactivation dramatically affects hemostasis while preserving platelet aggregation and secretion. Blood 2007; 110:3183-3191. (Pubitemid 350106310)
-
(2007)
Blood
, vol.110
, Issue.9
, pp. 3183-3191
-
-
Leon, C.1
Eckly, A.2
Hechler, B.3
Aleil, B.4
Freund, M.5
Ravanat, C.6
Jourdain, M.7
Nonne, C.8
Weber, J.9
Tiedt, R.10
Gratacap, M.-P.11
Severin, S.12
Cazenave, J.-P.13
Lanza, F.14
Skoda, R.15
Gachet, C.16
-
23
-
-
43549100273
-
GSK3beta is a negative regulator of platelet function and thrombosis
-
The authors provide evidence that GSK-3beta suppression (via pharmacologic inhibitors or haploinsufficiency) causes an increase in platelet activation. The authors speculate that pharmacologic blockade of GSK-3beta (as suggested for several disease states) may have prothrombotic effects
-
Li D, August S, Woulfe DS. GSK3beta is a negative regulator of platelet function and thrombosis. Blood 2008; 111:3522-3530. The authors provide evidence that GSK-3beta suppression (via pharmacologic inhibitors or haploinsufficiency) causes an increase in platelet activation. The authors speculate that pharmacologic blockade of GSK-3beta (as suggested for several disease states) may have prothrombotic effects.
-
(2008)
Blood
, vol.111
, pp. 3522-3530
-
-
Li, D.1
August, S.2
Woulfe, D.S.3
-
24
-
-
36348974550
-
Inhibition of glycogen synthase kinase 3beta during heart failure is protective
-
DOI 10.1161/CIRCRESAHA.107.160614
-
Hirotani S, Zhai P, Tomita H, et al. Inhibition of glycogen synthase kinase 3beta during heart failure is protective. Circ Res 2007; 101:1164-1174. (Pubitemid 350146443)
-
(2007)
Circulation Research
, vol.101
, Issue.11
, pp. 1164-1174
-
-
Hirotani, S.1
Zhai, P.2
Tomita, H.3
Galeotti, J.4
Marquez, J.P.5
Gao, S.6
Hong, C.7
Yatani, A.8
Avila, J.9
Sadoshima, J.10
-
25
-
-
37349109154
-
Amyloid-beta-induced neurotoxicity is reduced by inhibition of glycogen synthase kinase-3
-
Koh SH, Noh MY, Kim SH. Amyloid-beta-induced neurotoxicity is reduced by inhibition of glycogen synthase kinase-3. Brain Res 2008; 1188:254-262.
-
(2008)
Brain Res
, vol.1188
, pp. 254-262
-
-
Koh, S.H.1
Noh, M.Y.2
Kim, S.H.3
-
26
-
-
38949147126
-
Prophylactic P-selectin inhibition with PSI-421 promotes resolution of venous thrombosis without anticoagulation
-
The study provides evidence that an orally available p-selectin inhibitor, PSI-421, attenuates venous thrombosis and microparticle tissue factor activity in a nonhuman primate. The study demonstrates similar to better efficacy of PSI-421 compared with low-molecular-weight heparin
-
Meier TR, Myers DD Jr, Wrobleski SK, et al. Prophylactic P-selectin inhibition with PSI-421 promotes resolution of venous thrombosis without anticoagulation. Thromb Haemost 2008; 99:343-351. The study provides evidence that an orally available p-selectin inhibitor, PSI-421, attenuates venous thrombosis and microparticle tissue factor activity in a nonhuman primate. The study demonstrates similar to better efficacy of PSI-421 compared with low-molecular-weight heparin.
-
(2008)
Thromb Haemost
, vol.99
, pp. 343-351
-
-
Meier, T.R.1
Myers Jr., D.D.2
Wrobleski, S.K.3
-
27
-
-
54949095069
-
The humanized antiglycoprotein Ib monoclonal antibody h6B4-Fab is a potent and safe antithrombotic in a high shear arterial thrombosis model in baboons
-
This study demonstrated that an antibody to GP-1b-alpha which blocks binding to von Willebrand factor provides a significant reduction in cyclic flow reductions using a baboon model of injury and stenosis. The authors provide evidence that antithrombotic levels can be achieved without a significant induction of bleeding risk
-
Fontayne A, Meiring M, Lamprecht S, et al. The humanized antiglycoprotein Ib monoclonal antibody h6B4-Fab is a potent and safe antithrombotic in a high shear arterial thrombosis model in baboons. Thromb Haemost 2008; 100:670-677. This study demonstrated that an antibody to GP-1b-alpha which blocks binding to von Willebrand factor provides a significant reduction in cyclic flow reductions using a baboon model of injury and stenosis. The authors provide evidence that antithrombotic levels can be achieved without a significant induction of bleeding risk.
-
(2008)
Thromb Haemost
, vol.100
, pp. 670-677
-
-
Fontayne, A.1
Meiring, M.2
Lamprecht, S.3
-
28
-
-
37349040378
-
First-in-human evaluation of anti-von Willebrand factor therapeutic aptamer ARC1779 in healthy volunteers
-
DOI 10.1161/CIRCULATIONAHA.107.724864
-
Gilbert JC, DeFeo-Fraulini T, Hutabarat RM, et al. First-in-human evaluation of anti von Willebrand factor therapeutic aptamer ARC1779 in healthy volunteers. Circulation 2007; 116:2678-2686. (Pubitemid 350291240)
-
(2007)
Circulation
, vol.116
, Issue.23
, pp. 2678-2686
-
-
Gilbert, J.C.1
Defeo-Fraulini, T.2
Hutabarat, R.M.3
Horvath, C.J.4
Merlino, P.G.5
Marsh, H.N.6
Healy, J.M.7
Boufakhreddine, S.8
Holohan, T.V.9
Schaub, R.G.10
|