Thrombin–antithrombin III complex in acute retinal vein occlusion

Iijima, Hiroyuki; Gohdo, Takashi; Imai, Masahito; Tsukahara, Shigeo

doi:10.1016/s0002-9394(98)00226-8

Cited by 16 publications

(5 citation statements)

References 23 publications

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“…Some studies found an increased activation of clotting system and a decreased fibrinolytic potential in most patients with RVO. Moreover, increased levels of thrombin-antithrombin complexes (TAT) [ 31 , 32 ], fibrinopeptide A (FpA) [ 33 ], and plasminogen activator inhibitor-1 (PAI-1) [ 34 ] were also found in acute retinal vein occlusion, supporting our findings. Collectively, the results obtained from our study confirmed that important venous endothelial changes and fibrin production suggest that endothelial-mediated PS exposure and MP release may be linked to the pathogenesis of RVO.…”

Section: Discussionsupporting

confidence: 85%

The Exposure of Phosphatidylserine Influences Procoagulant Activity in Retinal Vein Occlusion by Microparticles, Blood Cells, and Endothelium

Deng

et al. 2018

Oxidative Medicine and Cellular Longevity

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The pathogenesis of hypercoagulability in retinal vein occlusion (RVO) is largely unknown. Whether the exposure of phosphatidylserine (PS) and microparticle (MPs) release will affect procoagulant activity (PCA) in RVO needs to be investigated. Objectives. To evaluate PS expression, circulating MPs, and the corresponding PCA in RVO patients. Twenty-five RVO patients were compared with 25 controls. PS-positive cells were detected by flow cytometry. Cell-specific MPs were measured by lactadherin for PS and relevant CD antibody. We explored PCA with coagulation time, purified coagulation complex assays, and fibrin production assays. In RVO, MPs from platelets, erythrocytes, leukocyte, and endothelial cells were increased and the exposure of PS was elevated significantly when compared with controls. In addition, we showed that circulating MPs in RVO patients were mostly derived from platelets, representing about 60–70% of all MPs, followed by erythrocytes and leukocytes. Moreover, PS exposure, ECs, and MPs in RVO lead to shortened clotting time with upregulation of FXa and thrombin formation obviously. Importantly, ECs treated with RVO serum which bounded FVa and FXa explicitly suggested the damage of retinal vein endothelial cells. Furthermore, lactadherin can inhibit the combination between PS and coagulation factors by approximately 70% and then exert an anticoagulant effect. In summary, circulating MPs and exposed PS from different cells may contribute to the increased PCA in patients with RVO. Lactadherin can be used for PS detection and an anticoagulant agent.

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Section: Discussionsupporting

confidence: 85%

The Exposure of Phosphatidylserine Influences Procoagulant Activity in Retinal Vein Occlusion by Microparticles, Blood Cells, and Endothelium

Deng

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…They concluded that these were not risk factors in 188 with the controls. Iijima et al [38], on evaluation of ten CRVO, six HCRVO, 33 major BRVO and eight macular BRVO cases, found levels of thrombin-antithrombin III complex significantly higher in CRVO and HCRVO than in BRVO and controls (P=0.02), with no difference between the BRVO and the controls. Tekeli et al [59] found decreased levels of protein C in six of 14 (42.9%) CRVO and three of 31 (9.7%) BRVO patients, and decreased protein S in one of 14 (7.1%) CRVO and one of 31 (3.2%) BRVO, and of antithrombin III in one of 31 (3.2%) BRVO, but in none of the 20 healthy controls; they concluded that there was a statistically significant difference in protein C deficiency between the CRVO and BRVO cases (P<0.05).…”

Section: Anticoagulant Proteinsmentioning

confidence: 96%

Hematologic abnormalities associated with various types of retinal vein occlusion

Hayreh

Zimmerman

Podhajsky

2002

Graefe's Arch Clin Exp Ophthalmol

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Our study showed that a variety of hematologic abnormalities may be seen in association with different types of RVO, and any generalization about these disorders applied to all RVO patients may be misleading. The evidence of our study and in the literature indicates that there is no good reason why all patients with RVO should be subjected to extensive, expensive, special hematologic and hypercoagulability investigations, unless, of course, there is some clear indication; the routine, inexpensive hematologic evaluation is usually sufficient for RVO patients. Treatment with anticoagulants or platelet anti-aggregating agents may adversely influence the visual outcome, without any evidence of protective or beneficial effect.

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“…Thrombin, one of the most potent thrombogenic factors, is formed at the site of intraocular hemorrhage and has previously been proposed to be important in the development of progressive retinal damage [16,17,18]. HCMV infection has been shown to initiate the generation of thrombin by having essential procoagulant phospholipid and tissue factor activity on the virus surface [19,20].…”

Section: Introductionmentioning

confidence: 99%

Thrombin induces Sp1-mediated antiviral effects in cytomegalovirus-infected human retinal pigment epithelial cells

Scholz

Vogel

Höver

et al. 2003

Med Microbiol Immunol

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Human cytomegalovirus (HCMV) retinitis causing retinal detachment and destruction of the blood-retina barrier is closely related to retinal hemorrhage/coagulation. However, the effects of procoagulants on HCMV (re)activation in retinal cells have not been investigated yet. Therefore, we studied whether thrombin modulates the expression of HCMV immediate early (IE) and late (L) genes in cultured human retinal pigment epithelial cells (RPE). Thrombin specifically stimulated the protease-activated receptor-1 (PAR-1) on RPE and, surprisingly, inhibited basal and 12,0-tetradecanoylphorbol 13-acetate-stimulated HCMV IE gene expression in infected RPE. On the other hand, HCMV strongly induced Sp1 DNA binding activity, which was prevented by thrombin/PAR1-mediated Sp1 hyperphosphorylation. Our data suggest that thrombin/PAR-1 may inhibit Sp1-dependent HCMV replication, which might be an important regulatory mechanism for HCMV persistence and replication in RPE.

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Thrombin–antithrombin III complex in acute retinal vein occlusion

Cited by 16 publications

References 23 publications

The Exposure of Phosphatidylserine Influences Procoagulant Activity in Retinal Vein Occlusion by Microparticles, Blood Cells, and Endothelium

The Exposure of Phosphatidylserine Influences Procoagulant Activity in Retinal Vein Occlusion by Microparticles, Blood Cells, and Endothelium

Hematologic abnormalities associated with various types of retinal vein occlusion

Thrombin induces Sp1-mediated antiviral effects in cytomegalovirus-infected human retinal pigment epithelial cells

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