Theories of Blood Coagulation

Howell, W. H.

doi:10.1152/physrev.1935.15.3.435

Cited by 80 publications

(30 citation statements)

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“…Key Words: coagulation Ⅲ cytosolic calcium Ⅲ factor VII Ⅲ phosphatidylserine Ⅲ tissue factor T he discovery of a thromboplastic activity in tissues inspired the hypothesis that blood coagulation is triggered by contact between intravascular and extravascular factors. [1][2][3][4] This 19 th century model of coagulation is supported by immunohistochemical studies of tissue factor (TF), the protein component of tissue thromboplastin. TF antigen was detected on cells surrounding blood vessels, but it was not visible on either endothelial cells or cells in the bloodstream.…”

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confidence: 99%

Tissue Factor Encryption

Bach

2006

ATVB

239

224

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Abstract-Tissue factor (TF) encryption is the post-translational suppression of TF procoagulant activity (PCA) on the cell surface. There is emerging evidence of encrypted TF in normal blood associated with monocytes and platelets. Expression of this latent TF PCA during the propagation phase of blood coagulation may contribute to hemostasis. One pathway leading to the decryption of TF PCA begins with an increase in cytosolic calcium. A large calcium influx triggers both the exposure of phosphatidylserine and the expression of TF PCA on cell surfaces. The connections between these events are reviewed along with evidence that lipid raft association may also contribute to TF encryption. The last step in the decryption of TF PCA is the proteolytic activation of zymogen factor VII. This event may be a key to understanding the different roles of intravascular and extravascular TF in the process of blood coagulation. Key Words: coagulation Ⅲ cytosolic calcium Ⅲ factor VII Ⅲ phosphatidylserine Ⅲ tissue factor T he discovery of a thromboplastic activity in tissues inspired the hypothesis that blood coagulation is triggered by contact between intravascular and extravascular factors. [1][2][3][4] This 19 th century model of coagulation is supported by immunohistochemical studies of tissue factor (TF), the protein component of tissue thromboplastin. TF antigen was detected on cells surrounding blood vessels, but it was not visible on either endothelial cells or cells in the bloodstream. 5 As important as the intact endothelium is to preventing TF-initiated coagulation, there are compelling reasons to believe this is not the entire story. Foremost is the emerging evidence of TF in normal blood. 6 -13 Because the levels are generally very low, it is difficult to detect TF antigen on the surface of blood cells. 5 However, the membrane-associated TF procoagulant activity (PCA) in blood is easily measured by more sensitive functional assays. 6,9 The quantity of TF on blood cells is small relative to that which is present on extravascular cells. This raises an obvious question. Is the level of intravascular TF too low to be of any significance? One study measured an average of Ϸ30 pg/mL for membrane-associated TF in the blood of normal subjects. 13 The estimate is based on functional assays of isolated mononuclear cells, platelets, and microparticles. The respective blood levels of the three TF pools were 15.9Ϯ14.7 pg/mL, 10.6Ϯ5.3 pg/mL, and 1.0Ϯ0.3 pg/mL. In a prothrombin time assay, this concentration of pure TF, optimally reconstituted into phospholipids vesicles, clots plasma in Ϸ60 seconds (R. Bach, unpublished, 2005). Thus, it is likely that more than an intact endothelium is required for blood to remain fluid.TF encryption is the post-translational suppression of TF PCA on the cell surface. It may be the primary mechanism controlling the expression of TF PCA by cells in blood. TF encryption was first observed in cell culture studies. Unperturbed cells express very little TF PCA despite the fact that TF, an integral membr...

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confidence: 99%

Tissue Factor Encryption

Bach

2006

ATVB

239

224

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“…It is well established that the platelets play an important role in blood coagulation (1). When exposed by bleeding, they exhibit a characteristic physicochemical behavior (swelling, agglutination, excresence formation, and partial disruption (2)) resembling osmotic phenomena of phospholipids, e.g., myelin figure formation (3).…”

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confidence: 99%

“…There is some debate as to the exact nature of the factors liberated by platelet disintegration. There can be no doubt as to a thermostable thromboplastic agent which has been identified with cephalin (5,6,7,8); it is questionable whether there is, in addition, a coagulant factor, either of prothrombin-like (1,8) or different (5,9) nature.…”

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The Lipid Distribution of Human Platelets in Health and Disease 1

Erickson¹,

Williams²,

Avrin³

et al. 1939

J. Clin. Invest.

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“…48,49 Building on studies of Doyon in France on the anticoagulant released from the liver after treating dogs with "peptone," in 1916 Jay McLean, a medical student working in Howell's laboratory at Johns Hopkins, isolated a fraction from hepatic tissue that "showed a marked power to inhibit coagulation," to which Howell gave the name heparin in 1918. 50,51 The carbohydrate chemistry was complex and so the clinical use of heparin was delayed until the studies of Murray and Best in Canada and Crafoord and Jorpes in Sweden between 1936 and 1937. [52][53][54] The recognition that heparin required a plasma cofactor for its full anticoagulant effect led to the identification of what was later called antithrombin III, and now just antithrombin.…”

Section: Brief Histories Of Select Topics In Hematologymentioning

confidence: 99%

“…[52][53][54] The recognition that heparin required a plasma cofactor for its full anticoagulant effect led to the identification of what was later called antithrombin III, and now just antithrombin. 50,55 The lysis of blood clots was recognized in antiquity, and in 1893 Dastre in France gave the term "fibrinolysis" to the effect of serum in lysing fibrin. 56 In 1933, Tillett and Garner in Baltimore identified a fibrinolysin in streptococcal lysates, and studies of the plasma cofactor required for this "streptokinase" activity led to its identification by Kaplan in North Carolina as plasminogen in 1944.…”

Section: Brief Histories Of Select Topics In Hematologymentioning

confidence: 99%

Blood at 70: its roots in the history of hematology and its birth

Coller

2015

Blood

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This year we celebrate Blood's 70th year of publication. Created from the partnership of the book publisher Henry M. Stratton and the prominent hematologist Dr William Dameshek of Tufts School of Medicine, Blood has published many papers describing major advances in the science and clinical practice of hematology. Blood's founding antedated that of the American Society of Hematology (ASH) by more than 11 years and Stratton and Dameshek helped galvanize support for the creation of ASH. In this review, I place the birth of Blood in the context of the history of hematology before 1946, emphasizing the American experience from which it emerged, and focusing on research conducted during World War II. I also provide a few milestones along Blood's 70 years of publication, including: the growth in Blood's publications, the evolution of its appearance, the countries of submission of Blood papers, current subscriptions to Blood, and the evolution of topics reported in Blood's papers. The latter provides a snapshot of the evolution of hematology as a scientific and clinical discipline and the introduction of new technology to study blood and bone marrow. Detailed descriptions of the landmark discoveries reported in Blood will appear in later papers celebrating Blood's birthday authored by past Editors-in-Chief.

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Theories of Blood Coagulation

Cited by 80 publications

References 0 publications

Tissue Factor Encryption

Tissue Factor Encryption

The Lipid Distribution of Human Platelets in Health and Disease 1

Blood at 70: its roots in the history of hematology and its birth

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