Mechanisms of Hemostasis: Contributions of Platelets, Coagulation Factors, and the Vessel Wall

Mußbacher, Marion; Kral-Pointner, Julia B.; Salzmann, Manuel; Schrottmaier, Waltraud C.

doi:10.1007/978-3-030-12270-6_8

Cited by 6 publications

(7 citation statements)

References 115 publications

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“…Although mainly active during embryonic development, vasculogenesis is a process also active during adult life, albeit rarely. Notch and ephrin proteins control differentiation pathways into vein and artery specific endothelial cells [ 111 ].…”

Section: Tissue Regeneration and Repair By Neovascularizationmentioning

confidence: 99%

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Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease

et al. 2021

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Currently, atherosclerosis, which affects the vascular bed of all vital organs and tissues, is considered as a leading cause of death. Most commonly, atherosclerosis involves coronary and peripheral arteries, which results in acute (e.g., myocardial infarction, lower extremities ischemia) or chronic (persistent ischemia leading to severe heart failure) consequences. All of them have a marked unfavorable impact on the quality of life and are associated with increased mortality and morbidity in human populations. Lower extremity artery disease (LEAD, also defined as peripheral artery disease, PAD) refers to atherosclerotic occlusive disease of the lower extremities, where partial or complete obstruction of peripheral arteries is observed. Decreased perfusion can result in ischemic pain, non-healing wounds, and ischemic ulcers, and significantly reduce the quality of life. However, the progressive atherosclerotic changes cause stimulation of tissue response processes, like vessel wall remodeling and neovascularization. These mechanisms of adapting the vascular network to pathological conditions seem to play a key role in reducing the impact of the changes limiting the flow of blood. Neovascularization as a response to ischemia induces sprouting and expansion of the endothelium to repair and grow the vessels of the circulatory system. Neovascularization consists of three different biological processes: vasculogenesis, angiogenesis, and arteriogenesis. Both molecular and environmental factors that may affect the process of development and growth of blood vessels were analyzed. Particular attention was paid to the changes taking place during LEAD. It is important to consider the molecular mechanisms underpinning vessel growth. These mechanisms will also be examined in the context of diseases commonly affecting blood vessel function, or those treatable in part by manipulation of angiogenesis. Furthermore, it may be possible to induce the process of blood vessel development and growth to treat peripheral vascular disease and wound healing. Reactive oxygen species (ROS) play an important role in regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. With regard to the repair processes taking place during diseases such as LEAD, prospective therapeutic methods have been described that could significantly improve the treatment of vessel diseases in the future. Summarizing, regenerative medicine holds the potential to transform the therapeutic methods in heart and vessel diseases treatment.

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Section: Tissue Regeneration and Repair By Neovascularizationmentioning

confidence: 99%

“…Moreover, knockdown of FGFR-3 mRNA inhibited proliferation of lymphatic endothelial cells, supporting this hypothesis. Lyve-1 and podoplanin are two other examples of lymphatic endothelium-specific markers [ 111 ].…”

Section: Tissue Regeneration and Repair By Neovascularizationmentioning

confidence: 99%

Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease

et al. 2021

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“…Interestingly, in vitro profiling of rDromaserpin's proteolytic activity shows its capacity to inhibit thrombin and Kallikrein, to slightly affect FXIa and FXIIa activity without any relevant effect on FIXa or FXa. The intrinsic pathway is triggered by the activation of FXII when blood comes in contact with a negatively charged surface [6]. FXIIa (activated FXII) promotes its own activation in turn by stimulating Kallikrein formation and activating the upstream factor, FXIa [6].…”

Section: Discussionmentioning

confidence: 99%

“…This system involves a set of well-regulated processes, including blood coagulation, platelet aggregation, and vasoconstriction, led by a complex series of cascade enzymatic reactions [5]. These reactions involve several serine proteases controlled by endogenous molecules including serine protease inhibitors (serpins) [6,7]. Several pathogeneses can ensue when serine protease activity or serpin-mediated regulation becomes unbalanced or dysfunctional [8].…”

Section: Introductionmentioning

confidence: 99%

rDromaserpin: A Novel Anti-Hemostatic Serpin, from the Salivary Glands of the Hard Tick Hyalomma dromedarii

Aounallah

Fessel

Goldfeder

et al. 2021

Toxins

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Hemostatic disorders are caused either by platelet-related dysfunctions, defective blood coagulation, or by a combination of both, leading to an increased susceptibility to cardiovascular diseases (CVD) and other related illnesses. The unique specificity of anticoagulants from hematophagous arthropods, such as ticks, suggests that tick saliva holds great promise for discovering new treatments for these life-threatening diseases. In this study, we combined in silico and in vitro analyses to characterize the first recombinant serpin, herein called Dromaserpin, from the sialotranscriptome of the Hyalomma dromedarii tick. Our in silico data described Dromaserpin as a secreted protein of ~43 kDa with high similarities to previously characterized inhibitory serpins. The recombinant protein (rDromaserpin) was obtained as a well-structured monomer, which was tested using global blood coagulation and platelet aggregation assays. With this approach, we confirmed rDromaserpin anticoagulant activity as it significantly delayed plasma clotting in activated partial thromboplastin time and thrombin time assays. The profiling of proteolytic activity shows its capacity to inhibit thrombin in the micromolar range (0.2 to 1 μM) and in the presence of heparin this inhibition was clearly increased. It was also able to inhibit Kallikrein, FXIa and slightly FXIIa, with no significant effect on other factors. In addition, the rDromaserpin inhibited thrombin-induced platelet aggregation. Taken together, our data suggest that rDromaserpin deserves to be further investigated as a potential candidate for developing therapeutic compounds targeting disorders related to blood clotting and/or platelet aggregation.

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“…The haemostatic work starts when the platelets come into contact with damaged endothelial wall or with circulatory coagulation factors, particularly thrombin, bringing about platelet activation, aggregation and clot formation. Thus, the endothelial dysfunction and the increase in vascular reactivity are proven to be involved in preeclampsia pathogenesis: the generalized endothelial alteration from preeclampsia causes vasoconstriction and promotes the adhesion and aggregation of the platelets, as well as the activation of the coagulation factors, inducing supplementary hypoxic injury of the endothelium [27].…”

Section: Discussionmentioning

confidence: 99%

To Determine the Frequency of Thrombocytopenia in Pre Eclamptic Presented at Isra University Hospital

Khatoon¹,

Ahmed²,

Naz³

et al. 2021

JPRI

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Objective: To determine the frequency of thrombocytopenia in pre-eclamptic women presented at Isra University Hospital Hyderabad. Patients and Methods: This cross sectional descriptive study of six months study was conducted at Isra university hospital from April 2019 to September 2019. All the patients between ≥18 - 45 years of age diagnosed preeclampsia were admitted and evaluated for thrombocytopenia. Results: During six month study period, total of 177 patients with preeclampsia were evaluated for thrombocytopenia. The majority of patients were from urban areas 125/177 (70.6%). The mean ±SD for maternal and gestational age of the preeclamptic patient was 32.75±8.85 and 28.75±7.63 whereas the mean platelet count was 93200±10.74 respectively. The majority of the patients were 21-30 years of age (54.8%) and the finding was statistically significant with gestational age [p=0.002]. The thrombocytopenia was observed in 99/177 (55.9%) and is statistically with relation to maternal age, gestational age and parity while in context to gravida and duration of disease it is non significant. Conclusion: A significantly high frequency of thrombocytopenia (55.9%) was recorded in the patients with preeclampsia and is statistically with relation to maternal and gestational age and parity.

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Mechanisms of Hemostasis: Contributions of Platelets, Coagulation Factors, and the Vessel Wall

Cited by 6 publications

References 115 publications

Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease

Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease

rDromaserpin: A Novel Anti-Hemostatic Serpin, from the Salivary Glands of the Hard Tick Hyalomma dromedarii

To Determine the Frequency of Thrombocytopenia in Pre Eclamptic Presented at Isra University Hospital

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