AM plays a role in the maintenance of blood circulation and has antithrombotic effects. There are two important factors that regulate blood coagulation which are plasma protease factor VII/VIIa (FVIIa) and tissue factor (TF). Their binding initiates the blood coagulation cascade (). The Tissue Factor Pathway Inhibitor (TFPI) is an inhibitor for TF-FVIIa complex which is secreted and synthesized by endothelial cells where the Heparan Sulfate Proteo Glycan (HSPG) helps TFPI to express at the cell surface. In thrombotic diseases the levels of AM and TFPI are increased, illustrating the possibility of existing correlations between them (). The cationic charge provided by the amino acid of AM is responsible for inducing the release of TFPI from the surface of ES, where TFPI binds to cell surface HSPG the via positively charged C-terminal region of the TFPI sequence. Additionally, in the ECs AM has the ability to induce antithrombin (AT) and urokinase type plasminogen activator (uPA) release (). AM has been shown to be a protection factor for organs in hypertension, oxidative stress, atherosclerosis, ischemia, and sepsis which results in multi organ failure. In rodent models, prolonged infusion or the overexpression of AM prevented thickness of the internal part of the capillary which is called intima by preventing the formation of fatty streaks and perivascular hyperplasia in order to protect the blood vessels. This shows AM is an important regulator for maintaining the circulatory system function (). The administration of AM systemically into the model of tail lymphoedema resulted in an improvement of lymphoedema compared to controls. The blood and lymphatic vessels number were shown to be increased at the site of injury. This finding emphasises the role of AM in angiogenic and lymphogenic processes (). AM has many other biological actions such as increasing cAMP in the cell, the
AM plays a role in the maintenance of blood circulation and has antithrombotic effects. There are two important factors that regulate blood coagulation which are plasma protease factor VII/VIIa (FVIIa) and tissue factor (TF). Their binding initiates the blood coagulation cascade (). The Tissue Factor Pathway Inhibitor (TFPI) is an inhibitor for TF-FVIIa complex which is secreted and synthesized by endothelial cells where the Heparan Sulfate Proteo Glycan (HSPG) helps TFPI to express at the cell surface. In thrombotic diseases the levels of AM and TFPI are increased, illustrating the possibility of existing correlations between them (). The cationic charge provided by the amino acid of AM is responsible for inducing the release of TFPI from the surface of ES, where TFPI binds to cell surface HSPG via the positively charged C-terminal region of the TFPI sequence. Additionally, in the ECs AM has the ability to induce antithrombin (AT) and urokinase type plasminogen activator (uPA) release (). AM has been shown to be a protection factor for organs in hypertension, oxidative stress, atherosclerosis, ischemia, and sepsis which results in multi organ failure. In rodent models, prolonged infusion or the overexpression of AM prevented thickness of the internal part of the capillary which is called intima by preventing the formation of fatty streaks and perivascular hyperplasia in order to protect the blood vessels. This shows AM is an important regulator for maintaining the circulatory system function (). The administration of AM systemically into the model of tail lymphoedema resulted in an improvement of lymphoedema compared to controls. The blood and lymphatic vessels number were shown to be increased at the site of injury. This finding emphasises the role of AM in angiogenic and lymphogenic processes (). AM has many other biological actions such as increasing cAMP in the cell, the
Emad%27s%20Thesis%20final%20after%20correction%201-12-2015%20last.docx