{"title":"Pulmonary Vascular Endothelial Cells","authors":"J. Gonzales, A. Verin","doi":"10.5772/INTECHOPEN.76995","DOIUrl":null,"url":null,"abstract":"Pulmonary vascular endothelial cells (ECs) line the surface of the lung vasculature and accommodate the various levels of blood flow. Pulmonary endothelium is a critical regu lator of vascular homeostasis by inhibiting coagulation of the blood. The ECs bind tis - sue factor pathway inhibitors (TFPI), modulate hemostasis with opposing effects such as antiplatelet, anticoagulant and fibrinolytic properties. Lung endothelium regulates synthesis and metabolism of vasoactive compounds such as nitric oxide and endothe-lin-1, both potent regulators of vascular tone. Cytokines, chemokines, interleukins, adhe - sion molecules, and growth factors can be secreted by pulmonary ECs with positive and adverse effects. Pulmonary endothelium exhibits heterogeneity with diverse expression of molecules and specific differences in signaling induced by various infections such as Gram-positive bacteria. The distinction of macro or microvascular endothelium occurs from the larger vessels to small capillaries in the lung alveoli system. Lectin-binding pat terns discriminate between pulmonary artery and pulmonary microvascular capillary endothelium. The lung is one of the body’s organs with the highest expression of vascu lar endothelial growth factor that stimulates small vessel formation of the microvascular endothelium. Acute respiratory distress syndrome and acute chest syndrome in sickle cell disease are two prototypes of devastating diseases caused by pulmonary EC dysfunction.","PeriodicalId":254860,"journal":{"name":"Endothelial Dysfunction - Old Concepts and New Challenges","volume":"51 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endothelial Dysfunction - Old Concepts and New Challenges","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5772/INTECHOPEN.76995","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
Pulmonary vascular endothelial cells (ECs) line the surface of the lung vasculature and accommodate the various levels of blood flow. Pulmonary endothelium is a critical regu lator of vascular homeostasis by inhibiting coagulation of the blood. The ECs bind tis - sue factor pathway inhibitors (TFPI), modulate hemostasis with opposing effects such as antiplatelet, anticoagulant and fibrinolytic properties. Lung endothelium regulates synthesis and metabolism of vasoactive compounds such as nitric oxide and endothe-lin-1, both potent regulators of vascular tone. Cytokines, chemokines, interleukins, adhe - sion molecules, and growth factors can be secreted by pulmonary ECs with positive and adverse effects. Pulmonary endothelium exhibits heterogeneity with diverse expression of molecules and specific differences in signaling induced by various infections such as Gram-positive bacteria. The distinction of macro or microvascular endothelium occurs from the larger vessels to small capillaries in the lung alveoli system. Lectin-binding pat terns discriminate between pulmonary artery and pulmonary microvascular capillary endothelium. The lung is one of the body’s organs with the highest expression of vascu lar endothelial growth factor that stimulates small vessel formation of the microvascular endothelium. Acute respiratory distress syndrome and acute chest syndrome in sickle cell disease are two prototypes of devastating diseases caused by pulmonary EC dysfunction.