scholarly journals Secretory Phospholipase A2 Tipe II (SPLA II) In Cardiovascular Disease

2015 ◽  
pp. 162-70
Author(s):  
Djanggan Sargowo
Keyword(s):  
Cardiovascular Disease ◽  
Phospholipase A2 ◽  
Inflammatory Mediator ◽  
Recent Literature ◽  
Acute Phase Reactant ◽  
Multiple Roles ◽  
Secretory Phospholipase A2 ◽  
Inflammatory Reactions ◽  
Secretory Phospholipase

Inflammatory reactions contribute to the pathogenesis of cardiovascular conditions such as atherosclerosis and ischemic damage in acute myocardial infarction (AMI). Among the mediators involved in inflammation are secretory phospholipase A2 group II (sPLA2-II) enzymes. Though some cells constitutively express Spla2-II, the synthesis by cells such as hepatocytes is typical for an acute-phase reactant. Recent literature suggest multiple roles for sPLA2-II in cardiovascular disease. In this review we discuss the role of sPLA2-II in included that sPLA2-II appears to be an inportant inflammatory mediator of cardiovascular disease.

Secretory phospholipase A2 predicts impending acute chest syndrome in sickle cell disease

Blood ◽  
2000 ◽  
Vol 96 (9) ◽  
pp. 3276-3278
Author(s):  
Lori A. Styles ◽  
Anton J. Aarsman ◽  
Elliott P. Vichinsky ◽  
Frans A. Kuypers
Keyword(s):  
Sickle Cell Disease ◽  
Phospholipase A2 ◽  
Cause Of Death ◽  
Sickle Cell ◽  
Inflammatory Mediator ◽  
Acute Chest Syndrome ◽  
Secretory Phospholipase A2 ◽  
Cell Disease ◽  
Secretory Phospholipase ◽  
Potent Inflammatory Mediator

Acute chest syndrome (ACS) is the leading cause of death in sickle cell disease. Severe ACS often develops in the course of a vaso-occlusive crisis (VOC), but currently there are no predictors for its development. Secretory phospholipase A2(sPLA2), a potent inflammatory mediator, is elevated in ACS, and previous work suggests that sPLA2 predicts impending ACS. We prospectively evaluated sPLA2concentration during 21 admissions for VOC; 6 of these patients went on to develop ACS. Elevation of sPLA2 was detected all 6 patients 24 to 48 hours before ACS was clinically diagnosed. Adding the requirement for fever raised the specificity of sPLA2 to 87% while retaining 100% sensitivity. These data indicate that sPLA2 can be useful in alerting the clinician to patients with impending ACS. In addition, sPLA2 may be useful for instituting early therapies to prevent or reduce the clinical morbidity of ACS.

scholarly journals Secretory Phospholipase A2-IIA and Cardiovascular Disease

2013 ◽  
Vol 62 (21) ◽  
pp. 1966-1976 ◽  
Author(s):  
Michael V. Holmes ◽  
Tabassome Simon ◽  
Holly J. Exeter ◽  
Lasse Folkersen ◽  
Folkert W. Asselbergs ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Phospholipase A2 ◽  
Secretory Phospholipase A2 ◽  
Secretory Phospholipase

Dendritic-cell activation by secretory phospholipase A2

Blood ◽  
2005 ◽  
Vol 105 (9) ◽  
pp. 3583-3587 ◽  
Author(s):  
Reinhold Ramoner ◽  
Thomas Putz ◽  
Hubert Gander ◽  
Andrea Rahm ◽  
Georg Bartsch ◽  
...  
Keyword(s):  
Phospholipase A2 ◽  
Cell Activation ◽  
Vaccine Development ◽  
Interleukin 1 ◽  
Immune Surveillance ◽  
Human Monocyte ◽  
Secretory Phospholipase A2 ◽  
Dendritic Cell Activation ◽  
Secretory Phospholipase

Abstract Dendritic cells (DCs), also referred to as the sentinels of the immune system, induce and coordinate important functions of immune surveillance. DCs acquire immunity-initiating capacity only after a process of maturation usually induced by ligands that bind to members of the tumor necrosis factor (TNF) or toll-like receptor families. Secretory phospholipase A2 (sPLA2), which hydrolyzes the sn-2 ester bond of glycerophospholipids, regulates a variety of cellular functions including migration of endothelial cells and neurite outgrowth. In the present study we investigated the role of sPLA2 in DC biology. We report that human monocyte-derived DC cultures lack sPLA2 activity but respond to exogenous sPLA2. sPLA2 alone and in cooperation with TNF-α and interleukin 1 β (IL-1β) induced fatty acid release from DC membranes, which was accompanied by upregulation of surface markers and by an increase in the migratory and immunostimulatory capacity of the DCs. Our findings indicate that secreted enzymes such as sPLA2 can contribute to DC maturation and emphasize the role of lipid mediators in the regulation of immune responses. This observation may also have implications for DC-based vaccine development.

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