Evaluation of Endocan as a Treatment for Acute Inflammatory Respiratory Failure.

Background: Acute respiratory distress syndrome (ARDS) is a life-threatening condition resulting from acute pulmonary inflammation. However, no specific treatment for ARDS has yet been developed. Previous findings suggest that lung injuries related to ARDS could be regulated by endocan (Esm-1).

Endothelial Cell-Specific Molecule-1 Inhibits Albuminuria in Diabetic Mice.

Background: Diabetic kidney disease (DKD) is the most common cause of kidney failure in the world, and novel predictive biomarkers and molecular mechanisms of disease are needed. Endothelial cell-specific molecule-1 (Esm-1) is a secreted proteoglycan that attenuates inflammation. We previously identified that a glomerular deficiency of Esm-1 associates with more pronounced albuminuria and glomerular inflammation in DKD-susceptible relative to DKD-resistant mice, but its contribution to DKD remains unexplored.

Cleaved endocan acts as a biologic competitor of endocan in the control of ICAM-1-dependent leukocyte diapedesis.

Dysregulated leukocyte diapedesis is a major contributor to acute severe inflammatory states like sepsis and acute respiratory distress syndrome, which are common conditions in critically ill subjects. Endocan is a circulating proteoglycan that binds to the leukocyte integrin LFA-1 and blocks its interaction with its endothelial ligand ICAM-1, subsequently leading to the inhibition of leukocyte recruitment. Recent data have highlighted the hypothetic role of p14, endocan's major catabolite found in the bloodstream of septic patients, as a potential antagonist of endocan, thus participating in the regulation of acute inflammation.

Endocan regulates acute lung inflammation through control of leukocyte diapedesis.

Acute respiratory distress syndrome is a severe form of respiratory failure, occurring in up to 20% of patients admitted to the intensive care unit with sepsis. Dysregulated leukocyte diapedesis is a major contributor to acute respiratory distress syndrome. Endocan is a circulating proteoglycan that binds to the leukocyte integrin leukocyte functional antigen-1 and blocks its interaction with its endothelial ligand, ICAM-1.

Endocan, sepsis, pneumonia, and acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) and hospital-acquired pneumonia (HAP) are major problems of public health in intensive care units (ICUs), occurring in 15% of critically ill patients. Among the factors explaining ARDS development, sepsis is known as a frequent cause. Sepsis, ARDS, and HAP increase morbidity, mortality, length of stay in the ICU, and the overall costs of healthcare.

Low endocan levels are predictive of Acute Respiratory Distress Syndrome in severe sepsis and septic shock.

Purpose: Endocan is a circulating proteoglycan measured at high blood levels during severe sepsis, with a likely lung anti-inflammatory function. The aim of this study was to assess whether paradoxically low endocan levels at Intensive Care Unit (ICU) admission could predict Acute Respiratory Distress Syndrome (ARDS) within 72 h in severe septic patients.

Materials And Methods: Patients admitted for severe sepsis in the ICU of a French University Hospital were included in a prospective single-center observational study between October 2014 and March 2016.

Endothelial Cell-Specific Molecule-1 in Critically Ill Patients With Hematologic Malignancy.

Objectives: To assess whether serum concentration of endothelial cell-specific molecule-1 (Endocan) at ICU admission is associated with the use of ICU resources and outcomes in critically ill hematology patients.

Design: Prospective multicenter cohort study.

Setting: Seventeen ICUs in France and Belgium.

Endocan is a stable circulating molecule in ICU patients.

Background: Endocan is a lung endothelial cell secreted proteoglycan, possessing multiple physiological roles and potential therapeutic and diagnostic utility as biomarker in pneumonia and acute respiratory distress syndrome. Endocan synthesis and secretion can be induced by proinflammatory cytokines such as TNF-α, but can also be subject of proteolytic degradation causing preanalytical variation.

Methods: We investigated the stability of endocan in conventional serum, plasma, anticoagulated whole blood, as well as whole blood and plasma stabilized with protease inhibitors.

Evaluation of endothelial biomarkers as predictors of organ failures in septic shock patients.

Background: Endothelial injury is recognized to trigger organ failures during the first 48h of septic shock. We evaluate endothelial biomarkers at ICU admission in their ability to predict severity, outcome, and organ failures in septic shock patients.

Methods: This prospective observational pilot study was conducted in a medical intensive care unit of a university hospital.

The non glycanated endocan polypeptide slows tumor growth by inducing stromal inflammatory reaction.

Endocan expression is increasingly studied in various human cancers. Experimental evidence showed that human endocan, through its glycan chain, is implicated in various processes of tumor growth. We functionally characterize mouse endocan which is also a chondroitin sulfate proteoglycan but much less glycanated than human endocan.

The disulfide bond between cysteine 10 and cysteine 34 is required for CCL18 activity.

Asthma is a Th2-mediated disease that involves Th2 cell and eosinophil migration into the bronchial mucosa which is dependent upon the expression of a specific set of chemokines within the lung. Among them, CCL18 seems to play a key role because of its preferential expression in the lung, and its up-regulation by Th2 cytokines. Here, we show that the optimal naïve T cell and basophil chemotaxis, and basophil histamine release induced by rhCCL18 occurred at a 100 time lower concentration with CHO-derived rhCCL18 than with E.

Identification of a 14 kDa endocan fragment generated by cathepsin G, a novel circulating biomarker in patients with sepsis.

Severe septic syndrome, which is the most prevalent and lethal cause of acute respiratory distress syndrome, remains one of the most frequent causes of admission and death in intensive care units (ICU). Inflammatory phenomenon leading to severe sepsis are multiple and not yet completely understood. The main target damage during severe sepsis is the endothelium.

Development of monoclonal antibodies and ELISA specific for the mouse vascular endocan.

Human vascular endocan is a proteoglycan exhibiting tumorigenic activity through both its glycan and protein cores. Endocan mRNA is identified as being one of the most significant molecular signatures defining a poor prognosis in lung, breast, kidney, prostate, and thyroid malignancies. The survival inversely correlates with endocan expression in tumor tissue from hepatocarcinoma, and in serum from lung cancer.