Endocan, a putative endothelial cell marker, is elevated in preeclampsia, decreased in acute pyelonephritis, and unchanged in other obstetrical syndromes

Adekola, Henry; Romero, Roberto; Chaemsaithong, Piya; Korzeniewski, Steven J.; Dong, Zhong; Yeo, Lami; Hassan, Sonia S.; Chaiworapongsa, Tinnakorn

doi:10.3109/14767058.2014.964676

Cited by 40 publications

(38 citation statements)

References 234 publications

(139 reference statements)

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“…Its synthesis and release of this molecule are raised by proinflammatory cytokines such as tumor necrosis factor (TNF)‐α and interleukin 1B [7]. In numerous studies (hepatocellular [8], renal cancers, lung, breast [9–11], acute myeloid leukemia [22], preeclampsia [12,13], acute migraine attack [23], obstructive sleep apnea [24]) Endocan levels were found to be high. In addition, it is also mentioned in these studies that Endocan can be a diagnostic and prognostic factor in pulmonary diseases.…”

Section: Discussionmentioning

confidence: 99%

“…Its synthesis is induced by pro‐inflammatory cytokines [7]. Endocan levels were found to be high in many diseases particularly in lung [8], renal cancers [9–11], preeclampsia [12,13], in which Endocan could be used as the biomarker. It is also mentioned that Endocan may have a diagnostic and prognostic role in pulmonary diseases [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Can endocan be a new biomarker in ventilator‐associated pneumonia?

Küpeli

Salcan

Kuzucu

et al. 2018

The Kaohsiung J of Med Scie

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Ventilator‐Associated Pneumonia (VAP) is a hospital‐acquired bacterial infection with high incidence and mortality rate. The aim of this study is to investigate the correlation between the Endocan level and development of VAP and whether or not this correlation was correlated with the clinical findings. Demographic data, white blood cell (WBC) count, procalcitonin (PCT), c‐reactive protein (CRP), and fever levels of 60 patients were recorded in serial measurements for 5 days. When there was the presence of fever or elevated Endocan, alveolar lavage culture was taken and chest radiographies were taken. Correlations of the Endocan levels with the culture results and laboratory values were examined. The rate of VAP was found as 10.4/1000 mechanical ventilator days. Endocan levels were significantly higher in patients with VAP (p < 0.05). However, there was no significant difference among PCT, WBC, CRP measurements (p > 0.05). No correlation was found between Endocan levels and PCT, WBC and CRP levels in those with VAP (p > 0.05). A significant correlation was found between the Endocan level and the elevated fever 24 h later (p:0.001). The serum Endocan level on the day 3 had a specificity of 73.3%, a sensitivity of 68.9%, positive predictive value of 44%, and negative predictive value of 88.5% at the cut off level of 9.17 ng/mL. In this study, it was determined that high Endocan levels were associated with the development of VAP. The present study suggested that Endocan can be used as a screening tool for the development of VAP. Clinical Trials.gov ID NCT02916277.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Can endocan be a new biomarker in ventilator‐associated pneumonia?

Küpeli

Salcan

Kuzucu

et al. 2018

The Kaohsiung J of Med Scie

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“…250 Circulating endothelial cells and other markers of endothelial activation/injury such as soluble VCAM-1, E-selectin and endocan are increased in preeclamptic compared with normal pregnant women. 149,184,260,261 Other studies have shown a decrease in circulating endothelial progenitor cells as a marker of endothelial damage in preeclamptic women. 262 …”

Section: Mmps and Vascular Dysfunction In Hypertensive Pregnancy Amentioning

confidence: 99%

Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia

Chen

Khalil

2017

Progress in Molecular Biology and Translational Science

234

168

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Normal pregnancy is associated with marked hemodynamic and uterine changes that allow adequate uteroplacental blood flow and uterine expansion for the growing fetus. These pregnancy-associated changes involve significant uteroplacental and vascular remodeling. Matrix metalloproteinases (MMPs) are important regulators of vascular and uterine remodeling. Increases in MMP-2 and MMP-9 have been implicated in vasodilation, placentation and uterine expansion during normal pregnancy. The increases in MMPs could be induced by the increased production of estrogen and progesterone during pregnancy. MMP expression/activity may be altered during complications of pregnancy. Decreased vascular MMP-2 and MMP-9 may lead to decreased vasodilation, increased vasoconstriction, hypertensive pregnancy and preeclampsia. Abnormal expression of uteroplacental integrins, cytokines and MMPs may lead to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate remodeling of spiral arteries, and reduced uterine perfusion pressure (RUPP). RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic vascular endothelial growth factor and placental growth factor, or stimulate the release of inflammatory cytokines, hypoxia-inducible factor, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could target MMPs in the extracellular matrix as well as endothelial and vascular smooth muscle cells, causing generalized vascular dysfunction, increased vasoconstriction and hypertension in pregnancy. MMP activity can also be altered by endogenous tissue inhibitors of metalloproteinases (TIMPs) and changes in the MMP/TIMP ratio. In addition to their vascular effects, decreases in expression/activity of MMP-2 and MMP-9 in the uterus could impede uterine growth and expansion and lead to premature labor. Understanding the role of MMPs in uteroplacental and vascular remodeling and function could help design new approaches for prediction and management of preeclampsia and premature labor.

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“…Studies have shown an increase in CEC number and other markers of EC damage such as soluble vascular cell adhesion molecule-1 (sVCAM-1), E-selectin and endocan in PE compared with Norm-Preg women (Canbakan et al, 2007; Adekola et al, 2015; Tuzcu et al, 2015; Cakmak et al, 2016), although some studies reported no difference in serum endocan levels (Yuksel et al, 2015). Other studies have shown a decrease in circulating endothelial progenitor cells as a marker of endothelial damage in PE women (Sakashita et al, 2014) (Table 1).…”

Section: Endothelial Dysfunction In Preeclampsiamentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

Possomato-Vieira

Khalil

2016

Advances in Pharmacology

191

117

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Preeclampsia is a pregnancy-related disorder characterized by hypertension, and could lead to maternal and fetal morbidity and mortality. Although the causative factors and pathophysiological mechanisms are unclear, endothelial dysfunction is a major hallmark of preeclampsia. Clinical tests and experimental research have suggested that generalized endotheliosis in the systemic, renal, cerebral and hepatic circulation could decrease endothelium-derived vasodilators such as nitric oxide, prostacyclin and hyperpolarization factor and increase vasoconstrictors such as endothelin-1 and thromboxane A2, leading to increased vasoconstriction, hypertension and other manifestation of preeclampsia. In search for the upstream mechanisms that could cause endothelial dysfunction, certain genetic, demographic and environmental risk factors have been suggested to cause abnormal expression of uteroplacental integrins, cytokines and matrix metalloproteinases, leading to decreased maternal tolerance, apoptosis of invasive trophoblast cells, inadequate spiral arteries remodeling, reduced uterine perfusion pressure (RUPP), and placental ischemia/hypoxia. RUPP may cause imbalance between the anti-angiogenic factors soluble fms-like tyrosine kinase-1 and soluble endoglin and the pro-angiogenic factors vascular endothelial growth factor and placental growth factor, or stimulate the release of other circulating bioactive factors such as inflammatory cytokines, hypoxia-inducible factor-1, reactive oxygen species, and angiotensin AT1 receptor agonistic autoantibodies. These circulating factors could then target endothelial cells and cause generalized endothelial dysfunction. Therapeutic options are currently limited, but understanding the factors involved in endothelial dysfunction could help design new approaches for prediction and management of preeclampsia.

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Endocan, a putative endothelial cell marker, is elevated in preeclampsia, decreased in acute pyelonephritis, and unchanged in other obstetrical syndromes

Cited by 40 publications

References 234 publications

Can endocan be a new biomarker in ventilator‐associated pneumonia?

Can endocan be a new biomarker in ventilator‐associated pneumonia?

Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia

Mechanisms of Endothelial Dysfunction in Hypertensive Pregnancy and Preeclampsia

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