Plasma sE-cadherin and the plasma sE-cadherin/sVE-cadherin ratio are potential biomarkers for chronic obstructive pulmonary disease

Shirahata, Toru; Nakamura, Hidetoshi; Nakajima, Takahiro; Nakamura, Miho; Chubachi, Shotaro; Yoshida, Shuichi; Tsuduki, Keishi; Mashimo, Shuko; Takahashi, Saeko; Minematsu, Naoto; Tateno, Hiroki; Asano, Koichiro; Fujishima, Seitaro; Betsuyaku, Tomoko

doi:10.1080/1354750x.2018.1434682

Cited by 15 publications

(11 citation statements)

References 32 publications

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“…We already know that it is not limited to bacteria since there is an apparent correlation between the levels of sE-cad in human immunodeficiency virus (HIV)-positive patients and their viral titers (Streeck et al, 2011). Moreover, abnormal concentrations of sE-cad in patients’ sera has been observed in several metabolic and inflammatory diseases (Pittard et al, 1996; Jiang et al, 2009; Shirahata et al, 2018; Sato et al, 2019). High concentration of sE-cad has also been found associated with cancer progression (Grabowska and Day, 2012; Salama et al, 2013; Repetto et al, 2014).…”

Section: Release Of Soluble E-cadherin After Bacterial Infection As Amentioning

confidence: 99%

The E-Cadherin Cleavage Associated to Pathogenic Bacteria Infections Can Favor Bacterial Invasion and Transmigration, Dysregulation of the Immune Response and Cancer Induction in Humans

2019

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Once bound to the epithelium, pathogenic bacteria have to cross epithelial barriers to invade their human host. In order to achieve this goal, they have to destroy the adherens junctions insured by cell adhesion molecules (CAM), such as E-cadherin (E-cad). The invasive bacteria use more or less sophisticated mechanisms aimed to deregulate CAM genes expression or to modulate the cell-surface expression of CAM proteins, which are otherwise rigorously regulated by a molecular crosstalk essential for homeostasis. Apart from the repression of CAM genes, a drastic decrease in adhesion molecules on human epithelial cells can be obtained by induction of eukaryotic endoproteases named sheddases or through synthesis of their own (prokaryotic) sheddases. Cleavage of CAM by sheddases results in the release of soluble forms of CAM. The overexpression of soluble CAM in body fluids can trigger inflammation and pro-carcinogenic programming leading to tumor induction and metastasis. In addition, the reduction of the surface expression of E-cad on epithelia could be accompanied by an alteration of the anti-bacterial and anti-tumoral immune responses. This immune response dysfunction is likely to occur through the deregulation of immune cells homing, which is controlled at the level of E-cad interaction by surface molecules αE integrin (CD103) and lectin receptor KLRG1. In this review, we highlight the central role of CAM cell-surface expression during pathogenic microbial invasion, with a particular focus on bacterial-induced cleavage of E-cad. We revisit herein the rapidly growing body of evidence indicating that high levels of soluble E-cad (sE-cad) in patients’ sera could serve as biomarker of bacterial-induced diseases.

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Section: Release Of Soluble E-cadherin After Bacterial Infection As Amentioning

confidence: 99%

The E-Cadherin Cleavage Associated to Pathogenic Bacteria Infections Can Favor Bacterial Invasion and Transmigration, Dysregulation of the Immune Response and Cancer Induction in Humans

2019

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“…Он состоит из трех доменов: С-концевой домен (локализован в цитоплазме клетки), трансмембранный и N-концевой домен (в межклеточном пространстве) [5]. Растворимый в крови (N-терминальный) Е-кадгерин представляет собой молекулу, которая высвобождается с поверхности эпителиальной клетки под воздействием протеаз, включая металлопротеиназы, проникает в кровь и становится доступной для определения [6]. Повышение содержания Е-кадгерина в крови может указывать на разрушение плотных запирательных контактов в слизистой оболочке пищевода [7].…”

Section: гастроэзофагеальнаяunclassified

The Role of E-Cadherin in the Assessment of Esophageal Mucosal Damage in Patients with Gastroesophageal Reflux Disease Associated with Obstructive Sleep Apnea/Hypopnea Syndrome

Шелкович

2019

Rossijskij žurnal gastroènterologii, gepatologii, koloproktolog

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Aim. To evaluate the E-cadherin content in the blood plasma of individuals with suffering from both gastroesophageal reflux disease (GERD) and GERD combined with obstructive sleep apnea/hypopnea syndrome (OSAHS).Materials and methods. 120 patients with GERD and/or OSAHS were examined. All the patients underwent esophagogastroduodenoscopy with the biopsy of the lower third of the esophagus in order to perform GERD morphological verification. The diagnostics of respiratory disorders during sleeping was performed using computer pulse oximetry. Group 1 (n = 29) consisted of GERD patients, group 2 (n = 35) of patients with GERD in combination with OSAHS, group 3 (n = 30) of patients with OSAHS, group 4 (n = 26) was the comparison group. The concentration of E-cadherin in the blood plasma was determined using enzyme immunoassay. Results. There were no statistically significant differences in the plasma level of the N-terminal E-cadherin fragment between GERD patients and the comparison group (0.207 (0.128; 0.295) and 0.128 (0.067; 0.281) ng/ml, respectively, p = 0.082). However, the patients with erosive esophagitis were characterized by a higher content of E-cadherin in the blood plasma than those of the comparison group (0.284 (0.176; 0.858) and 0.128 (0.067; 0.281) ng/ml, respectively, p = 0.03). In patients with GERD and OSAHS, statistically significantly higher plasma concentrations of E-cadherin were observed as compared to GERD patients (0.379 (0.277; 0.538) and 0.2007 (0.128; 0.295) ng/ml, respectively, p = 0.017). A positive dependence of E-cadherin concentration in the blood plasma on the apnea/hypopnea index was found (r = 0.43, p <0.05).Conclusions. OSAHS negatively affects the state of histoarchitecture of the esophageal mucosa of GERD patients, as evidenced by an increase in N-terminal E-cadherin in the blood plasma and may indicate a loss of E-cadherin in the esophageal mucosa with the development of an impaired function of tight junctions.

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“…These authors also stated that current tests for E‐cad lack sensitivity and specificity. Methodologies mainly used for E‐cad protein detection include immunohistochemistry or immunocytochemistry for tissue samples or cell lines, and ELISA tests for biological fluids , these last ones with a declared sensitivity of 0.039 ng mL −1 .…”

Section: Introductionmentioning

confidence: 99%

Disposable Amperometric Immunosensor for the Determination of the E‐Cadherin Tumor Suppressor Protein in Cancer Cells and Human Tissues

et al. 2018

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This paper describes the results obtained in the development of the first electrochemical immunosensor described to date for the detection of E‐cadherin (E‐cad) protein, a relevant biomarker of prognosis and metastasis in cancer, based on the use of magnetic microcarriers (MBs) and amperometric transduction at screen‐printed carbon electrodes (SPCEs). Thus, the determination of E‐cad protein involved the use of two specific antibodies against this protein (one of them labelled with HRP) in a sandwich configuration onto HOOC‐MBs. The magnetic bioconjugates were captured onto SPCEs and the amperometric transduction was performed using the H2O2/hydroquinone (HQ) system. Under optimal conditions, this bioplatform demonstrated a wide linear concentration range (0.50–25 ng mL−1) and a detection limit as low as 0.16 ng mL−1, well below the optimal cut‐off level for the E‐cad protein (defined as 10,000 ng mL−1 for soluble E‐cad levels in serum). The developed sensor also showed a good reproducibility among measurements with seven different sensors constructed in the same manner (RSD, 5.4 %), stability for more than 15 days and good specificity towards other proteins commonly found on biological samples. The applicability of this simple handling bioplatform for the direct determination of this protein in cell lysates with different metastatic potential and extracts from paraffined‐embedded human colorectal cancer tissues of different grade were also demonstrated.

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Plasma sE-cadherin and the plasma sE-cadherin/sVE-cadherin ratio are potential biomarkers for chronic obstructive pulmonary disease

Abstract: Plasma sE-cadherin levels and sE-cadherin/sVE-cadherin ratios are potential biomarkers for COPD.

Cited by 15 publications

References 32 publications

The E-Cadherin Cleavage Associated to Pathogenic Bacteria Infections Can Favor Bacterial Invasion and Transmigration, Dysregulation of the Immune Response and Cancer Induction in Humans

The E-Cadherin Cleavage Associated to Pathogenic Bacteria Infections Can Favor Bacterial Invasion and Transmigration, Dysregulation of the Immune Response and Cancer Induction in Humans

The Role of E-Cadherin in the Assessment of Esophageal Mucosal Damage in Patients with Gastroesophageal Reflux Disease Associated with Obstructive Sleep Apnea/Hypopnea Syndrome

Disposable Amperometric Immunosensor for the Determination of the E‐Cadherin Tumor Suppressor Protein in Cancer Cells and Human Tissues

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