Involvement of E-cadherin cleavage in reperfusion injury

Goto, Taichiro; Ishizaka, Akitoshi; Katayama, Masahiko; Kohno, Mitsutomo; Tasaka, Sadatomo; Fujishima, Seitaro; Kobayashi, Koichi

doi:10.1016/j.ejcts.2009.06.041

Cited by 7 publications

(6 citation statements)

References 24 publications

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“…It is expressed in epithelial tissues but in the normal lung, it is not present in the alveolar liquid lining. Hence, appearance of the soluble fragments of E-cadherin in the lavage fluid is a clear indication of epithelial cell injury [42], [46], [47]. We found the 85 kDa soluble fragments of E-cadherin in the lavage fluid of unventilated animals which is likely due to the combined effects of HCl injury and the lavage process itself (Fig.…”

Section: Discussionmentioning

confidence: 66%

Combined Effects of Ventilation Mode and Positive End-Expiratory Pressure on Mechanics, Gas Exchange and the Epithelium in Mice with Acute Lung Injury

et al. 2013

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The accepted protocol to ventilate patients with acute lung injury is to use low tidal volume (VT) in combination with recruitment maneuvers or positive end-expiratory pressure (PEEP). However, an important aspect of mechanical ventilation has not been considered: the combined effects of PEEP and ventilation modes on the integrity of the epithelium. Additionally, it is implicitly assumed that the best PEEP-VT combination also protects the epithelium. We aimed to investigate the effects of ventilation mode and PEEP on respiratory mechanics, peak airway pressures and gas exchange as well as on lung surfactant and epithelial cell integrity in mice with acute lung injury. HCl-injured mice were ventilated at PEEPs of 3 and 6 cmH2O with conventional ventilation (CV), CV with intermittent large breaths (CVLB) to promote recruitment, and a new mode, variable ventilation, optimized for mice (VVN). Mechanics and gas exchange were measured during ventilation and surfactant protein (SP)-B, proSP-B and E-cadherin levels were determined from lavage and lung homogenate. PEEP had a significant effect on mechanics, gas exchange and the epithelium. The higher PEEP reduced lung collapse and improved mechanics and gas exchange but it also down regulated surfactant release and production and increased epithelial cell injury. While CVLB was better than CV, VVN outperformed CVLB in recruitment, reduced epithelial injury and, via a dynamic mechanotransduction, it also triggered increased release and production of surfactant. For long-term outcome, selection of optimal PEEP and ventilation mode may be based on balancing lung physiology with epithelial injury.

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Section: Discussionmentioning

confidence: 66%

Combined Effects of Ventilation Mode and Positive End-Expiratory Pressure on Mechanics, Gas Exchange and the Epithelium in Mice with Acute Lung Injury

et al. 2013

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“…Goto et al applied this to a model of lung transplantation in rats and observed that rats with transplanted lungs had a higher level of sE-cad than the sham operated rats (68). Again, no direct evidence implicates a sheddase, but other studies have implicated MMP-7 in rodent lung damage studies (26, 55).…”

Section: Generation Of Se-cadmentioning

confidence: 99%

“…Patients with leukemia (myelogenous, monocytic, lymphatic) have increased levels of sE-cad ( P < 0.01), as do patients with leiomyosarcoma ( P < 0.05) (68). Multiple myeloma patients have five times higher levels of serum sE-cad than control samples ( P < 0.0001) (88).…”

Section: Se-cad Is Present In Patient Fluids In a Variety Of Condimentioning

confidence: 99%

Soluble E-cadherin: more than a symptom of disease

Grabowska

Day²

2012

Front Biosci

114

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Epithelial (E)-cadherin is a homophilic adhesion molecule which is responsible for maintenance of baso-lateral cell adhesion and polarity. E-cadherin can be lost from the cell surface by proteolytic cleavage, resulting in the generation of an 80kDa fragment referred to a soluble E-cadherin (sE-cad). Although originally discovered in the conditioned media of breast cancer cells and later verified in the fluids of cancer patients, today sE-cad has been reported in patients with viral and bacterial infections, organ failure, and benign disease. The proteases implicated in this cleavage event include members of the disintegrin family (ADAM10 and 15), bacterial proteases (gingipains and BFT), cathepsins (B, L, S), matrix metalloproteases (MMP-2, 3, 7, 9, and 14), Kallikrein-7 (KLK7), and plasmin. Stimulus that induces sE-cad generation by ADAMs, MMPs, KLK7, and plasmin in vitro ranges from serum withdrawal to pro-inflammatory cytokines to growth factors. The cellular or physiologic consequences of sE-cad accumulation include the disruption of adherens junctions, cellular migration and invasion, induction of MMPs, as well as cell signaling, suggesting that sE-cad may contribute to disease progression.

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“…Goto et al studied lung IR injury to investigate the role of E-cadherin. They found that E-cadherin concentration and expression are increased and undergo cleavage during IR 17 . Menezes et al studied renal IR.…”

Section: Discussionmentioning

confidence: 99%

E-cadherin and NF-κB expression in the vagina after ovarian ischemia and reperfusion

Yurci,

Zaman,

Sarı

et al. 2024

Acta Cir. Bras.

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Purpose: To investigate inflammation and cell adhesion molecules in the vagina after ovarian ischemia-reperfusion (IR) injury. Methods: 20 Wistar albino female rats were divided into two groups: control, and IR groups. In IR group, blood flow was restricted for 2 hours for ovarian ischemia. Then, tissues were re-blood 2 hours for reperfusion. Vagina tissues were excised and processed for histopathological analysis. Histopathological and biochemical follow-ups were performed. Results: Both malondialdehyde and myeloperoxidase values were increased in IR group compared to control group. Glutathione content was decreased in IR group compared to control group. Epithelial degeneration, inflammation, dilatation, and nuclear factor-κB (NF-κB) expression were increased in IR group compared to control group. E-cadherin expression was significantly decreased in IR group. In the IR group, E-cadherin showed a positive reaction in adenomas, gland-like cryptic structures, cellular junctions with clustered inflammatory cells. In the IR group, NF-κB expression was increased in basement membrane, inflammatory cells, in blood vessels. Conclusions: Ovarian ischemia caused degeneration of epithelial cells in the vaginal region and disruptions in the cell junction complex, which leads to activation of E-cadherin and NF-κB signaling pathway and alterations in reproductive and embryonal development in the vaginal region.

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Involvement of E-cadherin cleavage in reperfusion injury

Abstract: These results suggest that one potential mechanism of lung reperfusion injury involves the cleavage of E-cadherin.

Cited by 7 publications

References 24 publications

Combined Effects of Ventilation Mode and Positive End-Expiratory Pressure on Mechanics, Gas Exchange and the Epithelium in Mice with Acute Lung Injury

Combined Effects of Ventilation Mode and Positive End-Expiratory Pressure on Mechanics, Gas Exchange and the Epithelium in Mice with Acute Lung Injury

Soluble E-cadherin: more than a symptom of disease

E-cadherin and NF-κB expression in the vagina after ovarian ischemia and reperfusion

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