Involvement of E-cadherin cleavage in reperfusion injury

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

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Objective: E-cadherin is a major cell-to-cell adhesion molecule, of which the ectodomain is cleaved from epithelial cells to yield a soluble form after the pathological alteration of the alveolar epithelium. We investigated the excretion level of soluble E-cadherin in a rat lung isotransplant model, and demonstrated the involvement of this molecule in the pathogenesis of reperfusion injury after lung transplantation. Methods: Inbred male Lewis rats were used as both donor and recipient animals, and they were subjected to left lung isotransplantation. After 6 h of ischaemia, the left lung was transplanted into a recipient rat and reperfused for 4 h. The animals were injected intravenously with 125I-labelled albumin at 3 h after the onset of reperfusion as a marker of pulmonary albumin leakage. We assessed pulmonary alveolar septal damage quantitatively based on the 125I-albumin concentration ratio of bronchoalveolar lavage fluid (BALF) to plasma. Soluble E-cadherin fragments were detected in BALF on Western blot analysis using affinity-purified antibodies specific to rat E-cadherin synthetic peptides. Results: The BALF supernatant-to-plasma ratio of the graft lung was significantly increased compared to that of the control group. Western blot analysis showed a marked release of soluble E-cadherin into BALF, and its increase in BALF was associated with alveolar septal damage. Conclusions: These results suggest that one potential mechanism of lung reperfusion injury involves the cleavage of E-cadherin.

Original languageEnglish
Pages (from-to)426-431
Number of pages6
JournalEuropean Journal of Cardio-thoracic Surgery
Volume37
Issue number2
DOIs
Publication statusPublished - 2010 Feb

Fingerprint

Cadherins
Reperfusion Injury
Bronchoalveolar Lavage Fluid
Lung
Albumins
Inbred Lew Rats
Western Blotting
Isografts
Antibody Affinity
Lung Transplantation
Cell Adhesion Molecules
Lung Injury
Reperfusion
Ischemia
Epithelium
Epithelial Cells
Transplants
Control Groups
Peptides

Keywords

  • E-cadherin
  • Ectodomain shedding
  • Lung transplantation
  • Reperfusion injury
  • Soluble form

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery
  • Pulmonary and Respiratory Medicine

Cite this

Involvement of E-cadherin cleavage in reperfusion injury. / Goto, Taichiro; Ishizaka, Akitoshi; Katayama, Masahiko; Kohno, Mitsutomo; Tasaka, Sadatomo; Fujishima, Seitaro; Kobayashi, Koichi; Nomori, Hiroaki.

In: European Journal of Cardio-thoracic Surgery, Vol. 37, No. 2, 02.2010, p. 426-431.

Research output: Contribution to journalArticle

Goto, T, Ishizaka, A, Katayama, M, Kohno, M, Tasaka, S, Fujishima, S, Kobayashi, K & Nomori, H 2010, 'Involvement of E-cadherin cleavage in reperfusion injury', European Journal of Cardio-thoracic Surgery, vol. 37, no. 2, pp. 426-431. https://doi.org/10.1016/j.ejcts.2009.06.041
Goto, Taichiro ; Ishizaka, Akitoshi ; Katayama, Masahiko ; Kohno, Mitsutomo ; Tasaka, Sadatomo ; Fujishima, Seitaro ; Kobayashi, Koichi ; Nomori, Hiroaki. / Involvement of E-cadherin cleavage in reperfusion injury. In: European Journal of Cardio-thoracic Surgery. 2010 ; Vol. 37, No. 2. pp. 426-431.
@article{747f8762a0d54c718fd8feffc2d32523,
title = "Involvement of E-cadherin cleavage in reperfusion injury",
abstract = "Objective: E-cadherin is a major cell-to-cell adhesion molecule, of which the ectodomain is cleaved from epithelial cells to yield a soluble form after the pathological alteration of the alveolar epithelium. We investigated the excretion level of soluble E-cadherin in a rat lung isotransplant model, and demonstrated the involvement of this molecule in the pathogenesis of reperfusion injury after lung transplantation. Methods: Inbred male Lewis rats were used as both donor and recipient animals, and they were subjected to left lung isotransplantation. After 6 h of ischaemia, the left lung was transplanted into a recipient rat and reperfused for 4 h. The animals were injected intravenously with 125I-labelled albumin at 3 h after the onset of reperfusion as a marker of pulmonary albumin leakage. We assessed pulmonary alveolar septal damage quantitatively based on the 125I-albumin concentration ratio of bronchoalveolar lavage fluid (BALF) to plasma. Soluble E-cadherin fragments were detected in BALF on Western blot analysis using affinity-purified antibodies specific to rat E-cadherin synthetic peptides. Results: The BALF supernatant-to-plasma ratio of the graft lung was significantly increased compared to that of the control group. Western blot analysis showed a marked release of soluble E-cadherin into BALF, and its increase in BALF was associated with alveolar septal damage. Conclusions: These results suggest that one potential mechanism of lung reperfusion injury involves the cleavage of E-cadherin.",
keywords = "E-cadherin, Ectodomain shedding, Lung transplantation, Reperfusion injury, Soluble form",
author = "Taichiro Goto and Akitoshi Ishizaka and Masahiko Katayama and Mitsutomo Kohno and Sadatomo Tasaka and Seitaro Fujishima and Koichi Kobayashi and Hiroaki Nomori",
year = "2010",
month = "2",
doi = "10.1016/j.ejcts.2009.06.041",
language = "English",
volume = "37",
pages = "426--431",
journal = "European Journal of Cardio-thoracic Surgery",
issn = "1010-7940",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Involvement of E-cadherin cleavage in reperfusion injury

AU - Goto, Taichiro

AU - Ishizaka, Akitoshi

AU - Katayama, Masahiko

AU - Kohno, Mitsutomo

AU - Tasaka, Sadatomo

AU - Fujishima, Seitaro

AU - Kobayashi, Koichi

AU - Nomori, Hiroaki

PY - 2010/2

Y1 - 2010/2

N2 - Objective: E-cadherin is a major cell-to-cell adhesion molecule, of which the ectodomain is cleaved from epithelial cells to yield a soluble form after the pathological alteration of the alveolar epithelium. We investigated the excretion level of soluble E-cadherin in a rat lung isotransplant model, and demonstrated the involvement of this molecule in the pathogenesis of reperfusion injury after lung transplantation. Methods: Inbred male Lewis rats were used as both donor and recipient animals, and they were subjected to left lung isotransplantation. After 6 h of ischaemia, the left lung was transplanted into a recipient rat and reperfused for 4 h. The animals were injected intravenously with 125I-labelled albumin at 3 h after the onset of reperfusion as a marker of pulmonary albumin leakage. We assessed pulmonary alveolar septal damage quantitatively based on the 125I-albumin concentration ratio of bronchoalveolar lavage fluid (BALF) to plasma. Soluble E-cadherin fragments were detected in BALF on Western blot analysis using affinity-purified antibodies specific to rat E-cadherin synthetic peptides. Results: The BALF supernatant-to-plasma ratio of the graft lung was significantly increased compared to that of the control group. Western blot analysis showed a marked release of soluble E-cadherin into BALF, and its increase in BALF was associated with alveolar septal damage. Conclusions: These results suggest that one potential mechanism of lung reperfusion injury involves the cleavage of E-cadherin.

AB - Objective: E-cadherin is a major cell-to-cell adhesion molecule, of which the ectodomain is cleaved from epithelial cells to yield a soluble form after the pathological alteration of the alveolar epithelium. We investigated the excretion level of soluble E-cadherin in a rat lung isotransplant model, and demonstrated the involvement of this molecule in the pathogenesis of reperfusion injury after lung transplantation. Methods: Inbred male Lewis rats were used as both donor and recipient animals, and they were subjected to left lung isotransplantation. After 6 h of ischaemia, the left lung was transplanted into a recipient rat and reperfused for 4 h. The animals were injected intravenously with 125I-labelled albumin at 3 h after the onset of reperfusion as a marker of pulmonary albumin leakage. We assessed pulmonary alveolar septal damage quantitatively based on the 125I-albumin concentration ratio of bronchoalveolar lavage fluid (BALF) to plasma. Soluble E-cadherin fragments were detected in BALF on Western blot analysis using affinity-purified antibodies specific to rat E-cadherin synthetic peptides. Results: The BALF supernatant-to-plasma ratio of the graft lung was significantly increased compared to that of the control group. Western blot analysis showed a marked release of soluble E-cadherin into BALF, and its increase in BALF was associated with alveolar septal damage. Conclusions: These results suggest that one potential mechanism of lung reperfusion injury involves the cleavage of E-cadherin.

KW - E-cadherin

KW - Ectodomain shedding

KW - Lung transplantation

KW - Reperfusion injury

KW - Soluble form

UR - http://www.scopus.com/inward/record.url?scp=74149086563&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=74149086563&partnerID=8YFLogxK

U2 - 10.1016/j.ejcts.2009.06.041

DO - 10.1016/j.ejcts.2009.06.041

M3 - Article

C2 - 19643628

AN - SCOPUS:74149086563

VL - 37

SP - 426

EP - 431

JO - European Journal of Cardio-thoracic Surgery

JF - European Journal of Cardio-thoracic Surgery

SN - 1010-7940

IS - 2

ER -