MMP9 is involved in HO-1-mediated upregulation of apical junctional complex in Caco-2 cells under oxygen-glucose deprivation

MMP9 is involved in HO-1-mediated upregulation of apical junctional complex in Caco-2 cells under... Ischemia reperfusion injury is a critical factor in the recovery process after intestine trauma and the functional restoration of intestinal reconstruction. This study was the first to explore the expression of apical junctional complex (AJC) induced by heme oxygenase-1 (HO-1) in Caco-2 cells in oxygen-glucose deprivation (OGD) models. Here we showed that HO-1 was upregulated after OGD. Notably, activation of HO-1 largely enhanced the expression of AJC proteins including Claudin-4, E-cadherin and β-catenin in Caco-2 cells, but decreased the expression of matrix metalloproteinase 9 (MMP9). Knockdown of HO-1 attenuated the OGD-induced overexpression of AJC proteins but promoted the expression of MMP9. Interestingly, inhibition of MMP9 further enhanced AJC expression. These results suggest that HO-1 is involved in OGD-evoked upregulation of AJC proteins, which is partly mediated by MMP9 pathway. High expression of HO-1 may play an important role in the pathophysiological process of ischemia reperfusion injury and has potential clinical value for the treatment of intestine related diseases. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biochemical and Biophysical Research Communications Elsevier

MMP9 is involved in HO-1-mediated upregulation of apical junctional complex in Caco-2 cells under oxygen-glucose deprivation

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Publisher
Elsevier
Copyright
Copyright © 2018 Elsevier Ltd
ISSN
0006-291x
D.O.I.
10.1016/j.bbrc.2018.02.045
Publisher site
See Article on Publisher Site

Abstract

Ischemia reperfusion injury is a critical factor in the recovery process after intestine trauma and the functional restoration of intestinal reconstruction. This study was the first to explore the expression of apical junctional complex (AJC) induced by heme oxygenase-1 (HO-1) in Caco-2 cells in oxygen-glucose deprivation (OGD) models. Here we showed that HO-1 was upregulated after OGD. Notably, activation of HO-1 largely enhanced the expression of AJC proteins including Claudin-4, E-cadherin and β-catenin in Caco-2 cells, but decreased the expression of matrix metalloproteinase 9 (MMP9). Knockdown of HO-1 attenuated the OGD-induced overexpression of AJC proteins but promoted the expression of MMP9. Interestingly, inhibition of MMP9 further enhanced AJC expression. These results suggest that HO-1 is involved in OGD-evoked upregulation of AJC proteins, which is partly mediated by MMP9 pathway. High expression of HO-1 may play an important role in the pathophysiological process of ischemia reperfusion injury and has potential clinical value for the treatment of intestine related diseases.

Journal

Biochemical and Biophysical Research CommunicationsElsevier

Published: Mar 25, 2018

References

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