Abstract

In the human airway, the gelforming mucin subtypes MUC5B and MUC5AC play important roles in biophylaxis. However, the regulation of MUC5B production is less clear than that of MUC5AC. Therefore, the regulation of MUC5B production by cell attachment and Akt was investigated in human lung epithelial NCI-H292 cells. We found that low cell attachment to culture plates induced the upregulated production of both MUC5B and MUC5AC. Cell attachment induces the activation of Akt, a serine/threonine kinase. Cell treatment with Akt inhibitor I decreased Akt phosphorylation and activation. However, MUC5B production was unaffected by Akt inhibition, whereas MUC5AC production was upregulated. MUC5B production was also unaffected by Akt inhibition in cells cultured on type IV collagen or fibronectin. These results suggest that the production of both MUC5B and MUC5AC is regulated by cell attachment. However, the regulation of MUC5B is unaffected by Akt inhibition, in contrast to that of MUC5AC.

Highlights

  • The mucus layer in the human airway is produced by secretory epithelial cells and is an important component of primary host defense

  • We previously reported that Akt and low cell attachment are involved in the regulation of MUC5AC production [11] [23]

  • We previously reported that MUC5AC production was increased 10-fold by low cell attachment [11]

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Summary

Introduction

The mucus layer in the human airway is produced by secretory epithelial cells and is an important component of primary host defense. It traps and transports inhaled foreign particulates out of the airway through mucociliary clearance (MCC) by mucus flow and cough [1] [2]. Mucus is mainly composed of water and mucin, a highly. (2016) MUC5B Production Is Unaffected by Akt Inhibition in Human Lung Epithelial NCI-H292 Cells. 17 mucin genes have been identified in the human genome [3]. The principal mucin subtypes are MUC5AC and MUC5B. MUC5B is a major component of the biodefence activities of mucus in the healthy airway. The lack of MUC5B causes inefficient MCC in mice [6]-[8]

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