Epithelial-mesenchymal transition: Insights into nickel-induced lung diseases

Abstract

Nickel compounds are environmental toxicants, prevalent in the atmosphere due to their widespread use in several industrial processes, extensive consumption of nickel containing products, as well as burning of fossil fuels. Exposure to nickel is associated with a multitude of chronic inflammatory lung diseases including asthma, chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis. In addition, nickel exposure is implicated in the development of nasal and lung cancers. Interestingly, a common pathogenic mechanism underlying the development of diseases associated with nickel exposure is epithelial-mesenchymal transition (EMT). EMT is a process by which the epithelial cells lose their junctions and polarity and acquire mesenchymal traits, including increased ability to migrate and invade. EMT is a normal and essential physiological process involved in differentiation, development and wound healing. However, EMT also contributes to a number of pathological conditions, including fibrosis, cancer and metastasis. Growing evidence suggest that EMT induction could be an important outcome of nickel exposure. In this review, we discuss the role of EMT in nickel-induced lung diseases and the mechanisms associated with EMT induction by nickel exposure.

Keywords: Epigenetics; Epithelial-mesenchymal transition; HIF-1; Nickel; TGF-β.