Epithelial-Mesenchymal Transition in Human Alveolar Cells Exposed to Indium Chloride

Area of Science:

• Toxicology
• Cell Biology
• Occupational Health

Background:

• Occupational exposure to indium compounds is linked to pulmonary disorders and lung cancer.
• The underlying biological mechanisms of indium-induced lung disease remain unclear.
• Epithelial-mesenchymal transition (EMT) is implicated in fibrosis and cancer progression.

Purpose of the Study:

• To investigate whether indium exposure induces epithelial-mesenchymal transition (EMT) in vitro.
• To elucidate the cellular mechanisms of indium-induced lung injury.

Main Methods:

• A549 human alveolar epithelial cells were treated with indium chloride.
• Analysis of EMT marker mRNA and protein expression (CDH1, ZO1, SNAIL, Vimentin).
• Assessment of cellular morphology and cell-cell adhesion complexes.

Main Results:

• Indium chloride treatment dose-dependently downregulated the epithelial marker CDH1 and upregulated the mesenchymal marker SNAI1.
• Expression levels of EMT marker proteins were significantly altered.
• Indium exposure induced fibroblast-like cell morphology and disrupted cell-cell adhesion.

Conclusions:

• This study provides the first evidence that indium compounds induce EMT in lung epithelial cells.
• EMT induction is a potential mechanism underlying indium-induced lung disorders.
• Findings contribute to understanding indium lung disease pathophysiology.