Lung transplant remains the primary treatment option for patients with advanced lung disease or irreversible pulmonary failure. The major obstacle limiting longer survival in lung transplant patients is the development of chronic lung allograft dysfunction (CLAD). Our inventors have identified N-myc-interactor (NMI) as a critical regulator of epithelial-mesenchymal transition (EMT) — an important precursor to CLAD development. Tissue samples obtained from both healthy and explant lungs were compared for expression levels of epithelial and mesenchymal markers associated with CLAD development. Compared to control samples, NMI and protein expression was downregulated, while mesenchymal markers were upregulated in patients with CLAD. Therefore, reduction in NMI is an indicator of EMT in CLAD, which can lead to lung disease or tumor formation. Potential applications for these findings include development of NMI as a biomarker for early diagnosis of EMT and CLAD, as a novel drug target, and as recombinant protein or gene therapy.
Decreased NMI Expression Levels in Lungs of Transplant Patients that had Developed CLAD