Irene Tsilioni1, Aristotelis S Filippidis2, Theodora Kerenidi3, Andrei V Budanov4, Sotirios G Zarogiannis5, Konstantinos I Gourgoulianis3. 1. Department of Respiratory Medicine, Faculty of Medicine, University of Thessaly, Biopolis, Larissa, Greece; Department of Human and Molecular Genetics, Goodwin Research Laboratories, Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA; Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA, USA. Electronic address: eirini.tsilioni@tufts.edu. 2. Department of Neurosurgery, Boston University, Boston Medical Center, Boston, MA, USA. 3. Department of Respiratory Medicine, Faculty of Medicine, University of Thessaly, Biopolis, Larissa, Greece. 4. Department of Human and Molecular Genetics, Goodwin Research Laboratories, Massey Cancer Center, Virginia Commonwealth University, Richmond, VA, USA. 5. Department of Respiratory Medicine, Faculty of Medicine, University of Thessaly, Biopolis, Larissa, Greece; Department of Physiology, Faculty of Medicine, University of Thessaly, Biopolis, Larissa 41500, Greece.
Abstract
OBJECTIVES: Sestrin-2 (Sesn2) belongs to a family of highly conserved antioxidant proteins that were discovered as p53-inducible proteins and inhibits cell growth and proliferation. Our aim was to assess the levels of Sesn2 in malignant pleural effusions of lung cancer patients compared to benign pleural effusions. DESIGN AND METHODS: We enrolled 73 patients (55/males and 18/females) diagnosed with pleural effusion (PE). PEs were grouped as 44 malignant pleural effusions (MPEs; lung cancer) and 29 benign (BPE; 7 congestive heart failure, 9 tuberculosis, 13 parapneumonic). Pleural fluid (PF) Sesn2 levels were determined by enzyme-linked immunosorbent assay (ELISA) kit. Standard biochemical PF analysis was also performed and Sesn2 levels were correlated with PF lactate dehydrogenase (LDH), protein, cell counts and age. RESULTS: Sesn2 was detected in 24/44 patients with MPEs and in 3/29 patients with BPEs (p=0.0001). The mean value (mean±SEM) of Sesn2 in patients with MPEs was 0.54±0.22ng/mL while in BPEs it was 0.12±0.04ng/mL (p=0.0004). In MPEs Sesn2 pleural fluid levels did not correlate with PF LDH and cell counts (p=0.89 and p=0.64 respectively). CONCLUSIONS: Our study shows that Sesn2 is significantly increased in MPEs compared to BPEs. Moreover, the lack of correlation of Sesn2 levels with PF cell counts and PF LDH suggests that it is potentially secreted by pleural mesothelial cells.
OBJECTIVES:Sestrin-2 (Sesn2) belongs to a family of highly conserved antioxidant proteins that were discovered as p53-inducible proteins and inhibits cell growth and proliferation. Our aim was to assess the levels of Sesn2 in malignant pleural effusions of lung cancerpatients compared to benign pleural effusions. DESIGN AND METHODS: We enrolled 73 patients (55/males and 18/females) diagnosed with pleural effusion (PE). PEs were grouped as 44 malignant pleural effusions (MPEs; lung cancer) and 29 benign (BPE; 7 congestive heart failure, 9 tuberculosis, 13 parapneumonic). Pleural fluid (PF) Sesn2 levels were determined by enzyme-linked immunosorbent assay (ELISA) kit. Standard biochemical PF analysis was also performed and Sesn2 levels were correlated with PF lactate dehydrogenase (LDH), protein, cell counts and age. RESULTS:Sesn2 was detected in 24/44 patients with MPEs and in 3/29 patients with BPEs (p=0.0001). The mean value (mean±SEM) of Sesn2 in patients with MPEs was 0.54±0.22ng/mL while in BPEs it was 0.12±0.04ng/mL (p=0.0004). In MPEs Sesn2pleural fluid levels did not correlate with PF LDH and cell counts (p=0.89 and p=0.64 respectively). CONCLUSIONS: Our study shows that Sesn2 is significantly increased in MPEs compared to BPEs. Moreover, the lack of correlation of Sesn2 levels with PF cell counts and PF LDH suggests that it is potentially secreted by pleural mesothelial cells.
Authors: Ourania S Kotsiou; Rajesh M Jagirdar; Eleftherios D Papazoglou; Chrissi Hatzoglou; Konstantinos I Gourgoulianis; Sotirios G Zarogiannis Journal: Inflammation Date: 2019-12 Impact factor: 4.657