Background
Fibroblast dysfunction is the main pathogenic mechanism underpinning idiopathic pulmonary fibrosis (IPF). Potassium voltage-gated channel subfamily J member 2 (KCNJ2) plays critical roles in the proliferation of myofibroblasts and in the development of cardiac fibrosis. Objectives: This study aimed to evaluate the role of KCNJ2 in IPF.
Conclusion
KCNJ2 may participate in the development of IPF, and its protein level may be a candidate diagnostic and therapeutic molecule for IPF.
Methods
KCNJ2 mRNA expression was measured using real-time PCR in fibroblasts from IPF patients and normal controls (NCs). Protein concentrations were measured by ELISA in bronchoalveolar lavage (BAL) fluid obtained from NCs (n = 30), IPF (n = 30), IPF (n = 30), IPF (n = 30), IPF (n = 30), IPF (.
Results
KCNJ2 mRNA expression was measured using real-time PCR in fibroblasts from IPF patients and normal controls (NCs). Protein concentrations were measured by ELISA in bronchoalveolar lavage (BAL) fluid obtained from NCs (n = 30), IPF (n = 30), IPF (p < 0.001). KCNJ2 protein levels in BAL fluid were significantly higher in IPF (6.587 [1.441-26.01] ng/mL) than in NCs (0.084 [0.00-0.260] ng/mL, p < 0.001). KCNJ2 protein levels in BAL fluid were significantly higher in IPF (6.587 [1.441-26.01] ng/mL) than in NCs (0.084 [0.00-0.260] ng/mL, p < 0.001). KCNJ2 protein levels in BAL fluid were significantly higher in IPF (6.587 [1.441-26.01] ng/mL) than in NCs (0.084 [0.00-0.260] ng/mL, p < 0.001). KCNJ2 protein levels in BAL fluid were significantly higher in IPF (6.587 [1.441-26.01] ng/mL) than in NCs (0.084 [0.00-0.260] ng/mL, p < 0.001). KCNJ2 protein levels in BAL fluid were significantly higher in IPF (6.587 [1.441-26.01] ng/mL) than in NCs (0.084 [0.00-0.260] ng/mL.