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Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury Thomas KC; Roberts JK; Deering-Rice CE; Romero EG; Dull RO; Lee J; Yost GS; Reilly CAAm J Physiol Lung Cell Mol Physiol 2012[Jan]; 302 (1): L111-9Endogenous agonists of transient receptor potential vanilloid-1 (TRPV1) (endovanilloids) are implicated as mediators of lung injury during inflammation. This study tested the hypothesis that endovanilloids produced following lipopolysaccharide (LPS) treatment activate TRPV1 and cause endoplasmic reticulum stress/GADD153 expression in lung cells, representing a mechanistic component of lung injury. The TRPV1 agonist nonivamide induced GADD153 expression and caused cytotoxicity in immortalized and primary human bronchial, bronchiolar/alveolar, and microvascular endothelial cells, proportional to TRPV1 mRNA expression. In CF-1 mice, Trpv1 mRNA was most abundant in the alveoli, and intratracheal nonivamide treatment promoted Gadd153 expression in the alveolar region. Treatment of CF-1 mice with LPS increased Gadd153 in the lung, lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, and lung wet-to-dry weight ratio. Cotreating mice with LPS and the TRPV1 antagonist LJO-328 reduced Gadd153 induction and LDH in BAL but did not inhibit increases in lung wet-to-dry ratio. In Trpv1(-/-) mice treated with LPS, Gadd153 induction and LDH in BAL were reduced relative to wild-type mice, and the wet-to-dry weight ratios of lungs from both wild-type and Trpv1(-/-) mice decreased. Organic extracts of blood collected from LPS-treated mice were more cytotoxic to TRPV1-overexpressing cells compared with BEAS-2B cells and extracts from control mice, however, most pure endovanilloids did not produce cytotoxicity in a characteristic TRPV1-dependent manner. Collectively, these data indicate a role for TRPV1, and endogenous TRPV1 agonists, in ER stress and cytotoxicity in lung cells but demonstrate that ER stress and cytotoxicity are not essential for pulmonary edema.|*Lung/cytology/metabolism[MESH]|Animals[MESH]|Bronchi/metabolism[MESH]|Bronchoalveolar Lavage Fluid/chemistry[MESH]|Capsaicin/analogs & derivatives/pharmacology[MESH]|Cell Death[MESH]|Cell Line[MESH]|Cell Line, Transformed[MESH]|Cells, Cultured[MESH]|Endoplasmic Reticulum Stress/*genetics[MESH]|Humans[MESH]|Inflammation/metabolism[MESH]|L-Lactate Dehydrogenase/metabolism[MESH]|Lipopolysaccharides/pharmacology[MESH]|Lung Injury/*physiopathology[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Pulmonary Alveoli/*metabolism[MESH]|Pulmonary Edema/metabolism[MESH]|TRPV Cation Channels/*agonists/genetics[MESH]|Transcription Factor CHOP/genetics/metabolism[MESH] |