{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:47:02Z","timestamp":1787017622248,"version":"build-2736575974"},"reference-count":42,"publisher":"American Physiological Society","issue":"1","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["R01HL137807"],"award-info":[{"award-number":["R01HL137807"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"name":"JHU Blaustein Pain Research Fund Award","award":["80048814"],"award-info":[{"award-number":["80048814"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2020,1,1]]},"abstract":"<jats:p>\n                    We evaluated the mechanisms underlying protease-activated receptor 1 (PAR1)-mediated activation of nodose C-fibers in mouse lungs. The PAR1-induced action potential discharge at the terminals was strongly inhibited in phospholipase C-\u03b23 (PLC\u03b23)-deficient animals. At the level of the cell soma, PAR1 activation led to an increase in cytosolic calcium that was largely inhibited by transient receptor potential (TRP) A1 antagonism. Patch-clamp recordings, however, revealed that neither TRPA1 nor TRPV1 or any other ruthenium red-sensitive ion channels are required for the PAR1-mediated inward current or membrane depolarization in isolated nodose neurons. Consistent with these findings, PAR1-mediated action potential discharge in mouse lung nodose C-fiber terminals was unaltered in Trpa1\/ Trpv1 double-knockout animals and Trpc3\/ Trpc6 double-knockout animals. The activation of the C-fibers was also not inhibited by ruthenium red at concentrations that blocked TRPV1- and TRPA1-dependent responses. The biophysical data show that PAR1\/G\n                    <jats:sub>q<\/jats:sub>\n                    -mediated activation of nodose C-fibers may involve multiple ion channels downstream from PLC\u03b23 activation. TRPA1 is an ion channel that participates in PAR1\/G\n                    <jats:sub>q<\/jats:sub>\n                    -mediated elevation in intracellular calcium. There is little evidence, however, that TRPA1, TRPV1, TRPC3, TRPC6, or other ruthenium red-sensitive TRP channels are required for PAR1\/G\n                    <jats:sub>q<\/jats:sub>\n                    -PLC\u03b23-mediated membrane depolarization and action potential discharge in bronchopulmonary nodose C-fibers in the mouse.\n                  <\/jats:p>","DOI":"10.1152\/ajplung.00301.2019","type":"journal-article","created":{"date-parts":[[2019,10,30]],"date-time":"2019-10-30T15:28:05Z","timestamp":1572449285000},"page":"L192-L199","source":"Crossref","is-referenced-by-count":11,"title":["Role of TRP channels in G\n                    <sub>q<\/sub>\n                    -coupled protease-activated receptor 1-mediated activation of mouse nodose pulmonary C-fibers"],"prefix":"10.1152","volume":"318","author":[{"given":"Hui","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, 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