<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yarishkin O</submitter><funding>NEI NIH HHS</funding><funding>NCATS NIH HHS</funding><funding>U.S. Army Medical Research Acquisition Activity</funding><funding>National Institutes of Health</funding><pagination>805076</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9008486</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13</volume><pubmed_abstract>Trabecular meshwork (TM) cells are phagocytic cells that employ mechanotransduction to actively regulate intraocular pressure. Similar to macrophages, they express scavenger receptors and participate in antigen presentation within the immunosuppressive milieu of the anterior eye. Changes in pressure deform and compress the TM, altering their control of aqueous humor outflow but it is not known whether transducer activation shapes temporal signaling. The present study combines electrophysiology, histochemistry and functional imaging with gene silencing and heterologous expression to gain insight into Ca&lt;sup>2+&lt;/sup> signaling downstream from TRPV4 (Transient Receptor Potential Vanilloid 4), a stretch-activated polymodal cation channel. Human TM cells respond to the TRPV4 agonist GSK1016790A</pubmed_abstract><journal>Frontiers in immunology</journal><pubmed_title>Emergent Temporal Signaling in Human Trabecular Meshwork Cells: Role of TRPV4-TRPM4 Interactions.</pubmed_title><pmcid>PMC9008486</pmcid><funding_grant_id>R01 EY027920</funding_grant_id><funding_grant_id>R01EY027920, R01EY031817, P30EY014800, T32EY024234</funding_grant_id><funding_grant_id>P30 EY014800</funding_grant_id><funding_grant_id>VR200079</funding_grant_id><funding_grant_id>R01 EY031817</funding_grant_id><funding_grant_id>UL1 TR002538</funding_grant_id><funding_grant_id>T32 EY024234</funding_grant_id><pubmed_authors>Redmon SN</pubmed_authors><pubmed_authors>Hwang EM</pubmed_authors><pubmed_authors>Rudzitis CN</pubmed_authors><pubmed_authors>Freichel M</pubmed_authors><pubmed_authors>Overby D</pubmed_authors><pubmed_authors>Vazquez-Chona F</pubmed_authors><pubmed_authors>Baumann JM</pubmed_authors><pubmed_authors>Bertrand J</pubmed_authors><pubmed_authors>Yarishkin O</pubmed_authors><pubmed_authors>Phuong TTT</pubmed_authors><pubmed_authors>Krizaj D</pubmed_authors><pubmed_authors>van Battenburg-Sherwood J</pubmed_authors><pubmed_authors>Lakk M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Emergent Temporal Signaling in Human Trabecular Meshwork Cells: Role of TRPV4-TRPM4 Interactions.</name><description>Trabecular meshwork (TM) cells are phagocytic cells that employ mechanotransduction to actively regulate intraocular pressure. Similar to macrophages, they express scavenger receptors and participate in antigen presentation within the immunosuppressive milieu of the anterior eye. Changes in pressure deform and compress the TM, altering their control of aqueous humor outflow but it is not known whether transducer activation shapes temporal signaling. The present study combines electrophysiology, histochemistry and functional imaging with gene silencing and heterologous expression to gain insight into Ca&lt;sup>2+&lt;/sup> signaling downstream from TRPV4 (Transient Receptor Potential Vanilloid 4), a stretch-activated polymodal cation channel. Human TM cells respond to the TRPV4 agonist GSK1016790A</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-06-19T03:10:53.69Z</modification><creation>2025-02-19T00:56:46.114Z</creation></dates><accession>S-EPMC9008486</accession><cross_references><pubmed>35432302</pubmed><doi>10.3389/fimmu.2022.805076</doi></cross_references></HashMap>