<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10</volume><submitter>Sullivan MN</submitter><pubmed_abstract>&lt;b>Introduction:&lt;/b> Hypoxia-induced dilation of cerebral arteries orchestrated by Ca&lt;sup>2+&lt;/sup>-permeable transient receptor potential ankyrin 1 (TRPA1) cation channels on endothelial cells is neuroprotective during ischemic stroke, but it is unknown if the channel has a similar impact during hemorrhagic stroke. TRPA1 channels are endogenously activated by lipid peroxide metabolites generated by reactive oxygen species (ROS). Uncontrolled hypertension, a primary risk factor for the development of hemorrhagic stroke, is associated with increased ROS production and oxidative stress. Therefore, we hypothesized that TRPA1 channel activity is increased during hemorrhagic stroke. &lt;b>Methods:&lt;/b> Severe, chronic hypertension was induced in control (&lt;i>Trpa1&lt;/i> &lt;sup>fl/fl&lt;/sup>) and endothelia</pubmed_abstract><journal>Frontiers in molecular biosciences</journal><pagination>1129435</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9922848</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Endothelial cell TRPA1 activity exacerbates cerebral hemorrhage during severe hypertension.</pubmed_title><pmcid>PMC9922848</pmcid><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Sullivan MN</pubmed_authors><pubmed_authors>Krishnan V</pubmed_authors><pubmed_authors>Thakore P</pubmed_authors><pubmed_authors>Earley S</pubmed_authors><pubmed_authors>Feng Earley Y</pubmed_authors><pubmed_authors>Alphonsa S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Endothelial cell TRPA1 activity exacerbates cerebral hemorrhage during severe hypertension.</name><description>&lt;b>Introduction:&lt;/b> Hypoxia-induced dilation of cerebral arteries orchestrated by Ca&lt;sup>2+&lt;/sup>-permeable transient receptor potential ankyrin 1 (TRPA1) cation channels on endothelial cells is neuroprotective during ischemic stroke, but it is unknown if the channel has a similar impact during hemorrhagic stroke. TRPA1 channels are endogenously activated by lipid peroxide metabolites generated by reactive oxygen species (ROS). Uncontrolled hypertension, a primary risk factor for the development of hemorrhagic stroke, is associated with increased ROS production and oxidative stress. Therefore, we hypothesized that TRPA1 channel activity is increased during hemorrhagic stroke. &lt;b>Methods:&lt;/b> Severe, chronic hypertension was induced in control (&lt;i>Trpa1&lt;/i> &lt;sup>fl/fl&lt;/sup>) and endothelia</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-05T10:36:20.55Z</modification><creation>2025-04-05T10:36:20.55Z</creation></dates><accession>S-EPMC9922848</accession><cross_references><pubmed>36793787</pubmed><doi>10.3389/fmolb.2023.1129435</doi></cross_references></HashMap>