<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Walsh TG</submitter><funding>British Heart Foundation</funding><pagination>e24</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6241850</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>1(1)</volume><pubmed_abstract>Platelets are classically known for their roles in bleeding control and occlusive thrombus formation causing ischaemic tissue damage. Recently non-classical roles for platelets have been described, many of which may be mediated by the heterogeneous cargo that platelets secrete from granular stores upon activation. Using an in vitro model of ischaemic injury to ventricular cardiomyocytes, we observed that platelets, through secreted factors, delayed the rate of cardiomyocyte death during ischaemia. This protective effect appeared independent of platelet dense granule cargo, but required α-granule components stromal cell-derived factor (SDF)-1α and transforming growth factor (TGF) β1. Protein kinase C (PKC) activity within cardiomyocytes was responsible for mediating the protective signals i</pubmed_abstract><journal>TH open : companion journal to thrombosis and haemostasis</journal><pubmed_title>Platelets Protect Cardiomyocytes from Ischaemic Damage.</pubmed_title><pmcid>PMC6241850</pmcid><funding_grant_id>PG/13/14/30023</funding_grant_id><funding_grant_id>RG/15/16/31758</funding_grant_id><funding_grant_id>RG/10/006/28299</funding_grant_id><pubmed_authors>Poole AW</pubmed_authors><pubmed_authors>Walsh TG</pubmed_authors></additional><is_claimable>false</is_claimable><name>Platelets Protect Cardiomyocytes from Ischaemic Damage.</name><description>Platelets are classically known for their roles in bleeding control and occlusive thrombus formation causing ischaemic tissue damage. Recently non-classical roles for platelets have been described, many of which may be mediated by the heterogeneous cargo that platelets secrete from granular stores upon activation. Using an in vitro model of ischaemic injury to ventricular cardiomyocytes, we observed that platelets, through secreted factors, delayed the rate of cardiomyocyte death during ischaemia. This protective effect appeared independent of platelet dense granule cargo, but required α-granule components stromal cell-derived factor (SDF)-1α and transforming growth factor (TGF) β1. Protein kinase C (PKC) activity within cardiomyocytes was responsible for mediating the protective signals i</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2025-04-04T08:41:15.712Z</modification><creation>2019-03-27T00:08:45Z</creation></dates><accession>S-EPMC6241850</accession><cross_references><pubmed>30465040</pubmed><doi>10.1055/s-0037-1603928</doi></cross_references></HashMap>