<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>40(6)</volume><submitter>Young GH</submitter><pubmed_abstract>Our study aimed to establish the role of hemojuvelin (HJV) in acute ischemic stroke (AIS). We performed immunohistochemistry for HJV expression in human brain tissues from 10 AIS and 2 non-stroke autopsy subjects. Plasma HJV was measured in 112 AIS patients within 48 h after stroke. The results showed significantly increased HJV expression in brain tissues from AIS patients compare to non-stroke subjects. After adjusting for clinical variables, plasma levels of HJV within 48 h after stroke were an independent predictor of poor functional outcome three months post-stroke (OR:1.78, 95% CI: 1.03-3.07; &lt;i>P&lt;/i> = 0.038). In basic part, Western blotting showed that HJV expression in mice brains was apparent at 3 h after middle cerebral artery occlusion (MCAO), and increased significantly at 72 h. In cultured cortical neurons, expression of HJV protein increased remarkably 24 h after oxygen glucose deprivation (OGD), and small interfering RNAs (siHJV) transfected OGD neurons had a lower apoptotic rate. Importantly, 72 h post-MCAO, HJV knockout mice had significantly smaller infarcts and less expression of cleaved caspase-3 protein compared with wild-type mice. In summary, HJV participates in the mechanisms of post-stroke neuronal injury, and that plasma HJV levels can be a potential early outcome indicator for AIS patients.</pubmed_abstract><journal>Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism</journal><pagination>1316-1327</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7238368</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The functional role of hemojuvelin in acute ischemic stroke.</pubmed_title><pmcid>PMC7238368</pmcid><pubmed_authors>Wu VC</pubmed_authors><pubmed_authors>Jeng JS</pubmed_authors><pubmed_authors>Chiou HY</pubmed_authors><pubmed_authors>Tang SC</pubmed_authors><pubmed_authors>Wang KC</pubmed_authors><pubmed_authors>Hu CJ</pubmed_authors><pubmed_authors>Nong JY</pubmed_authors><pubmed_authors>Young GH</pubmed_authors><pubmed_authors>Hsu CY</pubmed_authors><pubmed_authors>Huang PY</pubmed_authors></additional><is_claimable>false</is_claimable><name>The functional role of hemojuvelin in acute ischemic stroke.</name><description>Our study aimed to establish the role of hemojuvelin (HJV) in acute ischemic stroke (AIS). We performed immunohistochemistry for HJV expression in human brain tissues from 10 AIS and 2 non-stroke autopsy subjects. Plasma HJV was measured in 112 AIS patients within 48 h after stroke. The results showed significantly increased HJV expression in brain tissues from AIS patients compare to non-stroke subjects. After adjusting for clinical variables, plasma levels of HJV within 48 h after stroke were an independent predictor of poor functional outcome three months post-stroke (OR:1.78, 95% CI: 1.03-3.07; &lt;i>P&lt;/i> = 0.038). In basic part, Western blotting showed that HJV expression in mice brains was apparent at 3 h after middle cerebral artery occlusion (MCAO), and increased significantly at 72 h. In cultured cortical neurons, expression of HJV protein increased remarkably 24 h after oxygen glucose deprivation (OGD), and small interfering RNAs (siHJV) transfected OGD neurons had a lower apoptotic rate. Importantly, 72 h post-MCAO, HJV knockout mice had significantly smaller infarcts and less expression of cleaved caspase-3 protein compared with wild-type mice. In summary, HJV participates in the mechanisms of post-stroke neuronal injury, and that plasma HJV levels can be a potential early outcome indicator for AIS patients.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Jun</publication><modification>2022-02-11T08:21:13.925Z</modification><creation>2022-02-11T08:21:13.925Z</creation></dates><accession>S-EPMC7238368</accession><cross_references><pubmed>31307288</pubmed><doi>10.1177/0271678x19861448</doi><doi>10.1177/0271678X19861448</doi></cross_references></HashMap>