{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"submitter":["del Zoppo GJ"],"funding":["NINDS NIH HHS"],"pagination":["919-32"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3345906"],"abstract":["Hemorrhage and edema accompany evolving brain tissue injury after ischemic stroke. In patients, these events have been associated with metalloproteinase (MMP)-9 in plasma. Both the causes and cellular sources of MMP-9 generation in this setting have not been defined. MMP-2 and MMP-9 in nonhuman primate tissue in regions of plasma leakage, and primary murine microglia and astrocytes, were assayed by immunocytochemistry, zymography, and real-time RT-PCR. Ischemia-related hemorrhage was associated with microglial activation in vivo, and with the leakage of plasma fibronectin and vitronectin into the surrounding tissue. In strict serum-depleted primary cultures, by zymography, pro-MMP-9 was generated by primary murine microglia when exposed to vitronectin and fibronectin. Protease secretion was enhanced by experimental ischemia (oxygen-glucose deprivation, OGD). Primary astrocytes, on each matrix, generated only pro-MMP-2, which decreased during OGD. Microglia-astrocyte contact enhanced pro-MMP-9 generation in a cell density-dependent manner under normoxia and OGD. Compatible with observations in a high quality model of focal cerebral ischemia, microglia, but not astrocytes, respond to vitronectin and fibronectin, found when plasma extravasates into the injured region. Astrocytes alone do not generate pro-MMP-9. These events explain the appearance of MMP-9 antigen in association with ischemia-induced cerebral hemorrhage and edema."],"repository":["biostudies-other"],"data_source":["Europe PMC"],"omics_type":["Unknown"],"volume":["32(5)"],"journal":["Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism"],"pmcid":["PMC3345906"],"funding_grant_id":["R01 NS026945","R01 NS053716","NS 026945","R01 NS038710","NS 053716","NS 038710","R37 NS038710"],"pubmed_authors":["Frankowski H","Osada T","Mabuchi T","Koziol JA","Hosomi N","Kanazawa M","Wang X","del Zoppo GJ","Milner R","Gu YH"],"additional_accession":[]},"is_claimable":false,"name":"Microglial cell activation is a source of metalloproteinase generation during hemorrhagic transformation.","description":"Hemorrhage and edema accompany evolving brain tissue injury after ischemic stroke. In patients, these events have been associated with metalloproteinase (MMP)-9 in plasma. Both the causes and cellular sources of MMP-9 generation in this setting have not been defined. MMP-2 and MMP-9 in nonhuman primate tissue in regions of plasma leakage, and primary murine microglia and astrocytes, were assayed by immunocytochemistry, zymography, and real-time RT-PCR. Ischemia-related hemorrhage was associated with microglial activation in vivo, and with the leakage of plasma fibronectin and vitronectin into the surrounding tissue. In strict serum-depleted primary cultures, by zymography, pro-MMP-9 was generated by primary murine microglia when exposed to vitronectin and fibronectin. Protease secretion was enhanced by experimental ischemia (oxygen-glucose deprivation, OGD). Primary astrocytes, on each matrix, generated only pro-MMP-2, which decreased during OGD. Microglia-astrocyte contact enhanced pro-MMP-9 generation in a cell density-dependent manner under normoxia and OGD. Compatible with observations in a high quality model of focal cerebral ischemia, microglia, but not astrocytes, respond to vitronectin and fibronectin, found when plasma extravasates into the injured region. Astrocytes alone do not generate pro-MMP-9. These events explain the appearance of MMP-9 antigen in association with ischemia-induced cerebral hemorrhage and edema.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 May","modification":"2019-03-27T00:53:11Z","creation":"2019-03-27T00:53:11Z"},"accession":"S-EPMC3345906","cross_references":{"pubmed":["22354151"],"doi":["10.1038/jcbfm.2012.11 "]}}