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Background:  The release of inflammatory molecules such as prostaglandins (e.g., PGF 2α ) is associated with brain damage following an intracerebral hemorrhagic (ICH) stroke; however, the role of PGF 2α  and its cognate FP receptor in ICH remains unclear. This study focused on investigating the role of the FP receptor as a target for novel neuroprotective drugs in a preclinical model of ICH, aiming to investigate the contribution of the PGF 2α -FP axis in modulating functional recovery and anatomical outcomes following ICH.   Results:  Neurological deficit scores in FP −/−  mice were significantly higher compared to WT mice 72 h after ICH (6.1 ± 0.7 vs. 3.1 ± 0.8;  P  < 0.05). Assessing motor skills, the total time mice stayed on the rotating rod was significantly less in FP −/− mice compared to WT mice 24 h after ICH (27.0 ± 7.5 vs. 52.4 ± 11.2 s;  P  < 0.05). Using grip strength to quantify forepaw strength, results showed that the FP −/−  mice had significantly less strength compared to WT mice 72 h after ICH (96.4 ± 17.0 vs. 129.6 ± 5.9 g;  P  < 0.01). In addition to the behavioral outcomes, histopathological measurements were made. In Cresyl violet stained brain sections, the FP −/−  mice showed a significantly larger lesion volume compared to the WT (15.0 ± 2.2 vs. 3.2 ± 1.7 mm 3 ;  P  < 0.05 mice.) To estimate the presence of ferric iron in the peri-hematoma area, Perls' staining was performed, which revealed that FP −/−  mice had significantly greater staining than the WT mice (186.3 ± 34.4% vs. 86.9 ± 13.0% total positive pixel counts,  P  < 0.05). Immunoreactivity experiments on brain sections from FP −/−  and WT mice post-ICH were performed to monitor changes in microgliosis and astrogliosis using antibodies against Iba1 and GFAP respectively. These experiments showed that FP −/−  mice had a trend toward greater astrogliosis than WT mice post-ICH.   Conclusion:  We showed that deletion of the PGF 2α  FP receptor exacerbates behavioral impairments and increases lesion volumes following ICH compared to WT-matched controls.Detailed mechanisms responsible for these novel results are actively being pursued.

Genetic Deletion of PGF2α-FP Receptor Exacerbates Brain Injury Following Experimental Intracerebral Hemorrhage