Spontaneous intracerebral hemorrhage (ICH) is a common and often fatal stroke subtype. If the patient survives the ictus, the resulting hematoma within the brain parenchyma triggers a series of events leading to secondary insults and severe neurological deficits. Clot lysis plays an important role in the secondary brain injury following ICH. It is the long-term goal of our laboratory to identify the mechanisms involved in brain damage following ICH. After an ICH, lysis of erythrocytes in the hematoma results in brain edema formation, neuronal death and neurological deficits. Our previous studies demonstrated that the release of hemoglobin and its degradation products including iron from erythrocytes are involved in brain injury following ICH. Recent studies found that enhancing microglia/macrophage-mediated hematoma clearance improves functional outcome after ICH, and CD47 has an important role in erythrophagocytosis. Our preliminary studies have showed that erythrophagocytosis occurs in the brain after ICH and erythrocytes express CD47. In this application, we propose to test the following specific aims: 1) To determine whether CD-47 mediates hematoma clearance;and 2) To determine whether enhanced clot clearance reduces ICH-induced brain injury and improves behavioral outcome following ICH. We believe that the pilot studies proposed here should form a strong basis for a NIH R01 application. The long-term goal of our studies is to limit brain damage following ICH.
After a cerebral hemorrhage, lysis of red blood cells causes a build up of iron in the brain and brain iron accumulation can cause brain cell death and neurological deficits. Recent studies suggest that hematoma clearance is a therapeutic target of brain hemorrhage and enhancing clot clearance reduces hemorrhage- induced neurological deficits. The purpose of this project is to investigate the role of CD47 in clot clearance and brai injury after cerebral hemorrhage. The long-term goal of our studies is to limit brain damage following cerebral hemorrhage.
| Liu, Ran; Cao, Shenglong; Hua, Ya et al. (2017) CD163 Expression in Neurons After Experimental Intracerebral Hemorrhage. Stroke 48:1369-1375 |
| Dang, Ge; Yang, Yuefan; Wu, Gang et al. (2017) Early Erythrolysis in the Hematoma After Experimental Intracerebral Hemorrhage. Transl Stroke Res 8:174-182 |
| Guo, Dewei; Wilkinson, D Andrew; Thompson, B Gregory et al. (2017) MRI Characterization in the Acute Phase of Experimental Subarachnoid Hemorrhage. Transl Stroke Res 8:234-243 |
| Cao, Shenglong; Zheng, Mingzhe; Hua, Ya et al. (2016) Hematoma Changes During Clot Resolution After Experimental Intracerebral Hemorrhage. Stroke 47:1626-31 |
| Mao, Shanshan; Xi, Guohua; Keep, Richard F et al. (2016) Role of Lipocalin-2 in Thrombin-Induced Brain Injury. Stroke 47:1078-84 |
| Garton, Thomas; Keep, Richard F; Hua, Ya et al. (2016) Brain iron overload following intracranial haemorrhage. Stroke Vasc Neurol 1:172-184 |
| Wan, Shu; Cheng, Yingying; Jin, Hang et al. (2016) Microglia Activation and Polarization After Intracerebral Hemorrhage in Mice: the Role of Protease-Activated Receptor-1. Transl Stroke Res 7:478-487 |
| Sun, Na; Keep, Richard F; Hua, Ya et al. (2016) Critical Role of the Sphingolipid Pathway in Stroke: a Review of Current Utility and Potential Therapeutic Targets. Transl Stroke Res 7:420-38 |
| Ni, Wei; Mao, Shanshan; Xi, Guohua et al. (2016) Role of Erythrocyte CD47 in Intracerebral Hematoma Clearance. Stroke 47:505-11 |
| Chaudhary, Neeraj; Pandey, Aditya S; Gemmete, Joseph J et al. (2015) Diffusion tensor imaging in hemorrhagic stroke. Exp Neurol 272:88-96 |
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