Hang Jin

Jilin University, Yung-chi, Jilin Sheng, China

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Publications (5)11.01 Total impact

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    ABSTRACT: Thrombin causes blood-brain barrier disruption, and this study examined whether thrombin can cause brain hemorrhage through protease-activated receptor-1 (PAR-1). Male wild type and PAR-1 knockout mice had an intracerebral injection of thrombin or saline. Mice then underwent serial T2 magnetic resonance imaging and were euthanized for brain hemoglobin, iron, and interleukin-1β measurements. Thrombin caused massive T2 lesions and brain hemorrhage in wild type mice. These effects were markedly reduced in PAR-1 knockout mice. Thrombin also increased brain interleukin-1β, and this was absent in PAR-1 knockout mice. In conclusion, thrombin increases interleukin-1β levels and induces intracerebral hemorrhage through PAR-1 activation.
    Translational Stroke Research 09/2013; 5(4). DOI:10.1007/s12975-013-0288-8 · 2.44 Impact Factor
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    ABSTRACT: Magnetic resonance imaging (MRI) has been widely used in intracerebral hemorrhage (ICH) animal models and patients. In the current study, we examined whether MRI can predict at-risk brain tissue during the acute phase and long-term brain tissue loss after ICH. Male Sprague-Dawley rats had an intracaudate injection of autologous whole blood (10, 50 or 100 μL). MRI (T2 and T2*) sequences were performed at days 1, 3, 7, 14, and 28. The volume of brain tissue at risk was calculated as the difference between T2 and T2* lesion volumes. Dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32) was used as a neuronal marker in the basal ganglia. Brain swelling at day 3 and brain tissue loss at day 28 after ICH were also measured. We found that the difference in lesion volumes between T2 and T2* measured by MRI coincided well with the difference between the volume of the DARPP-32-negative area and that of the hematoma measured in brain sections. Volumes of brain tissue at risk at day 3 correlated with the brain swelling at day 3 (p < 0.01) as well as the final brain tissue loss at day 28 (n = 9, p < 0.05). The results suggest that the difference between T2 lesions and T2* lesions could be an indicator of at-risk brain tissue and it could be used as a predictor of neuronal loss in ICH patients.
    Acta neurochirurgica. Supplement 04/2013; 118:151-5. DOI:10.1007/978-3-7091-1434-6_28
  • Hang Jin · Guohua Xi · Richard F Keep · Jiang Wu · Ya Hua
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    ABSTRACT: Quantification of acute brain injury in basal ganglia is essential for mechanistic and therapeutic studies in experimental intracerebral hemorrhage (ICH). Using conventional counting of degenerating cells based on morphological or immunohistochemical criteria, it is hard to define the boundary of the whole lesion area. Dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32) is a cytosolic protein highly enriched in medium-sized spiny neurons of the striatum. We developed new methods for quantifying lesion area by detecting the difference of the DARPP-32 negative area and the hematoma clot, and by measuring DARPP-32 protein level for semi-qualification in rat model of ICH. We found that DARPP-32 negative area around hematoma was present at day-1, peaked at day-3, and decreased at day-14 after ICH, a time course paralleled by DARPP-32 Western blots. The DARPP-32 negative area matched well with the necrotic area determined using propidium iodide. Treatment with an iron chelator, deferoxamine, attenuated the ICH-induced reduction in DARPP-32 protein levels. These results suggest that DARPP-32 is a simple and quantifiable indicator of ICH-induced neuronal death in basal ganglia.
    02/2013; 4(1):130-134. DOI:10.1007/s12975-012-0232-3
  • Jinhu Wang · Hang Jin · Ya Hua · Richard F Keep · Guohua Xi
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    ABSTRACT: Evidence suggests that the protease-activated receptor-1 (PAR-1), a thrombin receptor, mediates neuronal injury in experimental cerebral ischemia. The present study investigated whether PAR-1 plays a role in brain injury after global cerebral ischemia. Adult male wild-type or PAR-1 knockout mice underwent a 20-minute bilateral common carotid artery occlusion or a sham operation. Behavior tests were performed before ischemia and 1, 2, and 3 days after bilateral common carotid artery occlusion. Mice were euthanized at different time points for thrombin activity, brain edema, Western blot analysis, and brain histology. Thrombin activity and PAR-1 expression were increased in the brain after bilateral common carotid artery occlusion. Compared with wild-type mice, PAR-1 knockout mice had less brain edema formation, neuronal death, and behavior impairment after bilateral common carotid artery occlusion. In addition, bilateral common carotid artery occlusion-induced activation of mitogen-activated protein kinases was absent in PAR-1 knockout mice. PAR-1 contributes to the brain injury induced by global cerebral ischemia, which may be related to activation of mitogen-activated protein kinases.
    Stroke 07/2012; 43(9):2476-82. DOI:10.1161/STROKEAHA.112.661819 · 5.72 Impact Factor
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    ABSTRACT: Autophagy occurs in the brain after intracerebral hemorrhage (ICH) and thrombin contributes to ICH-induced brain injury and cell death. In this study, we investigated whether thrombin may activate autophagy (in vivo and in cultured astrocytes) and its potential role in ICH. Autophagy was examined using electron microscopy, conversion of light chain 3(LC3) from the LC3-I form to LC3-II, cathepsin D Western blotting and monodansylcadaverine (MDC) staining to detect autophagic vacuoles. 3-Methyladenine (3-MA) was used as an autophagy inhibitor. In vivo, we found that intracaudate injection of thrombin increased conversion of LC3-I to LC3-II, cathepsin D levels, and formation of autophagic vacuoles in the ipsilateral basal ganglia. ICH-induced upregulation of LC3-I to LC3-II conversion and cathepsin D levels was reduced by a thrombin inhibitor, hirudin. In cultured astrocytes, thrombin enhanced the conversion of LC3-I to LC3-II and increased MDC-labeled autophagic vacuoles. 3-MA inhibited thrombin-induced autophagic vacuole formation and exacerbated thrombin-induced cell death. These results indicate that thrombin activates autophagy in the brain and that thrombin has a role in ICH-induced autophagy.
    Brain research 11/2011; 1424:60-6. DOI:10.1016/j.brainres.2011.09.062 · 2.84 Impact Factor

Publication Stats

34 Citations
11.01 Total Impact Points


  • 2013
    • Jilin University
      Yung-chi, Jilin Sheng, China
  • 2011–2013
    • University of Michigan
      • Department of Neurosurgery
      Ann Arbor, Michigan, United States