Yi Yang

ORCID: 0000-0003-1493-2952
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About
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Research Areas
  • Barrier Structure and Function Studies
  • Neurological Disease Mechanisms and Treatments
  • Acute Ischemic Stroke Management
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Protease and Inhibitor Mechanisms
  • Intracerebral and Subarachnoid Hemorrhage Research
  • Signaling Pathways in Disease
  • S100 Proteins and Annexins
  • Cell Adhesion Molecules Research
  • Advanced Neuroimaging Techniques and Applications
  • Cerebrovascular and Carotid Artery Diseases
  • Cancer-related molecular mechanisms research
  • Extracellular vesicles in disease
  • Anesthesia and Neurotoxicity Research
  • Biochemical Analysis and Sensing Techniques
  • Heart Rate Variability and Autonomic Control
  • Immune cells in cancer
  • Eicosanoids and Hypertension Pharmacology
  • Neurological Disorders and Treatments
  • Vagus Nerve Stimulation Research
  • Cancer, Hypoxia, and Metabolism
  • Cardiac Ischemia and Reperfusion
  • Lipid metabolism and disorders
  • Bone and Joint Diseases
  • Peptidase Inhibition and Analysis

Hangzhou Normal University
2022-2025

University of New Mexico
2012-2025

First Hospital of Jilin University
2020-2023

Jilin University
2020-2023

National Yang Ming Chiao Tung University
2021

First People's Hospital of Chongqing
2020

Lovelace Respiratory Research Institute
2020

Biomedical Research Institute
2020

First Affiliated Hospital of Chinese PLA General Hospital
2000

Matrix metalloproteinases (MMPs) disrupt the blood—brain barrier (BBB) during reperfusion. Occludin and claudins are recently described tight junction proteins (TJPs) that form BBB. We hypothesized opening of BBB was because degradation TJPs by MMPs. Spontaneously hypertensive rats had a 90 mins middle cerebral artery occlusion with reperfusion for 2, 3, or 24 h. were measured immunohistochemistry in situ gel zymography. Real-time polymerase chain reaction (PCR) mRNAs MMP-2 −9, furin,...

10.1038/sj.jcbfm.9600375 article EN Journal of Cerebral Blood Flow & Metabolism 2006-07-19

Minocycline reduces reperfusion injury by inhibiting matrix metalloproteinases (MMPs) and microglia activity after cerebral ischemia. Prior studies of minocycline investigated short-term neuroprotective effects during subacute stage stroke; however, the late against early on neurovascular remodeling are less well studied. We have shown that spontaneous angiogenesis vessels in ischemic brain regions high blood–brain barrier (BBB) permeability due to lack major tight junction proteins (TJPs)...

10.1186/s12974-015-0245-4 article EN cc-by Journal of Neuroinflammation 2015-01-01

Increased permeability of the blood-brain barrier (BBB) is important in neurological disorders. Neuroinflammation associated with increased BBB breakdown and brain injury. Tumor necrosis factor (TNF)-α involved injury edema formation through a mechanism involving matrix metalloproteinase (MMP) up-regulation. There emerging evidence indicating that cyclooxygenase (COX) inhibition limits disruption following ischemic stroke bacterial meningitis, but mechanisms are not known. We used...

10.1124/jpet.107.127035 article EN Journal of Pharmacology and Experimental Therapeutics 2007-08-17

In cerebral ischemia, matrix metalloproteinases (MMPs) have a dual role by acutely disrupting tight junction proteins (TJPs) in the blood-brain barrier (BBB) and chronically promoting angiogenesis. Since TJP remodeling of neurovascular unit (NVU) is important recovery early inhibition MMPs neuroprotective, we hypothesized that short-term MMP would reduce infarct size promote angiogenesis after ischemia. Adult spontaneously hypertensive rats had transient middle artery occlusion with...

10.1038/jcbfm.2013.56 article EN Journal of Cerebral Blood Flow & Metabolism 2013-04-10

Small vessel disease is the major cause of white matter injury in patients with vascular cognitive impairment. Matrix metalloproteinase (MMP)-mediated inflammation may be involved damage oligodendrocyte (Ol) death. Therefore, we used spontaneously hypertensive stroke-prone rats to study role neuroinflammation damage.Permanent unilateral carotid artery occlusion was performed at 12 weeks age rats. Following surgery, were placed on a Japanese permissive diet and received 1% NaCl drinking...

10.1161/strokeaha.111.643080 article EN Stroke 2012-02-24

Angiogenesis, the growth of new blood vessels, is a natural defense mechanism helping to restore oxygen and nutrient supply affected brain tissue following an ischemic stroke. By stimulating vessel growth, angiogenesis may stabilize perfusion, thereby promoting neuronal survival, plasticity, neurologic recovery. However, therapeutic after stroke faces challenges: angiogenesis-induced vessels have higher than normal permeability, treatment promote exacerbate outcomes in patients. The...

10.2174/1570159x18666200720173316 article EN Current Neuropharmacology 2020-07-21

Hypertensive small vessel disease is a major cause of vascular cognitive impairment (VCI). Spontaneously hypertensive/stroke prone rats (SHR/SP) with unilateral carotid artery occlusion (UCAO) and Japanese permissive diet (JPD) have white-matter (WM) damage similar to that seen in VCI. We hypothesized WM injury was due hypoxia-mediated, blood–brain barrier (BBB) disruption. Twelve-week-old SHR/SP had UCAO/JPD were studied immunohistochemistry, biochemistry, multimodal magnetic resonance...

10.1038/jcbfm.2015.21 article EN Journal of Cerebral Blood Flow & Metabolism 2015-02-25

BackgroundVagus nerve stimulation (VNS) significantly reduces infarct volume in rat models of cerebral ischemia, but the mechanism this protective effect remains open.HypothesisThis study tested hypothesis that non-invasive VNS (nVNS), during transient middle artery occlusion (MCAO), protects blood-brain barrier (BBB), leading to reduced size ischemic brain.MethodsSpontaneous hypertensive rats (SHRs) were subjected a 90 min MCAO. nVNS treated received 5 stimulations (duration: 2 min; every...

10.1016/j.brs.2018.01.034 article EN cc-by-nc-nd Brain stimulation 2018-02-15

J. Neurochem. (2010) 112 , 134–149. Abstract Increased matrix metalloproteinase (MMP) activity is implicated in proteolysis of extracellular ischemic stroke. We recently observed intranuclear MMP brain neurons at early reperfusion, suggesting a possible role nuclear proteolysis. Nuclear proteins, poly‐ADP‐ribose polymerase‐1 (PARP‐1) and X‐ray cross‐complementary factor 1 (XRCC1), as well DNA repair enzymes, are important fragmentation cell apoptosis. hypothesized that facilitates oxidative...

10.1111/j.1471-4159.2009.06433.x article EN Journal of Neurochemistry 2009-10-15

Cyclooxygenase (COX)-2 and matrix metalloproteinase (MMP)-9 are two crucial mediators contributing to blood-brain barrier (BBB) damage during cerebral ischemia. However, it is not known whether MMP-9 activation involved in COX-2-mediated BBB disruption ischemic stroke. In this study, we hypothesized that genetic deletion or pharmacological inhibition of COX-2 reduces by reducing activity a mouse model Male knockout (COX-2-/-) wild-type (WT) mice were subjected 60 min middle artery occlusion...

10.3389/fneur.2020.00887 article EN cc-by Frontiers in Neurology 2020-08-20

Cerebral small vessel disease (SVD) contributes to approximately 50% of human dementias world-wide and pose a burden the health care system worldwide. Early endothelial/blood-brain barrier (BBB) dysfunction is an important contributor pathogenesis SVD. Sphingosine-1-phosphate (S1P), membrane-derived signaling sphingolipid, regulates BBB integrity by binding its receptor isoform 1 (S1PR1) on endothelial cells. We previously showed that activation S1PR1 using SEW2871, selective agonist,...

10.1161/str.56.suppl_1.wp391 article EN Stroke 2025-01-30

White matter (WM) injury after bilateral common carotid artery occlusion (BCAO) in rat is associated with disruption of the blood—brain barrier (BBB) by matrix metalloproteinases (MMPs). We hypothesized that WM as seen on magnetic resonance imaging (MRI) would correlate regions increased MMP activity. MRI was performed 3 days BCAO surgery rats. Apparent diffusion coefficients (ADC) were calculated and vascular permeability quantified multiple-time graphical analysis (MTGA) method, using...

10.1038/jcbfm.2008.121 article EN Journal of Cerebral Blood Flow & Metabolism 2008-10-22

Abstract Background and Purpose Oligodendrocyte (OL) death is important in focal cerebral ischemia. TIMP-3 promotes apoptosis ischemic neurons by inhibiting proteolysis of TNF-α superfamily receptors. Since OLs undergo during ischemia, we hypothesized that contributes to OL death. Methods Middle artery occlusion (MCAO) was induced Timp-3 knockout (KO) wild type (WT) mice with 24 or 72 h reperfusion. Cell white matter investigated stereology TUNEL. Mature immature were identified using...

10.1186/1742-2094-8-108 article EN cc-by Journal of Neuroinflammation 2011-08-29
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