Jinwei Pang

ORCID: 0000-0001-6559-3562
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About
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Research Areas
  • Intracranial Aneurysms: Treatment and Complications
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Intracerebral and Subarachnoid Hemorrhage Research
  • S100 Proteins and Annexins
  • Acute Ischemic Stroke Management
  • Mitochondrial Function and Pathology
  • Cancer-related molecular mechanisms research
  • Immune cells in cancer
  • Neurological Disease Mechanisms and Treatments
  • Barrier Structure and Function Studies
  • Moyamoya disease diagnosis and treatment
  • MicroRNA in disease regulation
  • Histone Deacetylase Inhibitors Research
  • Adipose Tissue and Metabolism
  • Endoplasmic Reticulum Stress and Disease
  • Lipid metabolism and disorders
  • Circular RNAs in diseases
  • Cancer, Hypoxia, and Metabolism
  • Neurosurgical Procedures and Complications
  • Mesenchymal stem cell research
  • Thyroid and Parathyroid Surgery
  • Cerebrovascular and Carotid Artery Diseases
  • Autophagy in Disease and Therapy
  • Eicosanoids and Hypertension Pharmacology

Affiliated Hospital of Southwest Medical University
2016-2025

Loma Linda University
2018-2024

Southwest Medical University
2021-2024

Shuguang Hospital
2008-2013

Shanghai University of Traditional Chinese Medicine
2008-2013

Oxidative stress and neuroinflammation play essential roles in ischemic stroke-induced brain injury. Previous studies have reported that Ezetimibe (Eze) exerts antioxidative anti-inflammatory properties hepatocytes. In the present study, we investigated effects of Eze on oxidative a rat middle cerebral artery occlusion (MCAO) model. One hundred ninety-eight male Sprague-Dawley rats were used. Animals assigned to MCAO given either or its control. To explore downstream signaling Eze, following...

10.1155/2020/4717258 article EN cc-by Oxidative Medicine and Cellular Longevity 2020-01-04

White matter injury (WMI) is associated with motor deficits and cognitive dysfunctions in subarachnoid hemorrhage (SAH) patients. Therapeutic strategy targeting WMI would likely improve the neurological outcomes after SAH. Low-density lipoprotein receptor-related protein-1 (LRP1), a scavenger receptor of apolipoprotein E (apoE), able to modulate microglia polarization towards anti-inflammatory M2 phenotypes during inflammatory oxidative insult. In present study, we investigated effects LRP1...

10.1016/j.redox.2019.101121 article EN cc-by-nc-nd Redox Biology 2019-01-27

Neuronal injury is the primary cause of poor outcome after subarachnoid hemorrhage (SAH). The apolipoprotein E (APOE) gene has been suggested to be involved in prognosis SAH patients. However, role APOE neuronal not well studied. In this study, was induced APOE-knockout (APOE-/-) and wild-type (WT) mice investigate impact deficiency on early phase SAH. experiments study were performed murine models vivo cultured microglia neurons vitro. model by endovascular perforation APOE-/- WT mice....

10.1155/2019/3832648 article EN Oxidative Medicine and Cellular Longevity 2019-12-26

Under subarachnoid hemorrhage (SAH) conditions, astrocytes undergo a marked intensification of glycolytic activity, resulting in the generation substantial amounts lactate to maintain energy demand for neurons and other brain cells. Lactate has garnered increasing attention recent years because its emerging role critical biological processes such as inflammation regulation neuroprotection, particularly through histone lactylation. Bromodomain-containing protein 4 (BRD4) plays crucial...

10.1186/s12974-024-03185-6 article EN cc-by-nc-nd Journal of Neuroinflammation 2024-07-30

β-Caryophyllene (BCP) mediates neuroprotection in cerebral ischemic animals. The neurovascular unit (NVU) acts as an intricate network to maintain the neuronal homeostatic microenvironment. However, effects exerted by BCP on NVU remain unclear. Therefore, we established vitro model investigate of oxygen-glucose deprivation and re-oxygenation (OGD/R)-induced injury. This involved co-culture brain microvascular endothelial cells, neurons, astrocytes. (10 μmol/L) was applied for 24 h prior...

10.1111/jnc.13833 article EN Journal of Neurochemistry 2016-08-27

BACKGROUND A carotid artery cavernous sinus fistula (CCF) is an abnormal shunt of blood vessels, allowing to flow directly or indirectly from the into sinus. The most common cause spontaneous CCF (s-CCF) ruptured internal carotid-cavernous aneurysms, while fibromuscular dysplasia (FMD) rare. FMD a rare, idiopathic, segmental, noninflammatory, and nonatherosclerotic disease medium-sized arteries, characterized by cell proliferation distortion arterial wall architecture. authors report case...

10.3171/case24622 article EN Journal of Neurosurgery Case Lessons 2025-03-31

Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is closely associated with neuroinflammation. Microglial activation an early event that leads to neuroinflammation after SAH. Peli1 E3 ubiquitin ligase mediates the induction of pro-inflammatory cytokines in microglia. Here we report contributions SAH mediated pathology. An model was induced by endovascular perforation adult male C57BL/6J mice. markedly mice brains a time-dependent manner and predominantly expressed...

10.3389/fnmol.2017.00398 article EN cc-by Frontiers in Molecular Neuroscience 2017-11-29

Subarachnoid haemorrhage (SAH) is a fatal neurovascular disease following cerebral aneurysm rupture with high morbidity and mortality rates. Long non-coding RNAs (lncRNAs) are type of mammalian genome transcript, abundantly expressed in the brain involved many nervous system diseases. However, little currently known regarding influence lncRNAs early injury (EBI) after SAH. This study analysed expression profiles mRNAs SAH tissues mice using high-throughput sequencing. The results showed...

10.1038/srep46577 article EN cc-by Scientific Reports 2017-04-18

Abstract Neuroinflammation has been reported to be associated with white matter injury (WMI) after subarachnoid hemorrhage (SAH). As the main resident immune cells of brain, microglia can activated into proinflammatory and anti‐inflammatory phenotypes. Toll‐like receptor 4 (TLR4), expressed on surface microglia, plays a key role in microglial inflammation. However, relationship between TLR4, polarization, WMI following SAH remains unclear. In this study, total 121 male adult C57BL/6...

10.1111/jnc.15851 article EN Journal of Neurochemistry 2023-06-13

Subarachnoid hemorrhage (SAH) is a devastating form of stroke, which poses series intractable challenges to clinical practice. Imbalance mitochondrial homeostasis has been thought be the crucial pathomechanism in early brain injury (EBI) cascade after SAH. Irisin, protein related metabolism and homeostasis, reported play pivotal roles post-stroke neuroprotection. However, whether this myokine can exert neuroprotection effects SAH remains unknown. In present study, we explored protective...

10.3389/fnagi.2021.640215 article EN cc-by Frontiers in Aging Neuroscience 2021-02-03

To investigate whether porotic changes occur in maxillary alveolar bone ovariectomized rats.Thirty-two 6-week-old female Sprague-Dawley rats were divided into an ovariectomy group (OVX) and a sham-ovariectomy (sham). Twelve weeks after surgery, maxillae of 16 (eight OVX eight sham) analyzed by micro-CT. Inter-radicular the first molar was reconstructed analyzed. The remaining used for histochemistry, including hematoxylin-eosin staining tartrate-resistant acid phosphatase enzyme...

10.1111/odi.12166 article EN Oral Diseases 2013-07-22

Neuroinflammation can be caused by various factors in early brain injury after subarachnoid hemorrhage (SAH). One of the most important features this process is M1 microglial activation. In turn, TLR4/NF-κB pathway plays an essential role activating phenotypic microglia. Biglycan, a small leucine-rich proteoglycan, functions as endogenous ligand TLR4 and TLR2 macrophages. However, underlying mechanisms associated with activation stroke pathogenesis are poorly understood. Here, we aimed to...

10.1111/jnc.14926 article EN Journal of Neurochemistry 2019-11-28

Traumatic brain injury (TBI) disrupts the blood–brain barrier (BBB) and reduces cerebral glucose uptake. Vascular endothelial growth factor (VEGF) is believed to play a key role in TBI, COG1410 has demonstrated neuroprotective activity several models of TBI. However, effects on VEGF metabolism following TBI are unknown. The current study aimed investigate expression C57BL/6J male mice subjected experimental results showed that controlled cortical impact (CCI)-induced vestibulomotor deficits...

10.1089/neu.2016.4485 article EN Journal of Neurotrauma 2016-07-14

COG1410, a mimetic peptide derived from the apolipoprotein E (apoE) receptor binding region, exerts positive effect on neurological deficits in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH). Currently neuroprotective of COG1410 includes inhibiting BBB disruption, reducing neuronal apoptosis and neuroinflammation. However, mechanism to subcellular organelles disorder have not been fully investigated. As main pathway for recycling long-lived proteins damaged...

10.3389/fnins.2018.00127 article EN cc-by Frontiers in Neuroscience 2018-03-04

// Jinwei Pang 1,* , Yue Wu 2,* Jianhua Peng 1 Ping Yang 3 Li Kuai 4 Xinghu Qin Fang Cao 5 Xiaochuan Sun 2 Ligang Chen Michael P. Vitek 6 and Yong Jiang Department of Neurosurgery, The Affiliated Hospital Southwest Medical University, Luzhou, China Departement First Chongqing Chongqing, Vasculocardiology, Ophthalmology, Neurovascular Disease, Zunyi College, Zunyi, Medicine (Neurology), Duke University Center, Durham, North Carolina, United States * co-first authors Correspondence to: Jiang,...

10.18632/oncotarget.10821 article EN Oncotarget 2016-07-24

Circular RNA phosphorylase kinase regulatory subunit alpha 2 (circPHKA2; hsa_circ_0090002) has a significantly, specifically different expression in acute ischemic stroke (AIS) patients' blood. Here, we intended to investigate the role and mechanism of circPHKA2 oxygen-glucose deprivation- (OGD-) induced stoke model human brain microvascular endothelial cells (HBMEC).Expression circPHKA2, microRNA- (miR-) 574-5p, superoxide dismutase-2 (SOD2) was detected by quantitative PCR western...

10.1155/2021/3823122 article EN cc-by Oxidative Medicine and Cellular Longevity 2021-01-01
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