Zhiping Mi

ORCID: 0000-0001-9499-6926
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • S100 Proteins and Annexins
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Neuropeptides and Animal Physiology
  • Ubiquitin and proteasome pathways
  • Nerve injury and regeneration
  • 14-3-3 protein interactions
  • Retinoids in leukemia and cellular processes
  • Cancer therapeutics and mechanisms
  • Metabolomics and Mass Spectrometry Studies
  • Pain Mechanisms and Treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Cell death mechanisms and regulation
  • Pharmacological Effects and Assays
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Peroxisome Proliferator-Activated Receptors
  • Protein Tyrosine Phosphatases
  • Melanoma and MAPK Pathways
  • RNA regulation and disease
  • Memory and Neural Mechanisms
  • Computational Drug Discovery Methods
  • Nuclear Receptors and Signaling
  • Neurological disorders and treatments

University of Pittsburgh
2013-2024

Shanxi Datong University
2024

VA Pittsburgh Healthcare System
2016-2023

Geriatric Research Education and Clinical Center
2016-2023

Barrow Neurological Institute
2016

University of Rochester Medical Center
2008-2011

Golisano Children's Hospital
2011

University of Rochester
2009

Boston Children's Hospital
2005-2006

Children's Hospital of Pittsburgh
2006

The α6 subunit of the γ-aminobutyric acid type A receptor (GABA<sub>A</sub>-R) has been implicated in mediating intoxicating effects ethanol and motor ataxic general anesthetics. To test this hypothesis, we used gene targeting embryonic stem cells to create mice lacking a functional gene. Homozygous are viable fertile have grossly normal cerebellar cytoarchitecture. Northern blot reverse transcriptase-polymerase chain reaction analyses demonstrated that event disrupted production mRNA....

10.1124/mol.51.4.588 article EN Molecular Pharmacology 1997-04-01

Ubiquitin C-terminal hydrolase L1 (UCHL1) is a unique brain-specific deubiquitinating enzyme. Mutations in and aberrant function of UCHL1 have been linked to many neurological disorders. activity protects neurons from hypoxic injury, binding stroke-induced reactive lipid species the cysteine 152 (C152) unfolds protein disrupts its function. To investigate role adduction by lipids inhibiting repair recovery following ischemic knock-in (KI) mouse expressing C152A mutation was generated....

10.1073/pnas.1821282116 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2019-02-13

Tenascin-C (TN-C) is an extracellular matrix glycoprotein linked to inflammatory processes in pathological conditions including Alzheimer disease (AD). We examined the distribution of TN-C immunoreactivity (ir) relation amyloid-β (Aβ) plaques and vascular Aβ deposits autopsy brain tissues from 14 patients with clinical neuropathological AD 10 aged-matched controls no cognitive impairment; 5 had did not. ir was abundant cortical white matter subpial cerebral gray all cases, whereas weak blood...

10.1093/jnen/nlw062 article EN public-domain Journal of Neuropathology & Experimental Neurology 2016-07-21

Background: Altered glutamatergic neurotransmission may contribute to impaired default mode network (DMN) function in Alzheimer’s disease (AD). Among the DMN hub regions, frontal cortex (FC) was suggested undergo a plasticity response prodromal AD, while status of synapses precuneus (PreC) during clinical-neuropathological AD progression is not known. Objective: To quantify vesicular glutamate transporter VGluT1- and VGluT2-containing synaptic terminals PreC FC across clinical stages AD....

10.3233/jad-221063 article EN Journal of Alzheimer s Disease 2023-05-19

Our previous studies demonstrated that p75NTR confers protection against oxidative stress-induced apoptosis upon PC12 cells; however, the mechanisms responsible for this effect are not known. The present reveal decreased mitochondrion membrane potential and increased generation of reactive oxygen species (ROS) in p75NTR-deficient cells as well diminution ROS after transfection a full-length construct into these cells. They also show deficiency attenuates activation phosphatidylinositol...

10.1111/j.1471-4159.2009.06137.x article EN Journal of Neurochemistry 2009-04-30

This post mortem immunohistochemical study examined the localization and distribution of ubiquilin‐1 ( UBL ), a shuttle protein which interacts with ubiquitin proteasome, in hippocampus from A lzheimer's disease AD ) dementia cases, age‐matched cases without dementia. In B raak stages 0– I – II immunoreactivity was detected dense fiber network neuropil, cell cytoplasm nucleoplasm neurons Cornu Ammonis CA fields dentate gyrus granular neurons. III ‐ IV V VI reduced neuropil majority CA1...

10.1111/neup.12055 article EN Neuropathology 2013-07-21

Studies of acetylcholine degrading enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) in Alzheimer's disease (AD) have suggested their potential role the development fibrillar amyloid‐β (Aβ) plaques (amyloid plaques). A recent genome‐wide association study analysis identified a novel between genetic variations BCHE locus amyloid burden. We studied BChE immunoreactivity hippocampal tissue sections from AD control cases, examined its relationship with plaques, neurofibrillary...

10.1111/neup.12241 article EN public-domain Neuropathology 2015-08-21

The p75 neurotrophin receptor (p75NTR) is an α‐and γ‐secretase substrate expressed preferentially in the cholinergic neurons of nucleus basalis Meynert, hippocampus, and cerebellum adult brain. Mutations γ‐secretase, presenilin, have been implicated familial Alzheimer′s disease. Furthermore, oxidative inflammatory injury to Meynert hippocampus plays a critical role pathology intracellular domain p75NTR (p75ICD) α‐ cleavage fragment holoreceptor that functions as antioxidant PC12 rat...

10.4161/oxim.2.4.9745 article EN cc-by Oxidative Medicine and Cellular Longevity 2009-01-01

The intracellular domain (ICD) of the neurotrophin receptor, p75NTR, exhibits variably pro- and antiapoptotic activity has been implicated in neurodegenerative neurodestructive disease. molecular determinants these cellular effects are not completely understood. "Chopper" p75ICD shown to be proapoptotic vitro systems which is proapoptotic. Chopper and, therefore, whether or accounts for variability known. We therefore examined deletion on cell culture antiapoptotic, respectively.In HN33.11...

10.1155/2011/391659 article EN Oxidative Medicine and Cellular Longevity 2011-01-01

IMMUNOCYTOCHEMICAL staining for serotonin (5-HT), tyrosine hydroxylase (TH) and galanin (GAL) was combined with horseradish peroxidase (HRP) retrograde tract-tracing technique to analyze the localizations of 5-HT-, catechalomine (CA)- GAL-containing neurons in brainstem which project nucleus parafascicularis (PF) rats. It is demonstrated that most retrogradely HRP-labeled (70%) bilateral periaqueductal gray (PAG) raphe nuclei are positively immunostained by antiserum 5-HT, (over 80%) locus...

10.1097/00001756-199202000-00003 article EN Neuroreport 1992-02-01

Ubiquitin C-terminal hydrolase L1 (UCHL1) is a neuronal protein important in maintaining axonal integrity and motor function may be the pathogenesis of many neurological disorders. UCHL1 ameliorate acute injury improve recovery after cerebral ischemia. In current study, hypothesis that UCHL1’s activity underlies its effect tested ischemic injury. Hydrolase was inhibited by treatment with inhibitor or employing knockin mice bearing mutation active site (C90A). Ischemic induced oxygen-glucose...

10.1177/0271678x241258809 article EN Journal of Cerebral Blood Flow & Metabolism 2024-06-04

To investigate the molecular mechanism of autophagy and apoptosis induced by ultrafine carbon black in human bronchial epithelial cells (BEAS-2B cells), to study intervention effect N-acetylcysteine (NAC) on black-induced oxidative damage BEAS-2B cells.

10.3760/cma.j.cn121094-20231010-00080 article EN PubMed 2024-09-20

Pyroglutamate-modified amyloid-β (AβNpE) peptides are present in amyloid deposits Alzheimer's disease (AD). The relationship of AβNpE with PET ligands such as Pittsburgh Compound-B (PiB) and cognitive status preclinical clinical AD is not fully understood. We reported that AβNpE3-42 Aβ1-42 dominated the insoluble Aβ pool posterior cingulate precuneus cortical association areas correlated antemortem cognition subjects no impairment (NCI), mild (MCI), AD. study quantified AβNpE3 full-length...

10.1016/j.jalz.2016.06.1548 article EN Alzheimer s & Dementia 2016-07-01
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