V
V. Wee Yong
Researcher at University of Calgary
Publications - 276
Citations - 21024
V. Wee Yong is an academic researcher from University of Calgary. The author has contributed to research in topics: Multiple sclerosis & Microglia. The author has an hindex of 73, co-authored 233 publications receiving 17556 citations. Previous affiliations of V. Wee Yong include Allen Institute for Brain Science & Foothills Medical Centre.
Papers
More filters
Journal ArticleDOI
Differential activation of ERKs to focal adhesions by PKC ε is required for PMA-induced adhesion and migration of human glioma cells
TL;DR: First evidence that PKC ε is able to activate ERK at focal adhesions to mediate glioma cell adhesion and motility is presented, providing a molecular mechanism to explain the different biological functions of PKC α and ε inglioma cells.
Journal ArticleDOI
Metalloproteinases are enriched in microglia compared with leukocytes and they regulate cytokine levels in activated microglia
Robert K. Nuttall,Claudia Silva,Walter Hader,Amit Bar-Or,Kamala D. Patel,Dylan R. Edwards,V. Wee Yong +6 more
TL;DR: It is concluded thatmicroglia bear a metalloproteinase signature distinct from systemic cells, and that following activation, microglia upregulate TNF‐α protein levels through a combination of elevated cytokine transcripts, increased metallobroteinase level and activity, and through the decrease of TIMP3.
Journal ArticleDOI
When encephalitogenic T cells collaborate with microglia in multiple sclerosis.
Yifei Dong,V. Wee Yong +1 more
TL;DR: Several challenges are involved in translating T cell–microglia interactions identified in vitro or in animal models to MS, so these findings should be considered carefully when generalizing to the human disease.
Journal ArticleDOI
Biochemically altered myelin triggers autoimmune demyelination.
Andrew V. Caprariello,James A. Rogers,Megan L. Morgan,Vahid Hoghooghi,Jason R. Plemel,Adam Koebel,Shigeki Tsutsui,Jeff F. Dunn,Lakshmi P. Kotra,Shalina S. Ousman,V. Wee Yong,Peter K. Stys +11 more
TL;DR: By showing that a primary biochemical myelinopathy can trigger secondary pathological inflammation, “cuprizone autoimmune encephalitis” potentially reconciles conflicting theories about MS pathogenesis and provides a strong rationale for investigating myelin as a primary target for early, preventative therapy.
Journal ArticleDOI
Microglia and macrophage phenotypes in intracerebral haemorrhage injury: therapeutic opportunities.
TL;DR: The preclinical data support the use of deactivator or inhibitor of pro-inflammatory microglia/macrophages, whilst enhancing the regulatory phenotype, as part of the therapeutic approach to improve the prognosis of intracerebral haemorrhage.