Premium
Lentiviral transduction of murine oligodendrocytes in vivo
Author(s) -
McIver Sally R.,
Lee ChulSang,
Lee JinMoo,
Green Steven H.,
Sands Mark S.,
Snider B. Joy,
Goldberg Mark P.
Publication year - 2005
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20626
Subject(s) - green fluorescent protein , biology , myelin basic protein , transduction (biophysics) , vesicular stomatitis virus , microbiology and biotechnology , viral vector , myelin , virology , gene , virus , recombinant dna , biochemistry , neuroscience , central nervous system
Lentiviral vectors are used widely to direct efficient gene transfer in vivo. We examined cell‐specific expression in adult murine white matter after stereotaxic microinjection of four lentiviral constructs. We synthesized vesicular stomatitis virus glycoprotein (VSV‐G) pseudotyped lentiviruses with combinations of two promoters, cytomegalovirus (CMV) or myelin basic protein (MBP), and two reporter sequences, cytosolic enhanced green fluorescent protein (eGFP) or a plasma membrane‐targeted eGFP (human lymphocyte‐specific protein tyrosine kinase [Lck]‐eGFP). For all constructs, intracerebral injections to lateral corpus callosum resulted in widespread GFP expression in forebrain white matter glial cells. Intense cellular GFP fluorescence was observed within 3 days after injection and lasted for at least 28 days. The CMV promoter directed GFP expression in multiple glial cell types, whereas the MBP promoter targeted GFP specifically to oligodendrocytes. Expression of the membrane‐targeted Lck‐eGFP construct distinctly labeled individual myelinating processes of oligodendrocytes. Lentiviral constructs expressing eGFP or Lck‐eGFP under the MBP promoter provide excellent visualization of oligodendrocyte morphology in intact white matter, and may prove valuable for delivering additional genes of interest to oligodendrocytes in vivo. © 2005 Wiley‐Liss, Inc.