Here researchers use our Olig2 antibody to study the differentiation state of Fetal Human Oligodendrocyte Progenitor Cells: Crystal R. McClain, Fraser J. Sim and Steven A. Goldman. Pleiotrophin Suppression of Receptor Protein Tyrosine Phosphatase-β/ζ Maintains the Self-Renewal Competence of Fetal Human Oligodendrocyte Progenitor Cells. The Journal of Neuroscience, 24 October 2012, 32(43): 15066-15075; doi: 10.1523/JNEUROSCI.1320-12.2012.
Abstract: Oligodendrocyte progenitor cells (OPCs) persist in human white matter, yet the mechanisms by which they are maintained in an undifferentiated state are unknown. Human OPCs differentially express protein tyrosine phosphatase receptor β/ζ (PTPRZ1) and its inhibitory ligand, pleiotrophin, suggesting the maintenance of an autocrine loop by which PTPRZ1 activity is tonically suppressed. PTPRZ1 constitutively promotes the tyrosine dephosphorylation of β-catenin and, thus, β-catenin participation in T cell factor (TCF)-mediated transcription. Using CD140a/PDGFRα-based fluorescence-activated cell sorting to isolate fetal OPCs from the fetal brain at gestational ages 16–22 weeks, we asked whether pleiotrophin modulated the expansion of OPCs and, if so, whether this was effected through the serial engagement of PTPRZ1 and β-catenin-dependent signals, such as TCF-mediated transcription. Lentiviral shRNAi knockdown of PTPRZ1 induced TCF-mediated transcription and substantially augmented GSK3β inhibition-induced TCF-reporter luciferase expression, suggesting dual regulation of β-catenin and the importance of PTPRZ1 as a tonic brake upon TCF-dependent transcription. Pharmacological inhibition of GSK3β triggered substrate detachment and initiated sphere formation, yet had no effect on either proliferation or net cell number. In contrast, pleiotrophin strongly potentiated the proliferation of CD140a+-sorted OPCs, as did PTPRZ1 knockdown, which significantly increased the total number of population doublings exhibited by OPCs before mitotic senescence. These observations suggest that pleiotrophin inhibition of PTPRZ1 contributes to the homeostatic self-renewal of OPCs and that this process is mediated by the tonic activation of β-catenin/TCF-dependent transcription.
Images: To verify that GSK3β inhibition was effecting TCF activation through altering localization of β-catenin, the Wnt signaling intermediate, β-catenin, was localized by confocal imaging in OPCs, validated as such by their coexpression of Olig2.
|CNPase||CH23013||Chicken IgY||H; M||ICC; IHC||100 ul||$89|
|Caspr2||SP15104||Sheep IgG||H; M||IHC; WB; E||100 ug||$365|
|HSP105||MO20028||Mouse IgG||H; M; R||IHC; WB||100 ul||$155|
|MAG/Siglec 4a||GT15152||Goat IgG||R||IHC; WB; E||100 ug||$365|
|MOG||GT15141||Goat IgG||H||IHC; WB; E||100 ug||$365|
|Mash1||GT15216||Goat IgG||M||IHC; WB; E||100 ug||$365|
|Mash1||MO15048||Rat IgG||H; M||ICC; WB; E||100 ug||$255|
|NOGO Receptor||GT15154||Goat IgG||H||IHC; WB; E||100 ug||$365|
|OMgp||GT15200||Goat IgG||H||WB; E||100 ug||$365|
|Olig1||RA14141||Rabbit IgG||R||IHC||100 ul|
100 ul @ 1mg/ml
|Olig1,2,3||MO15059||Mouse IgG||H; R||IHC||100 ug||$305|
|Olig2||GT15132||Goat IgG||H; M||IHC; WB; E||100 ug||$365|
|Olig2||RA25081||Rabbit IgG||H; M; R||ICC; IHC; WB; IP||100 ul||$395|
|Oligodendrocyte Marker O1||MO15001||Mouse IgM||H; M; R||IHC; FC||50 ug||$215|
|Oligodendrocyte Marker O4||MO15002||Mouse IgM||C; H; M; R||IHC||50 ug||$215|
|Oligodendrocyte Marker O4-Phycoerythrin Labeled||FC15013||Mouse IgM||H||FC||100 Tests||$305|
|PDGF R Alpha/CD140A||GT15150||Goat IgG||M||IHC; WB; E||100 ug||$365|