Figure 2.
Figure 2. Establishment of an orthotopic glioma model to study PDPN contribution to platelet aggregation. (A) Schematic representation of the genetic and the NSC-derived DKO orthotopic glioma models. NSCs were isolated DKO mice and analyzed by FACS for PDPN expression. (B) Histopathological features of a glioblastoma developed in a mouse with orthotopic transplantation of DKO-NSCs. Arrows indicate areas of microvascular proliferation; arrowheads indicate pseudopalisades. Scale bar, 50 µm. Section was stained with H&E. (C) Schematic representation of the genetic and the NSC-derived TKO orthotopic glioma models. NSCs were isolated from TKO mice and analyzed by FACS for PDPN expression. A FACS-sorted pure population of PDPN− NSCs (TKOPdpn neg-NSC) was isolated from TKO-NSC bulk cells. (D) Histopathological features of a glioblastoma developed in a mouse with orthotopic transplantation of TKOPdpn neg-NSCs. Scale bar, 50 µm. Section was stained with H&E.

Establishment of an orthotopic glioma model to study PDPN contribution to platelet aggregation. (A) Schematic representation of the genetic and the NSC-derived DKO orthotopic glioma models. NSCs were isolated DKO mice and analyzed by FACS for PDPN expression. (B) Histopathological features of a glioblastoma developed in a mouse with orthotopic transplantation of DKO-NSCs. Arrows indicate areas of microvascular proliferation; arrowheads indicate pseudopalisades. Scale bar, 50 µm. Section was stained with H&E. (C) Schematic representation of the genetic and the NSC-derived TKO orthotopic glioma models. NSCs were isolated from TKO mice and analyzed by FACS for PDPN expression. A FACS-sorted pure population of PDPN NSCs (TKOPdpn neg-NSC) was isolated from TKO-NSC bulk cells. (D) Histopathological features of a glioblastoma developed in a mouse with orthotopic transplantation of TKOPdpn neg-NSCs. Scale bar, 50 µm. Section was stained with H&E.

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