A transmission and scanning electron microscopic study of tumoral and peritumoral microblood vessels in human gliomas

Abstract

The tumor microblood vessels (MBVs) of 25 cases of gliomas of varying grades were studied and compared with those in peritumoral region using both transmission and scanning electron microscopy (TEM and SEM). The TEM study revealed numerous villous projections with pinocytotic vesicles (PCVs) and large vacuoles (LVs) concentrated mainly at the luminal aspect in tumor MBVs which increased with increasing severity of edema. The peritumoral MBVs, in addition to showing some increase in villous projections on the luminal surface, also showed increased number of PCVs and LVs concentrated at the abluminal aspect with some of them even communicating with the extravascular space. The SEM study largely corroborated the TEM findings. The sites of formation of PCVs and LVs appeared as small pits or large craters on the luminal surface of the endothelial cells of tumor MBVs. We feel that the morphological evidence of increased permeability in tumor MBVs represents their role in the development of edema and that the occurrence of reverse pinocytosis in peritumoral MBVs is a distinct possibility which may be associated with resorption of edema fluid.

Uniform brain tumor distribution and tumor associated macrophage targeting of systemically administered dendrimers

“…The vasculature and the amount of BBTB disruption have been demonstrated to differ significantly between the tumor core and a tumor border, which may play a significant role in drug accumulation [32]. In Fig.…”

Vaso-occlusive and prothrombotic mechanisms associated with tumor hypoxia, necrosis, and accelerated growth in glioblastoma

“…Neoplastic cells themselves could alter vascular integrity by invading perivascular spaces and vascular walls. 32 Lastly, intravascular thrombosis-the formation of a fibrinplatelet clot-occurs frequently in GBM and could cause vaso-occlusion and infarction. Procoagulation factors such as tissue factor (TF) and plasminogen activator inhibitor 1 (PAI-1) are increased in GBM and correlate with the extent of necrosis.…”

Glioblastoma-secreted factors induce IGFBP7 and angiogenesis by modulating Smad-2-dependent TGF-β signaling

“…GBM vessels lose many BBB properties, leading to clinical signs of brain edema due to increased vessel permeability (Long, 1970). Morphologically, GBM vessels are characterized by fenestrations, increased number of caveolae, wide intercellular junctions, abnormal pericytes and a discontinuous basement membrane (Hirano and Matsui, 1975;Dinda et al, 1993). GBM vessels express unique gene and protein biomarkers (Pen et al, 2007), often associated with angiogenesis and/or increased permeability, including aquaporin 4 (Davies, 2002), plasmalemmal vesicle associated protein-1 (Madden et al, 2004) and TEM7 (PLXDC1; Beaty et al, 2007).…”