Skip to main content

Advertisement

Figure 5 | Journal of Neuroinflammation

Figure 5

From: Regulation of CCL2 and CCL3 expression in human brain endothelial cells by cytokines and lipopolysaccharide

Figure 5

Surface localization of CCL2 and CCL3 by immunoelectron microscopy. (D, E) Surface localization of CCL2 on HBMEC by immunoelectron microscopy. (A) In resting monolayers, gold particles indicating the presence of CCL2 are bound mostly to the apical cell surface (arrow). (B) In cultures treated with TNF-α (100 U/ml) + IFN-γ (500 U/ml) for 24 hrs gold particles are preferentially bound to the subendothelial basal lamina-like material (arrows). Arrowheads in (A) and (B) indicate the basal cell surface. Scale bars = 0.25 μm. (C) Quantification of the number of gold particles bound to the apical and basal cell surface of unstimulated HBMEC shows no significant difference between apical and basal binding (p ≥ 0.1). In cytokine-treated HBMEC cultures, there is a significant increase in the number of gold particles bound to the basal cell surface and the basal lamina-like material versus the apical surface (p ≤ 0.01). The number of gold particles at the basal cell surface is significantly greater in activated versus resting HBMEC (p ≤ 0.01). (D, E) Surface localization of CCL3 on HBMEC by immunoelectron microscopy. (A) In resting monolayers occasional gold particles are bound to the basal cell surface only (arrow). (B) Following treatment with TNF-α (100 U/ml) + IFNγ (500 U/ml) for 24 hrs gold particles are preferentially bound to the apical surface (arrow). Arrowheads in (A) and (B) indicate the basal cell surface. Scale bars = 0.25 μm. (F) Quantification of the number of gold particles bound to the apical and basal cell surfaces of unstimulated and cytokine-treated HBMEC cultures shows no statistically significant differences between the different groups (p ≥ 0.15).

Back to article page