Confocal immunolocalization of VE‐cadherin‐ and CXC chemokine‐expressing endothelial cells in periapical granulomas

Abstract

VE-cadherin expression in ECs was lower than CXCL8 and CXCL10, suggesting that inflamed ECs in periapical granulomas could increase vascular permeability and that leukocyte chemotaxis mediated by ECs might occur. These findings may suggest the possibility that ECs could play a pivotal role in cell recruitment in periapical granulomas.

Vascular endothelial cadherin and vascular endothelial growth factor in periodontitis and smoking

“…Dramatic increase in permeability and vascular fragility via administration of anti‐VE‐cadherin in mouse model was observed (Corada et al , ). The relation between VE‐cadherin and vascular permeability in inflamed endothelial cells in cell cultures (Sheets et al , ), and a loss of cell adhesion (Takeichi et al , ), the barrier breakdown and increased paracellular permeability (Shen et al , ) as a result of altered expression of VE‐cadherin were also reported in different tissues. Therefore, alterations in VE‐cadherin expression (as VEGF expression) may be an important stage in the initiation and progression of inflammation.…”

A potential role for the silent information regulator 2 homologue 1 (SIRT1) in periapical periodontitis

“…Dual‐colour immunofluorescence imaging was used to identify cell proliferation associated with SIRT1 expression, as previously described (Takeichi et al . ). In brief, frozen tissue sections of periapical granulomas or healthy gingival tissues were treated with 10% (v/v) normal goat serum (Vector Laboratories, Burlingame, CA, USA) for 60 min to block nonspecific binding and incubated with a rabbit monoclonal anti‐human SIRT1 antibody (1/100; Abcam, Cambridge, UK) or a mouse monoclonal anti‐human Ki‐67 antibody (1/100; Abcam) at 4 °C overnight.…”

The Role of Chemokines and Cytokines in the Pathogenesis of Periodontal and Periapical Lesions: Current Concepts

“…Analysis of the chemokines KC/CXCL1 (the analogue of the human CXCL8), in an experimental model of PD in mice, revealed their expression in diseased tissues, preferentially in the junctional epithelium, and their correlation with the migration of PMNs . Furthermore, there was a significant increase in the expression of CXCL8 by epithelial cells from periapical granulomas, suggesting that those cells also could increase vascular permeability and leukocyte chemotaxis (Takeichi et al, 2008).…”