Role of high endothelial postcapillary venules and selected adhesion molecules in periodontal diseases: a review

Abstract

Periodontitis is accompanied by the proliferation of small blood vessels in the gingival lamina propria. Specialized postcapillary venules, termed periodontal high endothelial-like venules, are also present, and demonstrate morphological and functional traits similar to those of high endothelial venules (HEVs) in lymphatic organs. The suggested role of HEVs in the pathogenesis of chronic periodontitis involves participation in leukocyte transendothelial migration and therefore proinflammatory effects appear. Recent observations suggest that chronic periodontitis is an independent risk factor for systemic vascular disease and may result in stimulation of the synthesis of acute phase protein by cytokines released by periodontal high endothelial cells (HECs). However, tissue expression of HEV-linked adhesion molecules has not been evaluated in the gingiva of patients with chronic periodontitis. This is significant in relation to potential therapy targeting expression of the adhesion molecules. In this review, current knowledge of HEV structure and the related expression of four surface adhesion molecules of HECs [CD34, platelet endothelial cell adhesion molecule 1, endoglin and intercellular adhesion molecule 1 (ICAM-1)], involved in the key steps of the adhesion cascade in periodontal diseases, are discussed. Most studies on the expression of adhesion molecules in the development and progression of periodontal diseases pertain to ICAM-1 (CD54). Studies by the authors demonstrated quantitatively similar expression of three of four selected surface markers in gingival HEVs of patients with chronic periodontitis and in HEVs of reactive lymph nodes, confirming morphological and functional similarity of HEVs in pathologically altered tissues with those in lymphoid tissues.

Derivation of human decidua-like cells from amnion and menstrual blood

“…Antibodies against human CD9, CD10, CD13, CD14, CD16, CD19, CD29, CD31, CD34, CD44, CD45, CD54, CD55, CD59, CD73, CD90, CD105, CD133, CD146, CD166, HLA-ABC, and HLA-DR were purchased from Beckman Coulter, Immunotech (Marseille, France), BD Pharmingen and BioLegend (San Diego, CA, USA)2122. Supplementary table S1 shows the list of CD antigens investigated in this study3940414243444546474849.…”

Progranulin protects against endotoxin-induced acute kidney injury by downregulating renal cell death and inflammatory responses in mice

“…Among these mechanisms, a robust inflammatory process engaging both innate and adaptive immune responses is believed to cause the initial renal injury and mediate long-term structural changes [13,14]. Exposure of the kidney to high concentrations of LPS increases the production of pro-inflammatory mediators and upregulates adhesion molecules [15,16]. The infiltration of leukocytes induced by early inflammatory responses during kidney injury may lead to further damage [17].…”

Sirt1 Deletion Leads to Enhanced Inflammation and Aggravates Endotoxin-Induced Acute Kidney Injury

“…Sepsis also causes renal tubular damage and inflammation as shown by histological analysis [15]. Kidney inflammation is associated with increased production of pro-inflammatory mediators [16], and up-regulation of adhesion molecules such as Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) [17]. Those early inflammatory responses induce leukocyte infiltration during kidney injury [18], which may lead to further damage.…”