Adhesion molecules and pancreatitis

Abstract

Acute and chronic pancreatitises are gastrointestinal inflammatory diseases, the incidence of which is increasing worldwide. Most (~ 80%) acute pancreatitis (AP) patients have mild disease, and about 20% have severe disease, which causes multiple organ failure and has a high mortality rate. Chronic pancreatitis (CP) is characterized by chronic inflammation and destruction of normal pancreatic parenchyma, which leads to loss of exocrine and endocrine tissues. Patients with CP also have a higher incidence of pancreatic ductal adenocarcinoma. Although a number of factors are associated with the development and progression of AP and CP, the underlying mechanism is unclear. Adhesion molecules play important roles in cell migration, proliferation, and signal transduction, as well as in development and tissue repair. Loosening of cell-cell adhesion between pancreatic acinar cells and/or endothelial cells increases solute permeability, resulting in interstitial edema, which promotes inflammatory cell migration and disrupts tissue structure. Oxidative stress, which is one of the important pathogenesis of pancreatitis, leads to upregulation of adhesion molecules. Soluble adhesion molecules are reportedly involved in AP. In this review, we focus on the roles of tight junctions (occludin, tricellulin, claudin, junctional adhesion molecule, and zonula occludin), adherens junctions (E-cadherin and p120-, α-, and β-catenin), and other adhesion molecules (selectin and intercellular adhesion molecules) in the progression of AP and CP. Maintaining the normal function of adhesion molecules and preventing their abnormal activation maintain the structure of the pancreas and prevent the development of pancreatitis.

Polyethylene Glycol 35 (PEG35) Protects against Inflammation in Experimental Acute Necrotizing Pancreatitis and Associated Lung Injury

“…The process is controlled by complex interactions between surface receptors on neutrophils and their corresponding endothelial cell ligands [18]. To further study the protective function of PEG35 in ANP, we focused on the expression of two of the main adhesion molecules involved in this inflammatory disease: P-selectin and Intercellular Adhesion Molecule-1 (ICAM-1) [19]. A significant up-regulation in both adhesion molecules was evident in the pancreas and lung three hours after ANP induction compared to control-operated mice ( Figure 4A,B).…”

“…In recent years, several experimental studies have focused on the protective effects of PEGs. In lung endothelial cells, treatment with 15-20 kDa molecular weight PEG (PEG [15][16][17][18][19][20] was found to enhance cell function by activating endothelial cell-barrier signal transduction pathways and by contributing to cytoskeleton reorganization [8]. In addition, pre-treatment with PEG 15-20 in cultured ventricular myocytes subjected to hypoxia-reoxygenation reduced oxidative stress and apoptosis and increased cell survival [9].…”

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

“…β-Catenin, a type of transmembrane protein, is likely to play a crucial role in the progression and severity of AP [12]. Our previous research has determined that MSCs enhance the expression of β-catenin in SAP [20].…”

“…In recent years, increasing evidence has demonstrated that impaired autophagy has a crucial effect on the pathogenesis of SAP [ 9 – 11 ]. In addition, maintaining the normal action of adhesion molecules (such as β-catenin) and restricting their abnormal activation are beneficial in blocking the development of AP [ 12 ]. Therefore, investigations seeking to develop novel therapeutic tactics for SAP should concentrate on how to inhibit inflammatory responses, regulate autophagy, and maintain levels of adhesion molecules.…”

Long noncoding RNA H19 regulates the therapeutic efficacy of mesenchymal stem cells in rats with severe acute pancreatitis by sponging miR-138-5p and miR-141-3p

“…In recent years, increasing evidence has demonstrated that impaired autophagy has a crucial effect on the pathogenesis of SAP [9][10][11]. In addition, maintaining the normal action of adhesion molecules (such as β-catenin) and restricting their abnormal activation are bene cial in blocking the development of AP [12]. Therefore, investigations seeking to develop novel therapeutic tactics for SAP should concentrate on how to inhibit in ammatory responses, regulate autophagy and maintain levels of adhesion molecules.…”