concanavalin-a and Blood-Coagulation-Disorders

Autoimmune hepatitis (AIH) is an autoimmune disease characterized by liver parenchymal destruction and chronic fibrosis. Its exact etiology and pathogenesis are not yet fully understood.(Please connect with the following, do not leave a line) Concanavalin A (Con A)-induced mice hepatitis model is a liver injury mediated by T cell and macrophage activation, and its pathogenesis and pathological changes are similar to human AIH. The establishment of this model has greatly promoted the research progress of AIH pathogenesis. However, the exact mechanism of Con A induced liver injury in mice, and its possible defects or deficiencies, has not yet been described in a clear and detailed manner. Therefore, the model has some limitations when applied to the study of the pathogenesis and treatment mechanism of AIH. This article reveals the pathogenesis of Con A induced liver injury in mice from the aspects of immune disorder and coagulation mechanism, expounds the significance of non-coding RNA in this model, summarizes the signal transduction pathways involved in this model, and summarizes the advantages and disadvantages of the model, which provides a theoretical basis and research target for the application of Con A induced liver injury model in AIH in the future.

Topics: Animals; Blood Coagulation Disorders; Chemical and Drug Induced Liver Injury; Concanavalin A; Disease Models, Animal; Hepatitis, Autoimmune; Liver; Mice; RNA, Untranslated; Signal Transduction

Mechanisms for initiation of glomerular fibrin deposition were studied using renal tissue obtained from two patients with rapidly progressive, crescentic glomerulonephritis. Histological examination showed extensive glomerular monocyte infiltration and fibrin deposition in both patients. Sonicated cell suspensions of isolated glomeruli from these patients contained markedly augmented levels of procoagulant activity (PCA) compared with the levels found in normal glomeruli. This PCA was characterized as tissue factor by its functional dependence on Factors VII and V, independence of Factors VIII and XII, inhibition by concanavalin A and phospholipase C, and association with cell membranes. Its coagulant activity was also inhibited by a specific monoclonal anti-human tissue factor antibody. Tissue factor could be identified in glomeruli from these two patients by indirect immunofluorescence using this antibody. These studies implicate extrinsic pathway activation via tissue factor in intraglomerular deposition of fibrin in these patients. Activated monocytes, known to be a potent source of procoagulant activity and seen in large numbers within glomeruli from these patients, are a likely source of this tissue factor.

Topics: Adolescent; Aged; Blood Coagulation Disorders; Blood Coagulation Factors; Concanavalin A; Female; Glomerulonephritis; Humans; Kidney Cortex; Kidney Glomerulus; Male; Thromboplastin; Type C Phospholipases