Expression And Significance Of TRPC1and Beta-catenin On Intracranial Aneurysms Wall

Background and Objective：The etiology and pathogenesis of intracranial aneurysm （IA） is more complex,with the deepening of its studies, people have come to realize hemodynamic factorsplay a very important role in the occurrence, development and rupture process of theIA. Hemodynamic factors and its caused vascular wall changes in the roles ofoccurrence， development and rupture process of IA are receiving increasingattention．Recently, some articles reported that the vascular endothelial injury and thevessel wall inflammation caused by the hemodynamic changes may be the initiatinglink of intracranial aneurysms formation. That the hemodynamic changes led toendothelial damage and that appears vessel wall inflammatory cell infiltration andprotease degradation caused by vascular wall remodeling may be a majorpathophysiological aspects of the formation of IA. Thus, we speculate that theconnection and its associated signal in the vascular endothelial cells may be involvedin the formation process of the IA, the molecular mechanisms of vascular endodermisinjury of the process of IA formation, especially in terms of ion channels, remainsunclear by now. Our previous studies have found that the Beta-catenin is foundprimarily in the vascular endothelial cells of the arterial vascular wall, which is amajor component of the connection between the vascular endothelial cells, and playsa very important role in the adhesion between the mediated vascular endothelial cells.Beta-catenin directly bonding with vascular endothelial cadherin （VE-cadherin） formcomplexes, which is the most important catenin of vascular endothelial cells, and thenconnect with the actin cytoskeleton and different signaling proteins, maintain thestability and integrity of the vascular endothelial cells and signal transduction,regulating endothelial permeability and endothelial cell apoptosis and inflammatorycell infiltration play a very important role. Calcium (Ca²⁺) is a common secondmessenger, which main function is involved in cell signaling. Ca²⁺concentration inthe cells change is not only affecting the normal physiological function of the cell, butalso participate in the signal transduction process after the variety of receptor activation. Intracellular Ca²⁺concentration change and the release of intracellularcalcium stores or re-uptake of Ca²⁺and Ca²⁺transmembrane transport process areclosely related. There are many kinds of Ca²⁺channels in the endothelial cellmembrane, which main function control Ca²⁺influx and regulating endothelial cellmembrane potential. Classic transient receptor potential channel1（transient receptorpotential canonical TRPC1） has been confirmed to belong to the non-selective cationchannel, whose mainly through the cation is calcium ion. TRPC1in various types ofvascular smooth muscle cells, which are widely expressed and participate in a varietyof biological behavior of functional regulation. The TRPC1main function is involvedin receptor-mediated calcium-dependent secretion and contraction of smooth muscleand gland function, regulate physiological functions of vascular smooth muscle cellsand endothelial cells, and vascular remodeling impact. In this experiment, we havefound that based on the beta-catenin expression levels on intracranial aneurysms wassignificantly lower than that in normal blood vessels, combined with the latestbetween home and abroad the formation mechanism of IA and endothelial cells andits regulation of two research progress, by observing TRPC1and Beta-cateninexpression in human intracranial aneurysms, research aneurysmal vascularendothelial injury formed between the TRPC1and beta-catenin expression in theprocess of mutual adjustment, in order to further proven vascular endothelial cellconnection and its control signal molecular mechanisms involved in the formation ofIA.Methods：1. The experimental design is divided into two groups: the aneurysmal group andthe normal control group.25patients tissue samples with intracranial aneurysms ofaneurysmal group were selected from March2011to September2012, the FirstAffiliated Hospital of Nanchang University neurosurgical, microsurgical clipping theresected specimen, excised specimens were placed in frozen pipes and frozen inliquid nitrogen immediately after removed residual blood within the aneurysm wallby PBS solution, all patients with intracranial aneurysms diagnosed by the CTA orDSA in the First Affiliated Hospital of Nanchang University. Normal control groupeight cases, select from March2011to August2012temporal lobe epilepsy patients or Traffic accidents the temporal injury intracranial decompression after traumaticbrain injury caused by surgical removal of the temporal pole from the normal braincortex artery, and all tissue specimens collected were frozen in liquid nitrogen afterPBS solution processing.2. Detect aneurysmal group and the normal control group TRPC1andBeta-catenin expression by western blot （western blotting） experimental methods,detection data use applications of statistical spass17.0software for statistical analysis,and t-test.Results：1. Intracranial aneurysms wall have the TRPC1expression，and compare withthe control group, TRPC1expression of intracranial aneurysms group decreased.2. Intracranial aneurysms wall have the Beta-catenin expression，and comparewith the control group, Beta-catenin expression of intracranial aneurysms groupdecreased.Conclusion：TRPC1and Beta-catenin are expressed by detecting the intracranial aneurysmwall, but significantly decreased as compared with the expression amount of thenormal intracranial arterial vessel wall, our experimental results preliminarily showthat TRPC1and Beta-catenin may be involved in some way to adjust the formationand rupture of intracranial aneurysms. Vascular endothelial injury caused by bloodflow in intracranial aneurysm formation process, the existence of the intrinsic link orno between TRPC1and Beta-catenin needs further study.