The Expression Of ROCK-â…  And MYPT-1 In Splenic Vein Of Portal Hypertension

Background:Portal hypertension is a common clinical syndrome, it is characterized by a pathological increase in portal pressure. The elevated portal pressure leads to the formation of portosystemic collaterals, which makes the blood stream flow straight into the system circulation instead of the liver. The normal portal pressure is within 5 mmHg. When PHT happens, the pressure can raise up to above 10mmHg. The portal vein consists of splenic vein, superior mesenteric vein and inferior mesenteric vein. 20% of the portal blood flow is from splenic vein. The morphology and hemodynamic change in splenic vein in PHT has attracted more and more attention in the recent years. Researches show arterialization in splenic vein in PHT. It mainly includes diffused hyperplasia plaque in endomembrane which contains numerous smooth muscle cells, collagen fiber and lipid cells, thickness in tunica media which is caused by muscle fiber hyperplasia, and inflammation cell infiltration in tunica externa. This is called Para-atherosclerosis (PAS). Its mechanism has not been fully understood. Rho kinase, also known as Rho associated coiled-coil forming protein kinase (ROCK), is the major effectors of the small GTPase RhoA. Researches has shown that the RhoA/ROCK pathway regulates not only the polymerization of cytotactin in smooth muscle cell, but also the function of smooth muscle, such as: contraction, migration and proliferation. The myosine phosphatae targeting subunit 1(MYPT-1) in myosin light chain phosphatase (MLCP) is the substrate of ROCK. ROCK over expression has been found in the tissue of asthma, atheromatosis and hypertension.Objective:To explore the expression of Rho-associated kinase I(ROCK-I) in portal hypertensive splenic venous wall and the phosphorylation level of its substrate myosine phosphatae targeting subunit 1(MYPT-1). To discuss the role of Rock signal transduction pathway in the pathological changes of portal hypertensive splenic vein.Method:1,The level of ROCK-I and MYPT-1 expression in venous wall were detected by immunohistochemisty, and the expression of MYPT-1 was seen as a sign of Rock-I activation.2,The level of ROCK-I and MYPT-1 expression in venous wall were detected by Western Blot.3,To analyze the correlation between ROCK-I and MYPT-1.Result:1,Immunohistochemisty showed that the expression of ROCK-I and MYPT-1 were significantly upregulated in the wall of portal hypertensive splenic vein(P<0.01).2,Western Blot showed that the level of ROCK-I and MYPT-1 expression both rised in experimental group(P<0.01).3,ROCK-I and MYPT-1 was positively correlated(r=0.858,P<0.01).Conclusion:The ROCK-I expression in the wall of portal hypertension spleen vein was upregulated and activated, which gives a hint that Rho kinase signal transduction could play an important role in the pathogenesis of pathological changes in portal hypertensive spleen vein.