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The Effects of Angiotensin-(1-7) on Rat Hepatic Stellate Cell Contraction Mediated by Rho-Rock Pathway

Author: YingZuoZuo
Tutor: ZhangZhenShu；LiXu
School: Southern Medical University,
Course: Internal Medicine
Keywords: Angiotensin Rho - Rock Hepatic stellate cells Cell contraction
CLC: R575.2
Type: Master's thesis
Year: 2009
Downloads: 105
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Abstract


Background a variety of chronic liver disease may be the development of liver fibrosis to cirrhosis, portal hypertension is one of the main features of cirrhosis of the liver. Cirrhotic state, the increase in intrahepatic vascular resistance is an important factor to lead to portal hypertension. Hepatic stellate cells (hepatic stellate cell, HSC) is the main cells of the liver extracellular matrix, HSC activation of the formation of a series of processes play a key role in the development of liver fibrosis and portal hypertension. Activated HSC into myofibroblasts and fibroblasts continue to proliferate and contractible. When the latter is a strong contraction, resulting in the sinusoidal diameter reduced intrahepatic vascular resistance increases; at the same time can cause liver tissue scar contracture, further increase in intrahepatic vascular resistance, leading to portal hypertension. Visible, HSC contraction of the regulation mechanism is an important part of portal hypertension Mechanism. In recent years, the intrahepatic renin - angiotensin - aldosterone system (therenin-angiotensin-aldosterone system, RAAS) has become the hot spot of the liver fibrosis research areas, with the deepening understanding of the RAAS, found the RAAS many new group points, such as angiotensin-converting enzyme 2 (ACE2), angiotensin 1-7 (Ang-(1-7)), Ang-(1-7) receptor Mas. They constitute the ACE2-Ang-(1-7)-Mas receptor axis, become the RAAS another important branch, with significant inhibition of ACE-Ang II-AT1R axis. The intrahepatic ACE-ANG II-AT1R axis of portal hypertension is closely related to the formation. Is currently no information about the ACE2-Ang-(1-7)-Mas receptor axis studies have reported on the regulation of HSC contraction. Rho-Rock pathway regulation mechanism of HSC contraction in non-calcium pathway, is a research hotspot in recent years. Examined the effects of Ang-(1-7) to clarify the impact of regulation on the contraction of HSC HSC contraction and the expression of Rho-Rock signaling pathway components. Objective To investigate the angiotensin 1-7 (angiotensin1-7 Ang-(1-7)) on rat HSC contraction mediated by Rho kinase non-CA 2 -dependent signal transduction pathway. affected. Methods ① HSC-T6 cell line to give Ang-(1-7) 1 mmol / L treatment, the silicone membrane intuitive detection HSC contraction; (2) HSC-T6 cell line to give Ang-(1-7) 10 micromol / L treatment, detected by Western blot myosin light chain (myosin light chain, MLC) phosphorylation of MLC and alpha smooth muscle actin (alpha-SMA) expression levels. Observed Ang-(1-7), Ang II (angiotensin II), Ang-(1-7) the MAS receptor blocker A779, Ang II and Ang-(1-7) on the phosphorylation of MLC and alpha-SMA expression levels ; (3) reverse transcription polymerase chain reaction (RT-PCR) to detect the expression of Rho-Rock pathway Rock2 (Rho-kinase2), RhoAGTP, RhoGEF (Rho Guanine Nucleotide Exchange Factors, RhoGEF). Ang II treatment group phosphorylation of MLC protein expression was significantly increased (P = 0.000). Ang-(1-7) inhibits Ang II-induced contraction of HSC. Ang II Ang-(1-7) treated inhibit Ang II-induced the MLC protein phosphorylation level (P = 0.000) and Ang-(1-7) treated phosphorylated MLC protein levels were significantly higher Ang-(1-7 ) the A779 treated group, the difference was statistically significant (P = 0.000). ANG II treatment group alpha-SMA protein expression was significantly increased (P = 0.000), Ang II Ang-(1-7) treated inhibit Ang II-induced alpha-SMA protein expression levels, the difference was statistically significant (P = 0.000). Ang Ⅱ group RhoGEF mRNA was significantly higher than the negative control group (P = 0.000), Ang-(1-7) Ang II group RhoGEF mRNA expression of Ang Ⅱ group was significantly reduced (P = 0.000), Ang-(1-7) group RhoGEF mRNA significantly lower than the negative control group (P = 0.000), and the difference was statistically significant (P = 0.000). The Ang Ⅱ of group Rock2 mRNA was significantly higher than the negative control group (P = 0.000), Ang-(1-7) Ang II group Rock2 mRNA expression of Ang Ⅱ group was significantly reduced (P = 0.000), Ang-(1-7) group Rock2 mRNA significantly lower than the negative control group (P = 0.000), Ang-(1-7) the A779 Rock2 mRNA expression was significantly lower than the Ang-(1-7) group, the difference was statistically significant (P = 0.000). The Ang Ⅱ of group RhoAGTP mRNA was significantly higher than the negative control group (P = 0.000), Ang-(1-7) Ang II group of RhoAGTP mRNA expression of Ang Ⅱ group was significantly reduced (P = 0.000), Ang-(1-7) group RhoAGTP mRNA significantly lower than the negative control group (P = 0.000), Ang-(1-7) the A779 of RhoAGTP mRNA expression was significantly lower than the Ang-(1-7) group, the difference was statistically significant (P = 0.000). Conclusion Ang-(1-7) inhibition of Rho-Rock signaling pathway induced by Ang Ⅱ HSC contraction.

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CLC: > Medicine, health > Internal Medicine > Digestive and abdominal diseases > Liver and gall bladder disease > Cirrhosis
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