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C-jun Expression And SMC Phenotype Change In Pulmonary Arterioles Wall In The Development Of Ascites Syndrome In Broiler Chickens

Posted on:2006-04-24Degree:DoctorType:Dissertation
Country:ChinaCandidate:X F DongFull Text:PDF
GTID:1103360152492426Subject:Basic veterinary science
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Pulmonary vascular remodeling (PVR) may play an important role in the development of PH and AS in broiler chickens. Studies on human showed that the phenotypic change of vascular smooth muscle cell (VSMC) be the basis of VSMC proliferation and migration, while VSMC proliferation and migration was the pathological basis of PVR.The abnormal expression of proto-oncogene was the main process of the differentiaion and proliferation of VSMC. Calcium sigal played an important role in the development of PH in mammals. Studies on broilers suggested that the abnormal expression of proto-oncogene and calcium sigal may be invoved in the development of AS in broiler chickens. It is unclear that whether there be the phenotypic change and proliferation of VSMC and the abnormal expression of c-jun.in the development of AS induced by excess salt in broiler chickens. To clarify the mechanism of PVR and AS in broiler chickens, in the studies, the rule of phenotypic change and proliferation of SMC and expression of c-jun in the wall of pulmonary arterioles was investigated during the development of AS induced by excess salt in broiler chickens, and prophylactic effect of calcium antagonist verapamil on ascites syndrome caused by excess salt in broiler chickens.was also observed.200 commercial male Arbor Acres broiler chickens were randomly divided into four groups from day 8: control group (C) and three treated groups (T1, T2, T3). Pulmonary artery pressure (PAP), packed cell volume (PCV) and ascites heart index (AHI) of 6 randomly selected birds per group were measured at days 15, 22, 29, 36, 43 and 50 respectively. Lungs sections were respectively treated by different staining method for the analysis of pulmonary vascular remodeling, phenotypic change and proliferation of SMC and expression of c-jun. The incidence of AS was determined at the end of experiment. The results were as follows:1. Excess salt induced PH and AS in broiler chickens. Verapamil prevented PH and significantly decreased the incidence of AS caused by excess salt in broiler chickens. At the end of expriment, the incidence of AS in Ti group (16.0%) was significantly higher than that in C group (0.0%), T2 group (2.0%) and T3 group (0.0%) (P<0.01). At day 15 the mPAP in T, group and T2 group was significantly higher than that in C group and T3 group (P<0.01), and at days 36, 43 and 50 the mPAP in T1 group was significantly higher than that in C, T2 and T3 groups (.P<0.05 or P<0.01).2. Excess salt induced PVR, which was prevented by verapamil in broiler chickens. From days 36 to 50, the thickness of medial smooth muscle and vascular wall mainly in φ20~50μm pulmonary arterioles of broiler chickens were increased in T1 group. From days 29 to 50, the muscularization of non-muscular arterioles was observed in broiler chickens of T1 group. These changes were not found inother groups.3. Excess salt accelerated the proliferation and change from contractile phenotype to proliferative phenotype of SMC in pulmonary arterioles wall in the development of ascites syndrome in broiler chickens, and verapamil inhibited the proliferation and phenotypic change. At day 15 the phenotypic change was observed in broilers of T1 group, which was earlier than in C group at day 22. Theproliferation was observed in T1 group at day 22,which was earlier than in C group at day 29.Few proliferation and phenotypic change were found in T2 and T3 groups. The proliferation and phenotypic change in φ 20~50μm pulmonary arterioles was mainly affected.4. Excess salt induced the increase of expression of c-jun in pulmonary arterioles wall in the development of ascites syndrome in broiler chickens, and the increase of expression of c-jun was prevented by verapamil. At day 15 increase of expression of c-jun was observed in T1 group, which was earlier than in C group at day 22.In the later period, increase of expression of c-jun mainly was observed in φ20~50μm pulmonary arterioles wall. The increase of expression of c-jun was not found during theexpriment.These results first Showed that the proliferation...
Keywords/Search Tags:C-jun gene, Cell phenotype, Ascites syndrome, Verapamil, Excess salt
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