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ASSA13-03-45 Effects from Age to Wnt and NF-kB Signal Pathway in Heart of Mice
  1. Huang Ying,
  2. Ma Yitong,
  3. Yang Yingying,
  4. Liu Fen,
  5. Chen Bangdang,
  6. Li Xiaomei
  1. Cardiovascular Research Institute, 1st Affiliated Hospital of Xinjiang Medical University Urumqi, Xinjiang, China

Abstract

Background Wnt and NF-κB signal pathway are all related to cardiac remodelling post-infarction and there were age-related differences of outcome post infarction. We study changes of these two signal pathways in heart in old mice to prepare some materials for advanced study.

Methods We used 20 mice to study changes of these two signal pathways: 10 in young (3-mo) and old group (18-mo) respectively. They were detected expression of dvl-1, β-catenin, p/t GSK-3β and connexin 43 in the left ventricle (LV) by western-blot. And they were detected expression of p65 and p50 by immunohistochemistry and western-blot. At the same time they were detected expression of ICAM-1 and VCAM-1.

Results (1) Expression of dvl-1 increased by 2.41 fold in old group compared with young mice in the LV (P = 0.000). There were no statistically differences of expression of β-catenin between the old and young group (P = 0.647) in LV. Ratio of p/t GSK-3β is much lower in old compared with young (P = 0.000). When talking about connexin 43, there were statistically significant differences in old group compared with young (P = 0.001) in the LV. (2) There was no difference of numbers of p65 and p50 positive cells between old and young group by immunohistochemistry (P < 0.05). But expression of p65 and p50 in nuclear protein in old group is higher than it in young group (P = 0.000). There was no difference of ICAM-1 between old and young group (P = 0.401). Expression of VCAM-1 in old group was higher than it in young group (P = 0.000).

Conclusions There were age-related differences of protein associated with Wnt and NF-κB signal pathway in heart. Progressing study about changes in these two signal pathway post myocardial-infarction might find new mechanisms about age-related differences of cardiac remodelling.

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