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| PRKAG2基因G100S新突变对小鼠心肌细胞单磷酸腺苷活化蛋白激酶活性的影响 |
| 唐念中1,2,张艳飞3,陈挺4,郑兴1* |
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(1. 海军军医大学(第二军医大学)长海医院心血管内科, 上海 200433;
2. 海军军医大学(第二军医大学)长海医院虹口院区重症医学科, 上海 200081;
3. 海军军医大学(第二军医大学)长海医院虹口院区消毒供应科, 上海 200081;
4. 解放军东海舰队上海舰艇岸勤部医院, 上海 200940
*通信作者) |
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| 摘要: |
| 目的 探讨位于非胱硫醚β-合成酶（cystathionine β-synthase，CBS）区域的PRKAG2基因G100S突变对小鼠心肌细胞单磷酸腺苷活化蛋白激酶（AMPK）活性的影响。方法 建立人源PRKAG2（G100S）转基因小鼠模型，分别随机选取N4代4周龄、12周龄的转基因小鼠和同窝野生型小鼠各6只，用磷酸化检测试剂盒检测小鼠心肌细胞中AMPK活性，比较转基因小鼠与同窝野生型小鼠AMPK活性的差异，并观察随着周龄的增长转基因小鼠AMPK活性的变化。结果 4周龄和12周龄的转基因小鼠心肌细胞中AMPK活性均低于同窝野生型小鼠（0.042±0.013 vs 0.063±0.013，0.032±0.008 vs 0.062±0.018），差异均有统计学意义（P=0.019，P=0.004）。12周龄和4周龄的转基因小鼠心肌细胞中AMPK活性差异无统计学意义（P=0.135）。结论 PRKAG2基因G100S突变可导致转基因小鼠心肌细胞AMPK活性下降，而且AMPK活性并不随着转基因小鼠周龄的增长而变化。 |
| 关键词: PRKAG2基因 G100S新突变 单磷酸腺苷活化蛋白激酶 转基因小鼠 |
| DOI：10.16781/j.0258-879x.2019.01.0049 |
| 投稿时间：2018-09-11修订日期：2019-01-03 |
| 基金项目:国家自然科学基金（81170092）. |
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| Influence of PRKAG2 gene G100S novel mutation on adenosine monophosphate-activated protein kinase activity in cardiomyocytes of mice |
| TANG Nian-zhong1,2,ZHANG Yan-fei3,CHEN Ting4,ZHENG Xing1* |
(1. Department of Cardiovasology, Changhai Hospital, Naval Medical University(Second Military Medical University), Shanghai 200433, China;
2. Intensive Care Unit, Hongkou Branch of Changhai Hospital, Naval Medical University(Second Military Medical University), Shanghai 200081, China;
3. Department of Sterilization and Supply, Hongkou Branch of Changhai Hospital, Naval Medical University(Second Military Medical University), Shanghai 200081, China;
4. Hospital of Shanghai Warship Logistics Department, East China Sea Fleet, Shanghai 200940, China
*Corresponding author) |
| Abstract: |
| Objective To explore the effect of PRKAG2 gene G100S mutation in cystathionine β-synthase (CBS) region on adenosine monophosphate-activated protein kinase (AMPK) activity in cardiomyocytes of mice.Methods A human PRKAG2 (G100S) transgenic mouse model was established. Four-week-old and 12-week-old transgenic mice, and 4-week-old and 12-weekold wildtype littermate were randomly selected from N4 generation mice (n=6). The activity of AMPK in mouse cardiomyocytes was detected by phosphorylation assay kit. The difference of AMPK activity was compared between transgenic mice and wildtype littermate, and the changes of the activity of AMPK with the increase of age were observed in transgenic mice.Results The AMPK activities in cardiomyocytes of 4-week-old and 12-week-old transgenic mice were significantly lower than those of the wildtype littermate (0.042±0.013 vs 0.063±0.013, and 0.032±0.008 vs 0.062±0.018), and the differences were significant (P=0.019, P=0.004). There was no significant difference in the AMPK activity of cardiomyocytes between 4-week-old and 12-weekold transgenic mice (P=0.135).Conclusion The PRKAG2 gene G100S mutation can cause a reduction of AMPK activity in cardiomyocytes of transgenic mice, and AMPK activity does not significantly increase or decrease with the growth of the transgenic mice. |
| Key words: PRKAG2 gene G100S novel mutation adenosine monophosphate-activated protein kinase transgenic mice |
