Page 63 - 南京医科大学学报自然科学版

第42卷第6期 南京医科大学学报（自然科学版）
2022年6月 Journal of Nanjing Medical University（Natural Sciences） ·815 ·

·基础研究·

血小板受体C型凝集素样受体2在巨核细胞自噬中的作用

姜 江 ，丁育红 ，贾 慧 ，周 鹭 1*
3
1
1，2
南通大学附属医院血液内科，江苏 南通 226001；苏州大学附属第二医院核医学科，江苏 苏州 225556；南通大学医学
1 2 3
院，江苏 南通 226001

［摘 要］ 目的：用C型凝集素样受体⁃2（C⁃type lectin like receptor 2，CLEC⁃2）缺陷小鼠检测CLEC⁃2在自噬过程中的作用，从
而探究CLEC⁃2信号通路对巨核细胞发育的影响。方法：怀孕14.5 d的小鼠胚胎取出、分离并培养巨核细胞。体外雷帕霉素处
理巨核细胞，检测巨核细胞CLEC⁃2和CD41的表达。小鼠经雷帕霉素处理后，检测小鼠骨髓自噬蛋白的表达。结果：自噬基因
在胎肝来源的巨核细胞中表达，并且表达量很高。小鼠巨核细胞在雷帕霉素处理后，CLEC⁃2表达下调，提示CLEC⁃2参与调控
自噬。雷帕霉素处理后，与野生型小鼠相比，敲除小鼠的巨核细胞CD41和CD61蛋白表达明显降低（P < 0.001）。体内实验发
现雷帕霉素能显著增强敲除小鼠LC3蛋白的表达。CLEC⁃2的缺陷能显著降低自噬紊乱导致的高倍体巨核细胞数。CLEC⁃2
的缺陷降低雷帕霉素诱导胎肝来源的巨核细胞周期相关蛋白Cyclin D1、Cyclin D2的表达。结论：血小板受体CLEC⁃2在巨核
细胞自噬中具有重要的调控作用。
［关键词］ C⁃型凝集素样受体2；自噬；巨核细胞；雷帕霉素
［中图分类号］ R392.12 ［文献标志码］ A ［文章编号］ 1007⁃4368（2022）06⁃815⁃06
doi：10.7655/NYDXBNS20220608

Role of platelet receptor C⁃type lectin like receptor 2 in autophagy of megakaryocytes

1
1，2
3
JIANG Jiang ，DING Yuhong ，JIA Hui ，ZHOU Lu 1*
2
1 Hematology of Department，the Affiliated Hospital of Nantong University，Nantong 226001；Department of Nuclear
Medicine，the Second Affiliated Hospital of Soochow University，Suzhou 225556；Medical School，Nantong University，
3
Nantong 226001，China
［Abstract］ Objective：CLEC ⁃ 2 signaling pathway is involved in the regulation of autophagy in megakaryocytes. However，the
mechanism has not been fully elucidated. In this study，CLEC⁃2 deficient mice were used to detect whether CLEC⁃2 plays an important
role in autophagy. Methods：Megakaryocytes were isolated and cultured from 14.5 day pregnant mouse embryos. The expression of
CLEC⁃2 and CD41 in megakaryocytes were detected. After rapamycin treatment，the expression of autophagy protein was detected.
Results：Autophagy gene was highly expressed in megakaryocytes derived from fetal liver. After rapamycin treatment，the expression of
CLEC⁃ 2 was decreased，indicating that CLEC⁃ 2 was involved in the regulation of autophagy. Compared with wild⁃type mice，the
expression of CD41 and CD61 in megakaryocytes of CLEC⁃2 knockout mice was significantly decreased after rapamycin treatment. In

vivo，rapamycin can significantly enhance the expression of LC3 protein in knockout mice. The defect in CLEC⁃2 can significantly
reduce the number of polyploid megakaryocytes caused by autophagy disorder. And it also reduced the expression of cyclin D1 and
cyclin D2 in megakaryocyte derived from fetal liver induced by rapamycin. Conclusion：CLEC ⁃ 2 plays an important role in the
regulation of autophagy of megakaryocytes.
［Key words］ CLEC⁃2；autophage；megakaryocytes；rapamycin
［J Nanjing Med Univ，2022，42（06）：815⁃820］

自噬在造血干细胞中的缺失会导致多系血细
［基金项目］ 南通市科技计划指令性项目（JC2019039）
胞的异常分化 ［1-2］ 。许多血液病尤其是血小板相关
∗
通信作者（Corresponding author），E⁃mail：xueyezhoulu2007@si⁃
na.com 疾病伴随着自噬水平的上调，例如特发性血小板减