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Notch信号通路的抑制促进心外膜祖细胞向脂肪细胞的分化。

Inhibition of Notch Signaling Promotes the Differentiation of Epicardial Progenitor Cells into Adipocytes.

作者信息

Liu Bin, Wang Dinghui, Xiong Tianhua, Liu Yajie, Jing Xiaodong, Du Jianlin, She Qiang

机构信息

Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.

出版信息

Stem Cells Int. 2021 Apr 9;2021:8859071. doi: 10.1155/2021/8859071. eCollection 2021.

DOI:10.1155/2021/8859071
PMID:33897781
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8052169/
Abstract

BACKGROUND

The role of Notch signaling pathway in the differentiation of epicardial progenitor cells (EPCs) into adipocytes is unclear. The objective is to investigate the effects of Notch signaling on the differentiation of EPCs into adipocytes.

METHODS

Frozen sections of J mouse hearts were used to observe epicardial adipose tissue (EAT), and genetic lineage methods were used to trace EPCs. EPCs were cultured in adipogenic induction medium with Notch ligand jagged-1 or -secretase inhibitor DAPT. The adipocyte markers, Notch signaling, and adipogenesis transcription factors were determined.

RESULTS

There was EAT located at the atrial-ventricular groove in mouse. By using genetic lineage tracing methods, we found that EPCs were a source of epicardial adipocytes. EPCs had lipid droplet accumulation, and the expression of adipocyte markers FABP-4 and perilipin-1 was upregulated under adipogenic induction. Activating the Notch signaling with jagged-1 attenuated the adipogenic differentiation of EPCs and downregulated the key adipogenesis transcription factor peroxisome proliferator activated receptor- (PPAR-), while inhibiting the signaling promoted adipogenic differentiation and upregulated PPAR-. When blocking PPAR-, the role of Notch signaling in promoting adipogenic differentiation was inhibited.

CONCLUSIONS

EPCs are a source of epicardial adipocytes. Downregulation of the Notch signaling pathway promotes the differentiation of EPCs into adipocytes via PPAR-.

摘要

背景

Notch信号通路在心脏祖细胞（EPCs）向脂肪细胞分化中的作用尚不清楚。目的是研究Notch信号对EPCs向脂肪细胞分化的影响。

方法

用J小鼠心脏冰冻切片观察心外膜脂肪组织（EAT），并采用遗传谱系追踪方法追踪EPCs。将EPCs在含有Notch配体锯齿蛋白-1或γ-分泌酶抑制剂DAPT的成脂诱导培养基中培养。检测脂肪细胞标志物、Notch信号和脂肪生成转录因子。

结果

小鼠房室沟处存在EAT。通过遗传谱系追踪方法，我们发现EPCs是心外膜脂肪细胞的来源。EPCs有脂滴积累，在成脂诱导下脂肪细胞标志物脂肪酸结合蛋白-4（FABP-4）和 perilipin-1的表达上调。用锯齿蛋白-1激活Notch信号减弱了EPCs的成脂分化，并下调了关键脂肪生成转录因子过氧化物酶体增殖物激活受体-γ（PPAR-γ），而抑制该信号则促进成脂分化并上调PPAR-γ。当阻断PPAR-γ时，Notch信号在促进成脂分化中的作用受到抑制。

结论

EPCs是心外膜脂肪细胞的来源。Notch信号通路的下调通过PPAR-γ促进EPCs向脂肪细胞分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/10b6ca84f965/SCI2021-8859071.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/2eb82c39d39b/SCI2021-8859071.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/534833341064/SCI2021-8859071.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/e923825710db/SCI2021-8859071.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/947c4c23a740/SCI2021-8859071.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/0988b4cfadbd/SCI2021-8859071.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/c828d87db3f8/SCI2021-8859071.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/10b6ca84f965/SCI2021-8859071.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/2eb82c39d39b/SCI2021-8859071.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/534833341064/SCI2021-8859071.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/e923825710db/SCI2021-8859071.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/947c4c23a740/SCI2021-8859071.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/0988b4cfadbd/SCI2021-8859071.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/c828d87db3f8/SCI2021-8859071.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94b7/8052169/10b6ca84f965/SCI2021-8859071.007.jpg

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