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磷脂酶 A2(PLA2)损伤淋巴管内皮细胞,导致继发性淋巴水肿进展。

Phospholipase A2 (PLA2) injured lymphatic endothelial cells leading to progression of secondary lymphoedema.

机构信息

Department of Lymphatic Surgery, Capital Medical University Affiliated Beijing Shijitan Hospital, Beijing, China.

Department of Joint Surgery, Capital Medical University Affiliated Beijing Shijitan Hospital, Beijing, China.

出版信息

Biotechnol Genet Eng Rev. 2024 Nov;40(3):1511-1534. doi: 10.1080/02648725.2023.2195082. Epub 2023 Mar 27.

DOI:10.1080/02648725.2023.2195082
PMID:36971244
Abstract

Secondary lymphoedema is one of the common complications after lymph node dissection for gynecologic malignancies and breast cancer. In this study, the relationship between PLA2 and postoperative lymphoedema in cancer at the molecular level has been explored through transcriptomics and metabolomic assays. Transcriptome sequencing technology, as well as metabolomic assays, were utilized to explore the expression of PLA2 in lymphoedema patients, and search for potential pathways in the pathogenesis and exacerbation mechanism of lymphoedema. The effect of sPLA2 on human lymphatic endothelial cells was investigated by culturing human lymphatic endothelial cells. Secretory phospholipases A2 (sPLA2) showed high expression levels in lymphoedema tissues, however, cytoplasmic phospholipases A2 (cPLA2), showed low expression in lymphoedema, as demonstrated by RT-qPCR. By culturing human lymphatic vascular endothelial cells, the study found that sPLA2 causes HLEC vacuolization and has an inhibitory effect on HLEC proliferation and migration. By detecting sPLA2 in the serum of lymphoedema patients and analyzing clinical data, it was found that sPLA2 was positively correlated with the severity of lymphoedema. Secretory Phospholipase A2 (sPLA2) is highly expressed in lymphoedema tissue, damages lymphatic vessel endothelial cells, is strongly associated with disease severity, and can be used as a potential predictor of disease severity.: PLA2: Phospholipase A2; DEGs: differentially expressed genes; DMP: differential metabolic production.

摘要

继发性淋巴水肿是妇科恶性肿瘤和乳腺癌淋巴结清扫术后常见的并发症之一。本研究通过转录组学和代谢组学检测,从分子水平探讨 PLA2 与癌症术后淋巴水肿的关系。采用转录组测序技术和代谢组学检测方法,探讨 PLA2 在淋巴水肿患者中的表达情况,寻找淋巴水肿发病机制和加重机制中的潜在途径。通过培养人淋巴管内皮细胞,研究 sPLA2 对人淋巴管内皮细胞的作用。结果显示,淋巴水肿组织中 sPLA2 表达水平较高,而 RT-qPCR 显示淋巴水肿组织中细胞质型 PLA2(cPLA2)表达水平较低。通过培养人淋巴管内皮细胞,研究发现 sPLA2 导致 HLEC 空泡化,并对 HLEC 的增殖和迁移具有抑制作用。通过检测淋巴水肿患者血清中的 sPLA2 并分析临床资料,发现 sPLA2 与淋巴水肿的严重程度呈正相关。分泌型 PLA2(sPLA2)在淋巴水肿组织中高表达,损伤淋巴管内皮细胞,与疾病严重程度密切相关,可作为疾病严重程度的潜在预测指标。PLA2:磷脂酶 A2;DEGs:差异表达基因;DMP:差异代谢产物。

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Biotechnol Genet Eng Rev. 2024 Nov;40(3):1511-1534. doi: 10.1080/02648725.2023.2195082. Epub 2023 Mar 27.
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