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信号素3A与阿维A对HaCaT细胞增殖、迁移及凋亡影响的初步研究

A Preliminary Study of the Effect of Semaphorin 3A and Acitretin on the Proliferation, Migration, and Apoptosis of HaCaT Cells.

作者信息

Ding Wei, Cao Yi, Xing Fengling, Tao Maocan, Fu Hongyang, Luo Hongbin, Yang Xiaohong

机构信息

Department of Dermatology, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

Department of Dermatology, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

Indian J Dermatol. 2019 May-Jun;64(3):250. doi: 10.4103/ijd.IJD_179_18.

DOI:10.4103/ijd.IJD_179_18
PMID:31148871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6537688/
Abstract

BACKGROUND

Vascular endothelial growth factor (VEGF) is significantly elevated in psoriatic patients and is associated with the severity of the psoriasis. Due to the effect of inhibiting production of VEGF, acitretin can effectively treat psoriasis. Semaphorin 3A (Sema3A) restrain tumor growth and angiogenesis by partially reversing VEGF effects on tumor. However, the role of Sema3A in the pathogenesis of psoriasis is unclear.

AIMS AND OBJECTIVES

This study aimed to investigate the effect of VEGF, Sema3A, and acitretin on HaCaT cells, to see whether Sema3A could be a beneficial factor in psoriasis, as well as acitretin.

MATERIALS AND METHODS

Functional analysis of VEGF, Sema3A, and acitretin was carried out using HaCaT cells cultured under different treatments. Cell counting kit-8 method, colony formation assay, flow cytometry, transwell migration, reverse transcription-polymerase chain reaction, and Western blot test were performed to measure proliferation, colony formation, migration, apoptosis, and the expression of Bcl2, Bax, Caspase 3, and Caspase 9 of HaCaT cells.

RESULTS

Sema3A and acitretin inhibited the proliferation, colony formation, and migration of HaCaT cells, while induced the apoptosis of HaCaT cells by inhibiting the expression of Bcl2, and promoting the expression of Bax, Caspase 3, and Caspase 9, which were opposite to VEGF. Sema3A and acitretin partially reversed the function of VEGF.

CONCLUSIONS

Like acitretin, exogenous supplement of Sema3A may correct the abnormal proliferation and apoptosis procedure of HaCaT cells, and partially reverse the function of VEGF.

摘要

背景

血管内皮生长因子（VEGF）在银屑病患者中显著升高，且与银屑病的严重程度相关。由于阿维A具有抑制VEGF产生的作用，故能有效治疗银屑病。信号素3A（Sema3A）通过部分逆转VEGF对肿瘤的作用来抑制肿瘤生长和血管生成。然而，Sema3A在银屑病发病机制中的作用尚不清楚。

目的

本研究旨在探讨VEGF、Sema3A和阿维A对HaCaT细胞的影响，以确定Sema3A是否能像阿维A一样成为银屑病治疗中的有益因素。

材料与方法

使用在不同处理条件下培养的HaCaT细胞对VEGF、Sema3A和阿维A进行功能分析。采用细胞计数试剂盒-8法、集落形成试验、流式细胞术、Transwell迁移实验、逆转录-聚合酶链反应和蛋白质免疫印迹试验来检测HaCaT细胞的增殖、集落形成、迁移、凋亡以及Bcl2、Bax、Caspase 3和Caspase 9的表达。

结果

Sema3A和阿维A抑制HaCaT细胞的增殖、集落形成和迁移，同时通过抑制Bcl2的表达并促进Bax、Caspase 3和Caspase 9的表达来诱导HaCaT细胞凋亡，这些作用与VEGF相反。Sema3A和阿维A部分逆转了VEGF的功能。

结论

与阿维A一样，外源性补充Sema3A可能纠正HaCaT细胞异常的增殖和凋亡过程，并部分逆转VEGF的功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/68ad0965a9f7/IJD-64-250a-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/11379ea614b0/IJD-64-250a-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/24383ba45a17/IJD-64-250a-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/efa29a447f0a/IJD-64-250a-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/f7adba5d8b58/IJD-64-250a-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/116d7d364cc8/IJD-64-250a-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/68ad0965a9f7/IJD-64-250a-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/11379ea614b0/IJD-64-250a-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/24383ba45a17/IJD-64-250a-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/efa29a447f0a/IJD-64-250a-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/f7adba5d8b58/IJD-64-250a-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/116d7d364cc8/IJD-64-250a-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8121/6537688/68ad0965a9f7/IJD-64-250a-g006.jpg

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Sema3A drastically suppresses tumor growth in oral cancer Xenograft model of mice.Sema3A在小鼠口腔癌异种移植模型中显著抑制肿瘤生长。
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