Response by Cui et al to Letter Regarding Article, "RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis".
Response by Cui et al to Letter Regarding Article, "RGC-32 (Response Gene to Complement 32) Deficiency Protects Endothelial Cells From Inflammation and Attenuates Atherosclerosis".
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Cui 等人对有关文章“RGC-32（补体 32 的响应基因）缺乏可保护内皮细胞免受炎症并减轻动脉粥样硬化”的信件的回应。
DOI：
10.1161/atvbaha.118.311146
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Chen,Shi-You
中科院分区：
文献类型：
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作者：
Cui,Xiao-Bing;Luan,Jun-Na;Dong,Kun;Chen,Sisi;Wang,Yongyi;Watford,WendyT;Chen,Shi-You
我们欢迎罗斯等人来信评论我们最近的研究，该研究表明RGC-32（补体32应答基因）通过诱导内皮细胞间粘附分子-1和血管细胞粘附分子-1促进单核细胞-内皮细胞（EC）相互作用介导动脉粥样硬化的发展。1我们的结论是基于以下几个观察：（1）RGC-32在人和小鼠动脉粥样硬化病变的EC中被诱导;（2）RGC-32缺陷（Rgc32 −/−）减弱Apoe −/−小鼠自发形成和高脂饮食诱导的动脉粥样硬化;（3）移植野生型骨髓的Rgc32 −/−小鼠没有显著改变Rgc32 −/−表型;（4）Rgc32 −/−抑制内皮细胞间黏附分子-1和血管细胞黏附分子-1的表达及单核细胞-EC相互作用。1这些数据有力地表明，内皮RGC-32在动脉粥样硬化中起着重要作用。我们理解信中对我们和Vlaicu博士等人2研究中人类动脉粥样硬化病变中RGC-32表达差异的关注，并赞赏这种差异可能是不同动脉区域动脉粥样硬化病变差异的结果。通过重新查看两项研究中的相关数据，1我们意识到差异也可能是由不同的免疫组织化学染色程序引起的，如一抗浓度、二抗或底物孵育时间等。我们试图不过度染色组织切片以避免非特异性染色，如果我们的孵育时间延长或使用更大量的抗体，我们可以在平滑肌细胞（SMC）或其他细胞类型中观察到RGC-32染色。然而，来自Vlaicu等人2和我们的研究的结果表明，EC在人类病变中的细胞中表现出最强的RGC-32染色，这与我们的结论一致，即RGC-32主要但不仅仅在EC中表达。1我们报道RGC-32通过增强p34 CDC 2活性和诱导粘着斑接触和应力纤维形成促进损伤诱导的血管重塑和介导血小板源性生长因子-BB诱导的SMC增殖和迁移。3我们的结果确实与Badea等人4的发现一致，即RGC-32介导C5b-9诱导的SMC迁移和增殖。然而，动脉粥样硬化中SMC的功能比机械损伤诱导的血管重塑复杂得多。在早期病变中，平滑肌细胞除了增殖和迁移外，还可能成为巨噬细胞样细胞和泡沫细胞，这些细胞失去了SMC标志物的表达。5. RGC-32可能
We welcome the letter from Rus et al commenting on our recent study showing that RGC-32 (response gene to complement 32) mediates the development of atherosclerosis by facilitating monocyte–endothelial cell (EC) interaction through induction of endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. 1 Our conclusion is based on several observations:(1) RGC-32 is induced in ECs in both human and mouse atherosclerotic lesions;(2) RGC-32 deficiency (Rgc32−/−) attenuates the spontaneously-developed and high-fat diet–induced atherosclerosis in Apoe−/− mice;(3) Rgc32−/− mice transplanted with wild-type bone marrow does not significantly alter the Rgc32−/− phenotype;(4) Rgc32−/− inhibits endothelial intercellular adhesion molecule-1 and vascular cell adhesion molecule-1expression and monocyte–EC interaction. 1 These data strongly suggest that endothelial RGC-32 plays an essential role in atherosclerosis. We understand the concern in the letter about the differences in RGC-32 expression in human atherosclerotic lesions in our and Dr Vlaicu et al’s2 studies and appreciate the insights that the discrepancy may be the result of the differences in the atherosclerotic lesions from different arterial regions. By revisiting the relevant figures in both studies, 1 we have realized that the discrepancy could also be caused by different immunohistochemistry staining procedures, such as primary antibody concentration, secondary antibody, or substrate incubation time, etc. We have attempted to not overstain the tissue sections to avoid nonspecific staining, and we could observe RGC-32 staining in smooth muscle cells (SMC) or other cell types if our incubation times were prolonged, or greater amounts of antibodies were used. However, the results from both Vlaicu et al’s2 and our studies show that ECs exhibit the strongest RGC-32 staining among cells in human lesions, consistent with our conclusion that RGC-32 is predominantly, but not only, expressed in ECs. 1We reported that RGC-32 promotes injury-induced vascular remodeling and mediates platelet-derived growth factor-BB-induced SMC proliferation and migration by enhancing p34CDC2 activity and inducing focal adhesion contact and stress fiber formation, respectively. 3 Our results are indeed consistent with Badea et al’s4 findings that RGC-32 mediates C5b-9–induced migration and proliferation of SMCs. However, SMC functions are much more complicated in atherosclerosis than mechanic injury-induced vascular remodeling. In addition to the proliferation and migration, SMCs may become macrophage-like cells and foam cells in early stage lesions, which loss the SMC marker expression. 5 It is possible that RGC-32
影响因子：
20.1
作者：
Zeller I;Srivastava S
通讯作者：
Srivastava S
DOI：
10.1161/atvbaha.117.310656
发表时间：
2018-04
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Cui XB;Luan JN;Dong K;Chen S;Wang Y;Watford WT;Chen SY
通讯作者：
Chen SY
影响因子：
4.8
作者：
Tang, Rui;Zhang, Gui;Chen, Shi-You
通讯作者：
Chen, Shi-You