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Correction: Blood–brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism
Molecular Neurodegeneration ( IF 15.1 ) Pub Date : 2024-03-22 , DOI: 10.1186/s13024-024-00716-w
Qingyi Ma , Zhen Zhao , Abhay P. Sagare , Yingxi Wu , Min Wang , Nelly Chuqui Owens , Philip B. Verghese , Joachim Herz , David M. Holtzman , Berislav V. Zlokovic

Correction : Mol Neurodegener 13, 57 (2018)

https://doi.org/10.1186/s13024-018-0286-0

After publication of the first correction [1] to the original manuscript [2] regarding Fig. 4b, errors were noticed in the corrected Fig. 4B representative images for anti-LRP1 and RAP conditions:

  • In the merged column, representative images with similar pattern were noticed in anti-LRP1 and si.Lrp1 conditions, and in the Cy3-Aβ42 column, representative images with similar pattern were noticed in si.Lrp1 and RAP conditions.

  • The anti-LRP1 merged image, an incorrect cell tracker image was used for the merged overlay image. The merged image for anti-LRP1 has been corrected using images from the anti-LRP1 Cell tracker and Cy3-Aβ42 channels as originally presented in Fig. 4B.

  • The RAP Cy3-Aβ42 image is incorrect and was also incorrectly used for the RAP merged image. The authors have identified the correct RAP Cy3-Aβ42 image and replaced both the Cy3-Aβ42 and merged RAP images.

The single channel si.Lrp1 Cy3-Aβ42 image and si.Lrp1 merged image are both correct, and no change is needed. Importantly, these errors only pertain to the incorrect representative images in Fig. 4B and have no impact on the analysis or conclusions presented in the paper.

The corrected version of the entire Fig. 4 is shown ahead, and the authors apologize for these unintentional errors.

Fig. 4
figure 1

LRP1 mediates clearance of aggregated Cy3-Aβ42 by mouse pericytes. a-b Multiphoton/confocal laser scanning microscopy of multi-spot glass slides coated with Cy3-Aβ42 without cells (a), and with primary mouse brain pericytes cultured for 5 days in the presence of NI-IgG or anti-LRP1, after si.Lrp1 silencing compared to scrambled si.Control, and with RAP or vehicle (b). Scale bar, 50 μm. c Quantification of Cy3-Aβ42 relative signal intensityon multi-spot slides after 5 days without cells (open bar on the left) and with pericytes in the presence of vehicle (control), NI-IgG and anti-LRP1, after silencing with scrambled si.Control or si.Lrp1, and in the presence of RAP. N = 4 independent cultures (biological replicates, see Methods); mean ± s.e.m.; p < 0.05 by One-way ANOVA followed by Bonferroni post-hoc test. d Quantification of TUNEL + pericyte cell death at 3 and 7 days after seeding on multi-spot glass slides coated with Cy3-Aβ42 in the presence and absence of NI-IgG and anti-LRP1, and after si.Lrp1 silencing or si.Ctrl as in (b). N = 3 independent cultures per group; mean ± s.e.m.; p < 0.05 by One-way ANOVA followed by Bonferroni post-hoc test

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  1. Ma Q, Zhao Z, Sagare AP, et al. Correction: Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism. Mol Neurodegener. 2022;17:71. https://doi.org/10.1186/s13024-022-00573-5.

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  2. Ma Q, Zhao Z, Sagare AP, et al. Blood-brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism. Mol Neurodegener. 2018;13:57. https://doi.org/10.1186/s13024-018-0286-0.

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Author notes

  1. Qingyi Ma, Zhen Zhao and Abhay P Sagare contributed equally to this work.

Authors and Affiliations

  1. Center for Neurodegeneration and Regeneration, Zilkha Neurogenetic Institute and Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA

    Qingyi Ma, Zhen Zhao, Abhay P. Sagare, Yingxi Wu, Min Wang, Nelly Chuqui Owens & Berislav V. Zlokovic

  2. Lawrence D. Longo, MD Center for Neonatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA

    Qingyi Ma

  3. C2N Diagnostics, LLC, Saint Louis, MO, 63110, USA

    Philip B. Verghese

  4. Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX, USA

    Joachim Herz

  5. Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA

    Joachim Herz

  6. Department of Neurology and Neurotherapeutics and Center for Translational Neurodegeneration Research, University of Texas Southwestern Medical Center, Dallas, TX, USA

    Joachim Herz

  7. Department of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer’s Disease Research Center, Washington University School of Medicine, Saint Louis, MO, 63110, USA

    David M. Holtzman

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Corresponding author

Correspondence to Berislav V. Zlokovic.

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Ma, Q., Zhao, Z., Sagare, A.P. et al. Correction: Blood–brain barrier-associated pericytes internalize and clear aggregated amyloid-β42 by LRP1-dependent apolipoprotein E isoform-specific mechanism. Mol Neurodegeneration 19, 27 (2024). https://doi.org/10.1186/s13024-024-00716-w

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中文翻译：
纠正：血脑屏障相关周细胞通过 LRP1 依赖性载脂蛋白 E 异构体特异性机制内化并清除聚集的淀粉样蛋白 - β42

更正 ： Mol Neurodegene 13, 57 (2018)

https://doi.org/10.1186/s13024-018-0286-0

在针对图 4b 对原始手稿 [2] 进行第一次更正 [1] 后，在针对抗 LRP1 和 RAP 条件的校正后的图 4B 代表性图像中发现了错误：

  • 在合并列中，在抗 LRP1 和 si 中注意到具有相似模式的代表性图像。Lrp1条件下，在 Cy3-Aβ42 柱中，在 si 中注意到具有相似模式的代表性图像。Lrp1和 RAP 条件。

  • 抗LRP1合并图像，错误的细胞跟踪器图像被用于合并的覆盖图像。抗 LRP1 的合并图像已使用来自抗 LRP1 细胞追踪器和 Cy3-Aβ42 通道的图像进行校正，如图 4B 中最初所示。

  • RAP Cy3-Aβ42 图像不正确，并且也错误地用于 RAP 合并图像。作者已识别出正确的 RAP Cy3-Aβ42 图像，并替换了 Cy3-Aβ42 和合并的 RAP 图像。

单通道si。Lrp1 Cy3-Aβ42 图像和 si。Lrp1合并图像都是正确的，无需更改。重要的是，这些错误仅与图 4B 中不正确的代表性图像有关，对论文中提出的分析或结论没有影响。

整个图 4 的更正版本如前所示，作者对这些无意的错误表示歉意。

图4
图1

LRP1 介导小鼠周细胞清除聚集的 Cy3-Aβ42。a - b涂有 Cy3-Aβ42 且无细胞的多点载玻片的多光子/共焦激光扫描显微镜 ( a )，以及在 si 后在 NI-IgG 或抗 LRP1 存在下培养 5 天的原代小鼠脑周细胞。Lrp1沉默与扰乱 si 的比较。控制，并用RAP或车辆( b )。比例尺，50 μm。c在用乱序 si 沉默后，在没有细胞（左侧空心条）和有周细胞的情况下，在载体（对照）、NI-IgG 和抗 LRP1 存在下 5 天后，在多点载玻片上对 Cy3-Aβ42 相对信号强度进行定量。控制或si。Lrp1，并且在 RAP 存在的情况下。N  = 4 个独立培养物（生物重复，参见方法）；平均值±标准误； 通过单向方差分析和 Bonferroni 事后检验得出p < 0.05。 d 在存在和不存在 NI-IgG 和抗 LRP1 的情况下，以及在 si 后，在涂有 Cy3-Aβ42 的多点载玻片上接种后第 3 天和第 7 天对 TUNEL + 周细胞死亡进行定量。Lrp1沉默或 si。按 ( b ) 中的Ctrl 键。N  = 每组 3 个独立培养物；平均值±标准误； 单向方差分析p < 0.05，然后进行 Bonferroni 事后检验

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  1. 马Q，赵Z，Sagare AP，等。纠正：血脑屏障相关周细胞通过 LRP1 依赖性载脂蛋白 E 异构体特异性机制内化并清除聚集的淀粉样蛋白 - β42。摩尔神经退行性疾病。 2022；17:71。 https://doi.org/10.1186/s13024-022-00573-5。

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  2. 马Q，赵Z，Sagare AP，等。血脑屏障相关周细胞通过 LRP1 依赖性载脂蛋白 E 异构体特异性机制内化并清除聚集的淀粉样蛋白 - β42。摩尔神经退行性疾病。 2018；13:57。 https://doi.org/10.1186/s13024-018-0286-0。

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作者笔记

  1. 马清一、赵震和 Abhay P Sagare 对这项工作做出了同样的贡献。

作者和单位

  1. 南加州大学凯克医学院神经退行性和再生中心、Zilkha 神经发生研究所和生理学和神经科学系，洛杉矶，加利福尼亚州，90033，美国

    马清一、赵震、Abhay P. Sagare、吴英熙、王敏、Nelly Chuqui Owens 和 Berislav V. Zlokovic

  2. Lawrence D. Longo，医学博士 洛马琳达大学医学院基础科学系药理学部新生儿生物学中心，洛马琳达，加利福尼亚州，92350，美国

    马清一

  3. C2N Diagnostics, LLC，圣路易斯，密苏里州，63110，美国

    菲利普·B·维尔盖斯

  4. 分子遗传学系，德克萨斯大学西南医学中心，达拉斯，德克萨斯州，美国

    约阿希姆·赫兹

  5. 神经科学系，德克萨斯大学西南医学中心，达拉斯，德克萨斯州，美国

    约阿希姆·赫兹

  6. 德克萨斯大学西南医学中心神经病学和神经治疗学系和转化神经变性研究中心，美国德克萨斯州达拉斯

    约阿希姆·赫兹

  7. 神经内科，希望神经疾病中心，奈特阿尔茨海默病研究中心，华盛顿大学医学院，圣路易斯，密苏里州，63110，美国

    大卫·霍尔兹曼

作者
  1. 马清一查看作者出版物

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  2. 赵震查看作者出版物

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通讯作者

通讯作者：Berislav V. Zlokovic。

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Ma，Q.，赵，Z.，Sagare，AP等。更正：血脑屏障相关周细胞通过 LRP1 依赖性载脂蛋白 E 异构体特异性机制内化并清除聚集的淀粉样蛋白 - β42。摩尔神经变性 19 , 27 (2024)。 https://doi.org/10.1186/s13024-024-00716-w

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