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假基因 fms 相关酪氨酸激酶 1 假基因 1（FLT1P1）与 RNA 结合蛋白先天性角化不良症 1（DKC1）合作，通过靶向子痫前期中的 fms 相关酪氨酸激酶 1（FLT1）来抑制滋养细胞增殖和血管生成。

Pseudogene fms-related tyrosine kinase 1 pseudogene 1 (FLT1P1) cooperates with RNA binding protein dyskeratosis congenita 1 (DKC1) to restrain trophoblast cell proliferation and angiogenesis by targeting fms-related tyrosine kinase 1 (FLT1) in preeclampsia.

机构信息

Department of Obstetrics, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.

出版信息

Bioengineered. 2021 Dec;12(1):8885-8897. doi: 10.1080/21655979.2021.1988366.

DOI:10.1080/21655979.2021.1988366
PMID:34699328
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8806956/
Abstract

In preeclampsia (PE), preexistent maternal endothelial dysfunction leads to impaired placentation and vascular maladaptation. Long noncoding RNAs (lncRNAs) have been shown to participate in the placentation process. LncRNA fms-related tyrosine kinase 1 pseudogene 1 () was previously reported to be upregulated in PE. In this study, we verified the effect of and its cognate gene on trophoblast cell proliferation and angiogenesis by using Cell Counting Kit-8 (CCK-8) assay, tube formation assay, and western blot analysis. Their binding to RNA binding protein dyskeratosis congenita 1 () was validated by conducting RNA immunoprecipitation (RIP) and RNA pulldown assays. In this study, knockdown of or was found to promote cell proliferation and angiogenesis in trophoblasts. In addition, recruited to stabilize . Importantly, silencing or decreased the stability of . Rescue assays revealed that overexpression reversed the effect of silenced . Overall, cooperates with to restrain trophoblast cell proliferation and angiogenesis by targeting .

摘要

在子痫前期（PE）中，先前存在的母体血管内皮功能障碍导致胎盘功能障碍和血管适应不良。长链非编码 RNA（lncRNA）已被证明参与胎盘形成过程。先前有报道称，lncRNA fms 相关酪氨酸激酶 1 假基因 1（）在 PE 中上调。在这项研究中，我们通过使用细胞计数试剂盒-8（CCK-8）测定、管形成测定和 Western blot 分析来验证和其同源基因对滋养细胞增殖和血管生成的影响。通过进行 RNA 免疫沉淀（RIP）和 RNA 下拉测定验证了它们与 RNA 结合蛋白先天性角化不良症 1（）的结合。在这项研究中，发现敲低或可促进滋养细胞的增殖和血管生成。此外，募集到稳定。重要的是，沉默或降低的稳定性。挽救实验表明，过表达逆转了沉默的效果。总的来说，通过靶向，与合作来抑制滋养细胞的增殖和血管生成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/3267e1c2a40d/KBIE_A_1988366_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/c14a0b1f121d/KBIE_A_1988366_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/b638e6f64c8e/KBIE_A_1988366_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/d01ff07cc917/KBIE_A_1988366_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/060bfb201dde/KBIE_A_1988366_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/3267e1c2a40d/KBIE_A_1988366_F0005_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/c14a0b1f121d/KBIE_A_1988366_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/b638e6f64c8e/KBIE_A_1988366_F0002_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/d01ff07cc917/KBIE_A_1988366_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/060bfb201dde/KBIE_A_1988366_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fe1/8806956/3267e1c2a40d/KBIE_A_1988366_F0005_B.jpg

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