Reversal of H2O2-induced cell death by knockdown of HOTAIR in HTR-8/SVneo cells by mediation of miR-106b-5p/ACSL4 axis

被引：0
作者：
Minkai Cao
Weilai Jin
Ying Li
Mingxin Wang
Faguang Wan
Yongwei Ren
Ying Gu
Jinqi Ma
Le Zhang
机构：
[1] Wuxi Maternity and Child Health Care Hospital,Department of Obstetrics
[2] Women’s Hospital of Jiangnan University,Department of Neonatology
[3] Affiliated Children’s Hospital of Jiangnan University,Department of Obstetrics
[4] The Affiliated Wuxi People’s Hospital of Nanjing Medical University,School of Life Science and Technology
[5] China Pharmaceutical University,Department of Ultrasound Medicine
[6] The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University,State Key Laboratory of Reproductive Medicine, Research Institute for Reproductive Health and Genetic Diseases
[7] The Affiliated Wuxi Matemity and Child Health Care Hospital of Nanjing Medical University,undefined
来源：
Functional & Integrative Genomics | 2023年 / 23卷
关键词：
Preeclampsia; HOTAIR; miR-106b-5p; ACSL4; Ferroptosis;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Preeclampsia is a serious threat to the health of pregnant women. Injury of trophoblasts could contribute to the progression of preeclampsia, and H2O2 was able to induce apoptosis in trophoblasts. LncRNAs have been reported to be involved in the progression of preeclampsia. Additionally, lncRNA HOTAIR is upregulated in patients with preeclampsia. However, the function of HOTAIR in H2O2-treated trophoblasts remains unclear. To explore the function of HOTAIR in preeclampsia, HTR-8/SVneo cells were stimulated with H2O2. RT-qPCR was performed to measure HOTAIR expression in HTR-8/SVneo cells. The apoptosis of HTR-8/SVneo cells was measured using TUNEL staining. The mitochondrial membrane potential was measured using JC-1 staining. Western blotting was performed to detect the expression of ACSL4, GPX4, and FTH1 in HTR-8/SVneo cells. The level of HOTAIR in HTR-8/SVneo cells was upregulated by H2O2. In addition, H2O2 notably inhibited the proliferation of HTR-8/SVneo cells, whereas knockdown of HOTAIR reversed this phenomenon. The mitochondrial membrane potential in HTR-8/SVneo cells was significantly inhibited by H2O2 and partially abolished by HOTAIR silencing. Moreover, HOTAIR could bind to miR-106b-5p; ACSL4 was identified as the downstream target of miR-106b-5p. Furthermore, HOTAIR knockdown reversed H2O2-induced ferroptosis in HTR-8/SVneo cells by regulating miR-106b-5p/ACSL4. Collectively, the knockdown of HOTAIR reversed H2O2-induced ferroptosis in HTR-8/SVneo cells by mediating miR-106b-5p/ACSL4. Thus, HOTAIR may serve as a new therapeutic target against preeclampsia.
引用
收藏
相关论文
共 310 条
  • [1] Abildgaard U(2013)Pathogenesis of the syndrome of hemolysis, elevated liver enzymes, and low platelet count (HELLP): a review Eur J Obstet Gynecol Reprod Biol 166 117-123
  • [2] Heimdal K(2002)Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial Lancet 359 1877-1890
  • [3] Altman D(2018)Estradiol decreases blood pressure in association with redox regulation in preeclampsia Clin Exp Hypertens 40 281-286
  • [4] Carroli G(2021)Ferroptosis, trophoblast lipotoxic damage, and adverse pregnancy outcome Placenta 108 32-38
  • [5] Duley L(2014)Treatment of preeclampsia: current approach and future perspectives Curr Hypertens Rep 16 473-321
  • [6] Farrell B(2021)Legumain promotes tubular ferroptosis by facilitating chaperone-mediated autophagy of GPX4 in AKI Cell Death Dis 12 65-98
  • [7] Moodley J(2020)Association of lncRNA SH3PXD2A-AS1 with preeclampsia and its function in invasion and migration of placental trophoblast cells Cell Death Dis 11 583-1124
  • [8] Neilson J(2021)ACSL4 exacerbates ischemic stroke by promoting ferroptosis-induced brain injury and neuroinflammation Brain Behav Immun 93 312-763
  • [9] Smith D(2021)Identification of a small molecule as inducer of ferroptosis and apoptosis through ubiquitination of GPX4 in triple negative breast cancer cells J Hematol Oncol 14 19-6403
  • [10] Babic GM(2017)ACSL4 dictates ferroptosis sensitivity by shaping cellular lipid composition Nat Chem Biol 13 91-695
12345678910