gms | German Medical Science

73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

29.05. - 01.06.2022, Köln

Long Non-Coding RNA (Lnc RNA) NEAT1 is differentially expressed in ruptured and unruptured intracranial aneurysms (ICAs)

Expressionsunterschiede von NEAT1, einem langen nicht-kodierenden RNA (lnc-RNA) in rupturierten vs nicht rupturierten intrakraniellen Aneurysmen (ICAs)

Meeting Abstract

  • presenting/speaker Baolong Zheng - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Dilaware Khan - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Xuanchen Li - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Huakang Zhou - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Serdar Alpdogan - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Ann-Christin Nickel - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Ke Li - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Rui Zhang - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Jan Frederick Cornelius - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Daniel Hänggi - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland
  • Sajjad Muhammad - Universitätsklinikum Düsseldorf, Klinik für Neurochirurgie, Düsseldorf, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie. Köln, 29.05.-01.06.2022. Düsseldorf: German Medical Science GMS Publishing House; 2022. DocP091

doi: 10.3205/22dgnc401, urn:nbn:de:0183-22dgnc4017

Veröffentlicht: 25. Mai 2022

© 2022 Zheng et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objective: lncRNA NEAT 1 contributes to the regulation of oxidative stress, inflammation, cell proliferation, migration, phenotypic transformation via instructing gene expression. These processes are closely involved in pathophysiology of vascular diseases including atherosclerosis, hypertension, formation and rupture of intracranial aneurysms. In response to vascular injury vascular smooth muscle cells switch from contractile to proliferative phenotype thereby contributing to vascular repair. Recently, NEAT1 expression has been shown to control the phenotype switch of vascular smooth muscle cells contributing to neointima formation. Role of NEAT1 in intracranial aneurysms (ICA) is unexplored. This study was planned to investigate the expression, and clinical significance of NEAT1 in ICAs.

Methods: We collected specimens of ruptured and unruptured ICAs during the microsurgical clipping (n=5). Samples of superficial temporal artery were collected as controls. Using NucleoZOL, total RNA was extracted and then reverse transcribed to cDNA. Quantitative real-time PCR (qRT-PCR) analysis was performed to quantify the expression levels of NEAT1 that was then normalized to housekeeping gene (β-actin). SPSS software was used to analyze the data.

Results: NEAT1 expression was slightly increased in unruptured intracranial aneurysms as compared to healthy superficial temporal artery showing probably a measure of enhanced proliferative activity after vascular injury. Interestingly, NEAT1 expression was significantly lower in samples from ruptured ICAs as compared to unruptured ICAs. The relative expression to housekeeping gene (β-actin) was quantified (mean±SE) in three groups and compared using one way ANOVA (control=1.15±0.54 fold, ruptured ICAs=0.40±0.17 fold, unruptured ICAs=1.81±0.85 fold, p< 0.05).

Conclusion: NEAT1 expression was significantly lower in ruptured ICAs as compared to the unruptured ICAs. NEAT1 might be required in neointimal formation and repair of ICA wall. Further investigation with cell specific markers and in vivo studies are necessary to find the exact role of NEAT 1 in pathophysiology of ICAs.