Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMC

PSXV-9 A Novel Anti-sense LncRNA of CEBPA Inhibits Bovine Adipogenic Differentiation

Li A., Hu Y., Liu X., Zhao L., Tian Q., Du M.

Laboratory Study, published in J Anim Sci (2018) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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Study type
Laboratory Study
Journal
J Anim Sci (2018)
Reported sample size
—
Source database
Europe PMC
PMCID
PMC6285989

Abstract (original English)

Abstract Long non-coding RNAs (lncRNAs) have been revealed to play key role in the adipogenesis. Recently, a number of lncRNAs have been identified in adipose tissue by RNA sequencing, however the function of these lncRNAs remains largely undefined. In this study, we identified a novel bovine lncRNA located on bovine chromosome 18. It spans approximately 4.25 kb on the genome, containing two exons and one intron. The transcript is about 2608 bp which is an anti-sense lncRNA of CCAAT/enhancer-binding protein &alpha; gene (CEBPA), the product of which is known to regulate adipogenesis. To investigate the potential role of this LncRNA in adipogenesis, we cloned the anti-sense lncRNA of CEBPA into the pcDNA3.1+ vector. Then the construct was transfected into the bovine stromal vascular fraction (SVF) cells. Six hours (h) after transfection, an adipogenic inducing medium was applied. After 48 h following transfection, cells were collected. Compared to the pcDNA3.1+ vector only transfection, anti-sense lncRNA of CEBPA was dramatically enhanced due to LncRNA plasmid transfection (P < 0.01), while CEBPA and PPAR&gamma;2 were significantly down-regulated (P < 0.05). Oil Red O staining showed the over-expression of anti-sense lncRNA of CEBPA inhibited lipid accumulation in differentiated SVF cells. Interestingly, when we cloned the anti-sense lncRNA of CEBPA into the nuclear pZW1-snoVect

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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