Manara - Qatar Research Repository
Browse
P18 - Abstract - Muneera Vakayil.pdf (34.73 kB)

Uhrf1 regulates adipogenesis through GPNMB mediated TGFBeta axis

Download (34.73 kB)
poster
submitted on 2023-05-11, 06:21 and posted on 2023-05-17, 12:01 authored by Muneera Vakayil, Aisha Madani, Yasser Majeed, Nayef Mazloum

Poster by Muneera Vakayil (Weill Cornell Medicine - Qatar, Hamad Bin Khalifa University), Aisha Madani (Weill Cornell Medicine - Qatar), Yasser Majeed (Weill Cornell Medicine - Qatar), and Nayef Mazloum (Weill Cornell Medicine - Qatar)

Background: The increased prevalence of obesity has led to a concomitant increase in the incidence of type 2 diabetes (T2D). Obesity-linked inflammation is the major cause of insulin resistance, contributing to the onset of T2D. Therefore, understanding the cellular mechanisms responsible for adipogenesis, the conversion of preadipocytes to adipocytes, is critical for identifying anti-diabetic therapeutic targets. Uhrf1 is a key epigenetic regulator that coordinates DNA methylation and histone modifications; however, the function of Uhrf1 in metabolic diseases is not known. 

Objective: Therefore, here, we aimed to understand the role of Uhrf1 in adipogenesis by studying Uhrf1 loss of function cells.

Methods: We performed CRISPR/ Cas9 and shRNA-mediated gene silencing in addition to whole transcriptomics analysis on Uhrf1 KO cells.

Results: We identified altered molecular and cellular pathways indicating that Uhrf1 is a critical factor required for adipocyte metabolism, and in its absence, cells exhibit adipocyte dysfunctions with higher levels of inflammatory markers.

Conclusion: Our results highlight the possibility of Uhrf1 and its targets to have clinical applications in obesity and T2D treatment.

Funding

BMRP

History

Language

  • English

Publication Year

  • 2023

Institution affiliated with

  • Weill Cornell Medical College in Qatar
  • Hamad Bin Khalifa University
  • Qatar Biomedical Research Institute

Usage metrics

    Manara - Qatar Research Repository

    Licence

    Exports

    RefWorks
    BibTeX
    Ref. manager
    Endnote
    DataCite
    NLM
    DC