Luiza Ghila's picture

Luiza Ghila

  • E-mailLuiza.Ghila@uib.no
  • Phone+47 413 09 216
  • Visitor Address
    Barne- og ungdomssjukehuset (BUS1)
    Haukelandsbakken 15
    5021 Bergen
    6110, 6th floor
  • Postal Address
    Postboks 7804
    5020 Bergen

My research aims at studying the molecular switches acting as regenerative/cell-plasticity breaks by actively maintaining the cell fate, thereby ensuring the strict regulation of cell identity and/or numbers.

For example, by using genetic cell fate-tracing techniques, I studied a spontaneous age-dependent regeneration process in the mammalian pancreas, based on a cell-fate conversion. Although a natural attempt of mammalian regeneration, this regenerative mechanism was extremely inefficient, with only 2% of the cells converting at any given time point (Thorel et al., Nature, 2010; Chera et al. Nature, 2014). We investigated the cellular and molecular mechanisms behind this restricted cell identity change and revealed that Insulin and Hedgehog signalling pathways act as natural cell-plasticity breaks by actively maintaining cell-identity (Cigliola*, Ghila*, Thorel* et al., Nature Cell Biology, 2018; *equal contribution). These results are neither organ-specific nor isolated, with an incremental body of literature reporting cell-plasticity breaks in many mammalian tissue and organs. Several recent studies pointed towards a short list of signalling pathways involved, reviewed by us in Cigliola, Ghila et al., 2020, Stem Cells. 

I am currently investigating the molecular mechanisms acting during cell reprogramming and differentiation using mouse models and hiPS-derived human cell models.  

Academic article
  • Show author(s) 2020. In vivo environment swiftly restricts human pancreatic progenitors toward mono-hormonal identity via a HNF1A/HNF4A mechanism. Frontiers in Cell and Developmental Biology. 1-14.
  • Show author(s) 2020. Encapsulation boosts islet-cell signature in differentiating human induced pluripotent stem cells via integrin signalling . Scientific Reports. 1-16.
  • Show author(s) 2020. Bioinformatic analyses of miRNA-mRNA signature during hiPSC differentiation towards insulin-producing cells upon HNF4α mutation. Biomedicines. 1-20.
  • Show author(s) 2019. The effect of WnT pathway modulators on human iPSC-derived pancreatic beta cell maturation. Frontiers in Endocrinology. 1-13.
  • Show author(s) 2019. Reprogrammed cells display distinct proteomic signaturesAssociated with colony morphology variability. Stem Cells International. 1-16.
  • Show author(s) 2019. In vivo hyperglycemia exposure elicits distinct period-dependent effects on human pancreatic progenitor differentiation, conveyed by oxidative stress. Acta Physiologica. 1-16.
  • Show author(s) 2019. Diabetes relief in mice by glucose-sensing insulin-secreting human α-cells. Nature. 43-48.
  • Show author(s) 2018. Pancreatic islet-autonomous insulin and smoothened-mediated signalling modulate identity changes of glucagon+ α-cells. Nature Cell Biology. 1267-1277.
  • Show author(s) 2018. Novel protein signatures suggest progression to muscular invasiveness in bladder cancer. PLOS ONE. 1-15.
  • Show author(s) 2017. Probing the missing mature β-cell proteomic landscape in differentiating patient iPSC-derived cells. Scientific Reports. 1-14.
Popular scientific article
  • Show author(s) 2019. Encapsulation boosts islet-cell signature in differentiating human induced pluripotent stem cells via integrin signalling. bioRxiv - the preprint server for biology.
Academic literature review
  • Show author(s) 2019. Tissue repair brakes: A common paradigm in the biology of regeneration: Concise review. Stem Cells. 330-339.

More information in national current research information system (CRIStin)

2016-2019 Characterization of regulatory mechanisms in differentiating MODY-iPS-derived pancreatic cells (postdoctoral project funded by UiB, PI)

2019-2020 Differentiating insulin-producing cells from induced pluripotent stem cells derived from diabetes patients (funded by Diabetesforbundet, PI)

2020-2023 Supportive therapy for diabetes by increasing the stress endurance and regenerative capacity of beta-cells (funded by EEA and Norway Grants funding scheme, RoNo2019)