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Biology subjects

Granskog, R.

Publications and source records attributed to Granskog, R..

2 recordsLinked to original sources

Precursor of chemically expanded hepatocytes (pre-cHep) with 1-million-fold expansion potential and liver repopulation capacity

Primary human hepatocytes (PHHs) are the gold standard for toxicology and drug metabolism studies in industry. However, their limited availability, substantial batch-to-batch variability, and high cost restrict their use. Here, we report a novel culture condition that reprograms PHHs into a proliferative state. These proliferating cells, termed precursors of chemically expanded hepatocytes (pre-cHep), expand over 106-fold within 30 days while retaining liver repopulation capacity comparable to PHHs. pre-cHep can further differentiate into chemically expanded hepatocytes (cHep) as three-dimensional (3D) spheroids within 7 days in vitro, exhibiting global gene expression profiles, albumin production, and cytochrome P450 (CYP) activities similar to 3D-cultured PHH spheroids (3D PHH). Efficient genetic manipulation of pre-cHep using CRISPR/Cas9 is also achievable. Together, pre-cHep and cHep represent a promising alternative to high-quality PHHs, providing a more affordable, reproducible, and scalable source of human hepatocytes for toxicology, drug metabolism studies, disease modelling, towards precision drug development.

bioengineering↗

Hsa-miR-92a-3p regulates cell-cycle and signaling programs during human extra-embryonic lineage commitment

MicroRNA (miRNA) levels increase during human embryonic genome activation (EGA) and have been implicated in the first lineage decisions. Re-analyzing single-cell and bulk small RNA-seq (sRNA-seq) from human and mouse embryos, together with new sRNA-seq of naive human embryonic stem cells (hESCs) differentiated into hypoblast-like cells (HLCs) and extra-embryonic mesoderm (EXM)-like cells (EXMCs), we identify hsa-miR-92a-3p as highly expressed from oocyte to morula stage and dynamically regulated during HLC and EXMC formation. Functional inhibition of hsa-miR-92a-3p delays RACL (HLC/EXMC) differentiation, maintains epiblast-like and promotes trophectoderm (TE)-like transcriptional features, and reduces hypoblast and EXM marker acquisition. Transcriptome analyses revealed derepression of hsa-miR-92a-3p targets, including FGF2, and shifts in developmental and cell-cycle programs. The patterns of FGF protein stainings and flow cytometry-based cell-cycle analysis further implicate these pathways in RACL differentiation. Our findings position hsa-miR-92a-3p as a central regulator coordinating signaling and cell-cycle cues during extra embryonic lineage progression.

developmental biology↗