Search bioRxiv⌕ Search

Biology subjects

Caserta, C.

Publications and source records attributed to Caserta, C..

2 recordsLinked to original sources

Ex Vivo Expansion of Hematopoietic Stem and Progenitor Cells from Human Mobilized Peripheral Blood for Gene Therapy Applications

Ex vivo expansion of mobilized peripheral blood (mPB) hematopoietic stem cells (HSCs) represents a promising approach to advance cell and gene therapy strategies yet is hampered by loss of stem cell function when applying commonly used culture protocols. We performed in-depth characterization of mPB expansion cultures by single cell RNA sequencing, which highlighted differentiation trajectories with preservation of lineage fidelity in committed progenitors. Defining a putative HSC cluster allowed an estimation of transduction efficiency in ex vivo cultures, which correlated with long-term gene marking in xenografts and patients enrolled in a gene therapy study. We then developed a clinically translatable, GMP-compliant process to expand lentivirus (LV)-transduced HSCs from mPB of pediatric patients and adult donors, by biologically informed protocol improvements of cytokine supplementation, media choice, timing of LV transduction and combinations of small molecules preventing the activation of differentiation programs. Our optimized process outperforms validated state-of-the-art cord blood expansion protocols when applied to mPB. LV integration site analysis and genomic barcode-based clonal tracking provided definitive proof for symmetric HSC self-renewal divisions occurring during ex vivo culture. These results warrant clinical testing of this HSC transduction/expansion process in an upcoming clinical gene therapy trial for autosomal recessive osteopetrosis (EU CT 2024-518972-30). One Sentence SummaryA mobilized peripheral blood HSC expansion protocol optimized for gene therapy allows robust polyclonal long-term engraftment of LV-transduced cells.

cell biology↗

The mitochondrial NAD transporter SLC25A51 is a modulator of beta cell senescence and type 2 diabetes

AbstractNicotinamide adenine dinucleotide (NAD+) is an essential redox cofactor and signaling molecule linked to age-dependent metabolic decline, with its compartmentalization regulated by the mitochondrial carrier SLC25A51. The mechanisms contributing to declining NAD+ levels during aging and the consequences of altered NAD+ homeostasis across tissues are poorly understood. Here, we show that SLC25A51 is upregulated in aging and aging-associated conditions, particularly in senescent cells. In a mouse model of beta-cell senescence, upregulated SLC25A51 was associated with beta-cell identity loss, senescence progression, and a reduced NAD+/NADH ratio. SLC25A51 was elevated following p16INK4a-, replicative-, irradiation-, and H2O2-induced senescence, with NRF2 implicated as a potential transcriptional regulator. Overexpression of SLC25A51, but not a transport-dead mutant, induced senescence factors, while its deletion prevented this effect. Beta-cell-specific deletion of SLC25A51 lowered p16INK4a levels in pancreatic islets, circulating insulin, and glucose levels, improving insulin sensitivity and indicating its role in cellular senescence and the metabolic control of beta-cell function.

cell biology↗