Cyclin D1/CDK coordination with the cellular prion protein upregulated cell proliferation signaling and preserved neurological function in acute IS rats.

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

Abstract (original English)

We tested how the coordination between cyclin D1/cyclin-dependent kinase (CDK) and the cellular prion protein (PrP C ) activates mitogenic/cell proliferation signaling to improve neurological outcomes in acute ischemic stroke (AIS) rats. Compared with those in adipose-derived mesenchymal stem cells (ADMSCs) and the N2a cell line, the cell viability, cell proliferation, cell-stress signaling, and wound healing rates were significantly increased upon overexpression of PrP C (PrP C-OE ) in ADMSCs (all P< 0.001). The cell viability, proliferation. mitochondrial mass, and protein expression of mitogenic signaling markers (cyclin D1, cyclin E1, CDK2, and CDK4) were significantly increased upon PrP C-OE in ADMSCs compared to ADMSCs that were subjected to a significant reversal of PrP C-OE by treatment with promazine (a PrP C formation inhibitor) (all P< 0.001). After 3 h of serum-free/hypoxic conditions, the protein expression levels of cyclin D1/CDK, p-Akt and mitogenic signaling markers were significantly increased upon PrP C-OE in ADMSCs compared with ADMSCs that were treated with palbociclib (a cyclin D1/CDK inhibitor). Adult male Sprague-Dawley rats (n=40) were grouped into Groups 1 (AC), 2 (AIS), 3 (AIS + ADMSCs), and 4 (AIS + ADMSCs with PrP C-OE ). By Day 28 after AIS induction, the neurological function and numbers of NeuN+ cells and myelin basic protein ( MBP )+ cells were l

Evidence level

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

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.