Growth factors like NGF are known to increase the expression of PrP gene, a housekeeping gene which is responsible for susceptibility to transmissible spongiform encephalopathies. We evaluated in vitro the effect of recombinant human growth hormone (hGH) and one of its in vivo effectors, the insulin-like growth factor I (IGF-I), on PrP gene expression in PC12 cells. We observed a 30% increase of PrP mRNA level after 7 day treatment by hGH at 10 micrograms/ml and potentiation of NGF effect (reaching four times baseline expression as opposed to three times baseline with NGF alone). IGF-I induced a dose-dependent increase of PrP mRNA up to twice baseline at a dose of 100 ng/ml and had an additive effect with NGF at 10 ng/ml. These preliminary results indicate that growth promoting factors may play a role in the PrP gene regulation within neuron-like cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1006/bbrc.1993.2373 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Effects of adipose allograft matrix on viability of humeral head cartilage and rotator cuff tendon.
BMC Musculoskelet Disord
January 2025
Department of Clinical Sciences, College of Veterinary Medicine, Columbus, OH, USA.
Background: Rotator cuff repairs may fail because of compromised blood supply, suture anchor pullout, or poor fixation to bone. To augment the repairs and promote healing of the tears, orthobiologics, such a platelet-rich plasma (PRP), and biologic scaffolds have been applied with mixed results. Adipose allograft matrix (AAM), which recruits native cells to damaged tissues, may also be a potential treatment for rotator cuff tears.
View Article and Find Full Text PDFIn vivo base editing extends lifespan of a humanized mouse model of prion disease.
Nat Med
January 2025
Merkin Institute of Transformative Technologies in Healthcare, Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Prion disease is a fatal neurodegenerative disease caused by the misfolding of prion protein (PrP) encoded by the PRNP gene. While there is currently no cure for the disease, depleting PrP in the brain is an established strategy to prevent or stall templated misfolding of PrP. Here we developed in vivo cytosine and adenine base strategies delivered by adeno-associated viruses to permanently modify the PRNP locus to achieve PrP knockdown in the mouse brain.
View Article and Find Full Text PDFCRISPR/Cas9-editing of PRNP in Alpine goats.
Vet Res
January 2025
UVSQ, INRAE, BREED, Université Paris-Saclay, 78350, Jouy-en-Josas, France.
Misfolding of the cellular PrP (PrP) protein causes prion disease, leading to neurodegenerative disorders in numerous mammalian species, including goats. A lack of PrP induces complete resistance to prion disease. The aim of this work was to engineer Alpine goats carrying knockout (KO) alleles of PRNP, the PrP-encoding gene, using CRISPR/Cas9-ribonucleoproteins and single-stranded donor oligonucleotides.
View Article and Find Full Text PDFDemyelinating neuropathy as the initial presentation of familial E200K Creutzfeldt-Jakob disease in two patients.
Ann Clin Transl Neurol
January 2025
Institut du Cerveau et de la Moelle Épinière, ICM, Sorbonne Université, INSERM, CNRS, Paris, France.
Objective: To describe peripheral neuropathy associated with familial Creutzfeldt-Jakob disease.
Methods: We report two unrelated patients with genetic Creutzfeldt-Jakob disease with demyelinating peripheral neuropathy as initial presentation, with a comprehensive clinical, electrophysiological and neuropathological description.
Results: Both patients exhibited gait disturbance and paresthesia.
Comparative assessment of chondral defect repair using human bone marrow- and adipose tissue-derived mesenchymal stem cells, adult and foetal articular cartilage-derived chondrocytes, and chondroprogenitors: an ex-vivo model.
Biotechnol Lett
January 2025
Faculty of Health and Medical Sciences, The University of Adelaide, Adelaide, SA, Australia.
Purpose: Cartilage repair necessitates adjunct therapies such as cell-based approaches, which commonly use MSCs and chondrocytes but is limited by the formation of fibro-hyaline cartilage. Articular cartilage-derived chondroprogenitors(CPs) offer promise in overcoming this, as they exhibit higher chondrogenic and lower hypertrophic phenotypes. The study aimed to compare the efficacy of various cell types derived from adult and foetal cartilage suspended in platelet-rich plasma(PRP) in repairing chondral defects in an Ex-vivo Osteochondral Unit(OCU) model.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!