Nicotine-induced fibroblast growth factor-2 restores the age-related decline of precursor cell proliferation in the subventricular zone of rat brain.

6533b85bfe1ef96bd12bb4ca

RESEARCH PRODUCT

Nicotine-induced fibroblast growth factor-2 restores the age-related decline of precursor cell proliferation in the subventricular zone of rat brain.

Kjell Fuxe Monica Frinchi Alessandra Bonomo Valentina Di Liberto Giuseppa Mudò Natale Belluardo

subject

Male medicine.medical_specialty Aging Nicotine Basic fibroblast growth factor Subventricular zone Cell Count Nerve Tissue Proteins Biology Fibroblast growth factor Settore BIO/09 - Fisiologia Antibodies Subgranular zone Nestin chemistry.chemical_compound Intermediate Filament Proteins Internal medicine Precursor cell Lateral Ventricles Glial Fibrillary Acidic Protein medicine Animals Nicotinic Agonists Rats Wistar Molecular Biology Cell Proliferation Analysis of Variance Cell growth General Neuroscience Dentate gyrus Fibroblast growth factor receptor 1 Brain Precursor proliferationFGF-2 FGFR1 SVZ Nicotine Aged Rats Adult Stem Cells Endocrinology medicine.anatomical_structure nervous system chemistry Bromodeoxyuridine Gene Expression Regulation Fibroblast Growth Factor 2 Neurology (clinical)Developmental Biology

description

Precursor cell proliferation is present in the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus of adult rat and persists during aging although at reduced levels. Previous studies have shown that acute intermittent nicotine treatment significantly increases fibroblast growth factor-2 (FGF-2) expression in several brain regions of aged rats. The aim of the present investigation was to test the hypothesis that nicotine-induced expression of FGF-2 may restore the age-related decline of precursor cell proliferation. It was first demonstrated that nicotine treatment increases both mRNA and protein FGF-2 in the SVZ of aged male rats (18 months old). The effect of nicotine on precursor cell proliferation in the SVZ was studied by i.p. injection of 5-bromo-2'-deoxyuridine (BrdU) 40 mg/kg to label dividing cells. The nicotine treatment was found to significantly enhance precursor cell proliferation in the SVZ. This increase was sufficiently large to restore the age-related decline of proliferating precursor cells observed in aged rats to that found in young adult rats (3 months old). FGF-2 was expressed in GFAP-positive cells and may act via its receptor FGFR1 that was found expressed in nestin-positive cells of the SVZ. The data obtained demonstrated that the age-related decline of precursor cell proliferation may be counteracted by activating a trophic mechanism mediated by FGF-2.

year	journal	country	edition	language
2007-10-07	Brain research

10.1016/j.brainres.2007.11.069 https://pubmed.ncbi.nlm.nih.gov/18190895