VEGF reduces astrogliosis and preserves neuromuscular junctions in ALS transgenic mice.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease resulting from motor neuron loss in the spinal cord and brain stem. In the present study, we found that systemic administration of recombinant vascular endothelial growth factor (VEGF) significantly diminished astrogliosis and increased the number of neuromuscular junctions in a Cu/Zn superoxide dismutase (SOD1) transgenic mouse model of ALS. Our results thus demonstrate a novel regulatory role of VEGF on astrocytes and are suggestive of protective effects of VEGF both in the peripheral and central nervous system in the SOD1 transgenic mouse model. These findings warrant further evaluation of the mechanism(s) of regulatory effects of VEGF on neuronal and non-neuronal cells, and the relation of these events to motor neuron degeneration and the onset and progression of ALS.
Zheng
Chengyun
C
Childhood Cancer Research Unit, Department of Woman and Child Health, Karolinska Institutet, Karolinska University Hospital, 171 76 Stockholm, Sweden.
Sköld
Mattias K
MK
Li
Jian
J
Nennesmo
Inger
I
Fadeel
Bengt
B
Henter
Jan-Inge
JI
D000690:Amyotrophic Lateral Sclerosis / Q000378:metabolism / Q000473:pathology*; D000818:Animals; D001253:Astrocytes / Q000166:cytology* / Q000187:drug effects* / Q000473:pathology; D002454:Cell Differentiation / Q000187:drug effects*; D006801:Humans; D051379:Mice; D008822:Mice, Transgenic; D009469:Neuromuscular Junction / Q000166:cytology / Q000187:drug effects*; D011994:Recombinant Proteins / Q000008:administration & dosage / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000008:administration & dosage / Q000494:pharmacology*
D011994:Recombinant Proteins; D042461:Vascular Endothelial Growth Factor A