Fibroblast Growth Factor Type 1 (FGF1)-Overexpressed Adipose-Derived Mesenchaymal Stem Cells (AD-MSC FGF1 ) Induce Neuroprotection and Functional Recovery in a Rat Stroke Model.
Ghazavi H., Hoseini SJ., Ebrahimzadeh-Bideskan A., Mashkani B., Mehri S., Ghorbani A.
Animal Study on Stroke Research, published in Stem Cell Rev Rep (2017) — summary generated from the PubMed abstract.
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
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- Study type
- Animal Study
- Journal
- Stem Cell Rev Rep (2017)
- Country
- United States
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 28795363
- DOI
- 10.1007/s12015-017-9755-z
- Citations
- 40
Abstract (original English)
Stroke, as the second most common cause of death, imposes a great financial burden on both the individual and society. Mesenchymal stem cells from rodents have demonstrated efficacy in experimental animal models of stroke due to enhanced neurological recovery. Since FGF1 (fibroblast growth factor 1) displays neuroprotective properties, for the first time, we investigated the effect of acute intravenous administration of FGF1 gene transfected adipose-derived mesenchymal stem cell (AD-MSC FGF1 ) on transient experimental ischemic stroke in rats. Stroke induction was made by transient middle cerebral artery occlusion (tMCAO). 2 × 10 6 AD-MSC FGF1 was administrated intravenously 30 min after carotid reperfusion. The ability of technetium 99m -hexamethyl propylene amine oxime ( 99m Tc-HMPAO)-labeled AD-MSC FGF1 to enter into ischemic brain was evaluated 2 h post injection. 24 h post operation, the neurological recovery (rotarod and Roger's tests), the infarct volume (2, 3, 5-triphenyltetrazolium chloride, TTC assay), apoptosis rate (TUNEL assay), and the expression of FGF1 protein (western blotting) in the ischemic hemisphere were assessed. The 99m Tc-HMPAO-labeled AD-MSC FGF1 could enter into the ischemic brain. Ischemic hemisphere activity was significantly higher than that observed in the contralateral hemisphere (p = 0.002). The administration of AD-MSC FGF1 resulted in signific
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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