Journal
STEM CELL RESEARCH & THERAPY
Volume 10, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s13287-019-1322-x
Keywords
Adipose tissue; Behavioral outcome; Brain repair; Experimental model; Hyperglycemia; Mesenchymal stem cells
Funding
- RESSTORE project - European Commission under the Horizon2020 program [681044]
- RESSTORE project - European Commission under the Juan de la Cierva postdoctoral fellowship [IJCI-2017-33505]
- European Social Fund -European Commission [FI17/00188]
- INVICTUS PLUS network of the Carlos III Health Institute (ISCIII), Ministry of Science and Innovation of Spain [RD16/0019/0005]
- European Regional Development Fund (FEDER Funding)
- RESSTORE project - European Commission under the Miguel Servet [CP15/00069]
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Background: Over 50% of acute stroke patients have hyperglycemia, which is associated with a poorer prognosis and outcome. Our aim was to investigate the impact of hyperglycemia on behavioral recovery and brain repair of delivered human adipose tissue-derived mesenchymal stem cells (hAD-MSCs) in a rat model of permanent middle cerebral artery occlusion (pMCAO). Methods: Hyperglycemia was induced in rats by the administration of nicotinamide and streptozotocin. The rats were then subjected to stroke by a pMCAO model. At 48 h post-stroke, 1x10(6) hAD-MSCs or saline were intravenously administered. We evaluated behavioral outcome, infarct size by MRI, and brain plasticity markers by immunohistochemistry (glial fibrillary acidic protein [GFAP], Iba-1, synaptophysin, doublecortin, CD-31, collagen-IV, and alpha-smooth muscle actin [alpha-SMA]). Results: The hyperglycemic group exhibited more severe neurological deficits; lesion size and diffusion coefficient were larger compared with the non-hyperglycemic rats. GFAP, Iba-1, and alpha-SMA were increased in the hyperglycemic group. The hyperglycemic rats administered hAD-MSCs at 48h after pMCAO had improved neurological impairment. Although T2-MRI did not show differences in lesion size between groups, the rADC values were lower in the treated group. Finally, the levels of GFAP, Iba-1, and arterial wall thickness were lower in the treated hyperglycemic group than in the nontreated hyperglycemic group at 6 weeks post-stroke. Conclusions: Our data suggest that rats with hyperglycemic ischemic stroke exhibit increased lesion size and impaired brain repair processes, which lead to impairments in behavioral recovery after pMCAO. More importantly, hAD-MSC administration induced better anatomical tissue preservation, associated with a good behavioral outcome.
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