1
Furthermore, behavioral recovery was similar with both striatal and femoral hUCB delivery.
2
Renal functional decline and tubular injury after IRI were attenuated by HUCB-MSC treatment.
3
Our results suggest a promising role for HUCB-MSCs in the treatment of renal IRI.
4
SDF-1 induced the migration of hUCB-MSCs in a dose-dependent manner.
5
We further investigated how hUCB-MSCs enhance cellular survival and inhibit apoptosis in NPC mice.
6
However, migration signaling pathways required for homing and recruitment of hUCB-MSCs are not fully understood.
7
HUCB-MSCs treatment also prevented the induction of TIMPs expression.
8
In contrast, hUCB-MSC injection did not elicit these responses.
9
Rats receiving HUCB cells have a less severe inflammatory response compared to MCAO stroke rats.
10
Mononuclear HUCB cells were added to half the cultures at the beginning of the hypoxia conditions.
11
Our data suggest that HUCB cells may produce a soluble factor that decreases viability of microglia.
12
In inflammatory conditions simulated in a cell culture experiment, VEGF secretion from HUCB-MSCs was substantially enhanced.
13
Interestingly, repeated administration of hUCB-MSCs was not found to elicit additional or synergistic improvements over monotherapy.
14
We showed that hUCB-MSCs have the migration ability toward the glioma cell lines and primary glioma cells.
15
We hypothesized that HUCB-MSCs could suppress the inflammatory response in postischemic kidneys and attenuate early renal injury.
16
To test this hypothesis, hUCB-MSCs were transplanted into the hippocampus of NPC mice in the early asymptomatic stage.