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Reduced lymphocyte proliferation capacity was observed in CMZ-treated mice.
The proliferation capacity was determined by cell counting assays.
In addition, they maintained high viability and proliferation capacity.
Fig. 1 Effects of Ca2+/hypoxia on the proliferation capacity of hUCB-MSCs.
Fig. 2 Ca2+/hypoxia-treated hUCB-MSCs maintained their proliferation capacity in long-term culture.
MSCs cultured on these surfaces exhibit improved proliferation capacity, maintenance of phenotype, and increased differentiation potential.
E. granulosus germinal cells grew beyond 100 passages and showed no signs of reduced proliferation capacity.
We report that an optimized CaCl2 protocol reliably influences ASCs osteogenesis while conserving the proliferation capacity.
We then examined whether HIF-1α was involved in the Ca2+/hypoxia-dependent enhancement of the hUCB-MSC proliferation capacity.
In another randomized research, HCO hemofiltration restored the monocyte proliferation capacity of septic patients, probably by eliminating immunomodulatory mediators [31].
These results suggest that Ca2+/hypoxia enhanced the proliferation capacity of hUCB-MSCs through an HIF-1α-dependent signaling pathway.
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