Taurine postponed the replicative senescence of rat bone marrow-derived multipotent stromal cells in vitro.
"Taurine exhibited anti-replicative senescence effect on rat BMSCs by promoting colony forming unit-fibroblast formation and cell proliferation, shortening cell population doubling time, enormously inhibiting senescence-associated beta-galactosidase activity and slowing the loss of differentiation potential, while having no significant effect on the maximum passage number and total culture time, and slight influences on the cell surface CD molecules expressions. Taurine is a quite safe antioxidant and nutrient extensively used in food addition and clinical treatment. Taurine is a promising anti-replicative senescence additive for ex vivo expansion of BMSCs in experimental and clinical cell therapies."
"As a cellular redox-controlling molecule, taurine protect the molecular constituents of cells against reactive species (SP)-induced damages"
"The addition of 100–2,000 mg/l taurine afforded virtually complete protection, in terms of both cell viability and of cell swelling. The maximal effect of taurine on neural progenitor cell proliferation was at 1,000 mg/l, though a significant increase was observed already at 100 mg/l"
Taurine may increase the number of mesenchymal stem cells available for chondrogenic differentiation thus helping you grow taller.
However Taurine may decrease chondrocyte cell volume:
The role of a swelling-activated taurine transport pathway in the regulation of articular chondrocyte volume.
"Swelling articular chondrocytes by reducing osmolarity stimulates a taurine transport pathway, which is implicated in regulatory volume decrease (RVD) in various cell types. The present study investigated factors controlling the activity of this pathway in chondrocytes, in particular (1) the effects of the acute (seconds) and chronic (hours) exposure of chondrocytes to anisotonic media, and (2) whether there is a role for metabolites from the arachidonic acid cascade in activating the taurine transport pathway. For in situ and isolated chondrocytes, the point at which swelling-activated [14C]taurine efflux was stimulated (the "set-point") corresponded closely to the osmolarity of the incubation medium (180, 280 or 380 mosmol/l). However, the volume of chondrocytes isolated into these media and measured by confocal microscopy was not different ( congruent with 645 microm3){so taurine did not reduce volume}. Activity of the swelling-activated taurine transport pathway was inhibited by REV5901 (an inhibitor of steps of the arachidonic acid cascade; K0.5 8+/-4 microM), NDGA (a general lipoxygenase inhibitor; K0.5 28+/-5 microM), or MK886 (an inhibitor of the 5-lipoxygenase-activating protein; 91% inhibition at 10 microM), but weakly by the more potent 5-lipoxygenase inhibitor REV5901 para (K0.5 350+/-100 microM). Addition of the leukotriene (LT) B4 or D4 receptor antagonists, CP-105,696 and L660,711 respectively, or of the leukotrienes LTB4, LTC4, LTD4 and LTE4 or lipoxins (hepoxylin A3 or B3) had no effect on the activity of the pathway in isotonic or hypotonic media. The role of the pathway in RVD was determined in isolated calcein-loaded chondrocytes using fluorescence imaging. RVD was observed and inhibited by REV5901 (50 microM) and by NDGA (75 microM). Despite chronic exposure of chondrocytes to anisotonic media, the cells maintain a pre-determined volume that is the "set-point" for the activation of the taurine transport pathway following acute hypotonic challenge{so the volume of chondrocytes is set by other compounds and not by taurine itself}."
"The proteoglycans surrounding the chondrocytes of articular cartilage carry a high density of immobile negative charges, resulting in high concentrations of free cations (e.g. Na+, 250-350 mM) and low concentrations of free anions(e.g. Cl- 60-90 mM)"
"[Regulatory Volume Decrease] is stimulated following hypotonicity, and leads to osmolyte loss and recovery of cell volume."
"Although the volume of chondrocytes isolated into 180, 280 or 380 mosmol/l media are the same, matrix synthesis rates are very different"
"when osmolarity was altered over 280-480 mosmol/l and matrix synthesis measured using 35SO4 incorporation over 2 h, the maximum rate was 380 mosmol/l, i.e. close to the in situ osmolarity. However, when synthesis was determined over 2 h following 24 h of incubation in 280 mosmol/l, the optimal rate was then at 280 mosmol/l."<-So the optimal matrix synthesis is based on the mean default osmolarity.
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