Fig. 6.

ACTH induces transient elevations in [Ca²⁺]_i through an influx of extracellular calcium in rat BMSC enriched for mesenchymal progenitors. This influx is enhanced with dexamethasone priming. In the presence of extracellular calcium (EC Ca²⁺), ACTH induces transient increases in [Ca²⁺]_i in a manner consistent with dose in BMSC left untreated (a & e). When rat MSC are treated with 10⁻⁸ M dexamethasone for 48 h (+Dex) these increases are enhanced (b & e). Some cultures, left untreated (c & f) or treated with 10⁻⁸ M dexamethasone (d & f), were re-suspended in buffer without Ca²⁺ and exposed to ACTH over a range of doses (10⁻⁸ M to 10⁻⁶ M). After ~3 min Ca²⁺ (1.8 mM) was added back to the medium and Ca²⁺ influx was measured. Times of Ca²⁺ addition are indicated by the lines above the traces. The dose of ACTH in moles/L is indicated under or next to the corresponding trace. In e & f are bar graphs of the results shown in a–d and indicate the Δ in [Ca²⁺]_i from baseline. Data are presented as mean ± SD, n = 3. Individual comparisons were made after a significant two-way ANOVA using the Bonferroni correction. * -significantly different from DEX treated counterpart. Neither α-MSH (10⁻⁶ M) nor γ₂–MSH (10⁻⁶ M) elicit changes in [Ca²⁺]_i in untreated control (g & i) or dexamethasone treated (h & j) cultures. Arrows indicate time of ACTH, α-MSH or γ₂–MSH addition. α-MSH or γ₂–MSH were added at 10⁻⁶ M. Traces are representative of 3 separate experiments.