Bone Abstracts

Calcium represents one of the most versatile and universal signalling particles regulating many different cellular processes. Changes in [Ca²⁺]_i give rise to a vast diversity of modulatory events, amongst others, influencing activities of kinases and ion channels.

It was demonstrated that nuclear magnetic resonance therapy (NMRT) treatment in osteoarthritis led to reduced pain and improved function followed by increase in quality of life. Less is known about how NMRT influences cellular processes, a modulation of ion channels is discussed. Likewise, NMRT might transmit its signal activity by generating mechanical forces to the cell’s surface, activating signal transmission.

To investigate NMRT influencing the cellular messenger [Ca²⁺]_i, cells were stimulated with NMRT for 1 h ± IL1β. Induction of calcium release was initiated by histamine application (1–100 μM). Fura-2 functioned as indicator for calcium imaging, Ca²⁺ concentration was calculated by determining the 340:380 nm ratio. A functional involvement of MAPKs was investigated by applying U0126 (MAPK/ERK inhibitor) and SB203580 (p38/MAPK inhibitor) prior to calcium measurements. The influence of NMRT on protein kinase activity was further investigated via a phospho-MAPK array.

Our preliminary results demonstrate NMRT to influence basal intracellular calcium levels; peak calcium concentrations induced by histamine application were not affected. Interestingly without IL1β NMRT treatment depicted lower levels of basal and peak [Ca²⁺]_i. U0126 or SB203580 modulated the intracellular calcium release in general and the basal calcium under NMRT in particular. A first brief screening regarding the activity of kinases revealed an apparent up-regulation of MAPK/ERK and p38 MAPK in NMRT stimulated cells.

Obviously under inflammatory conditions NMRT influences [Ca²⁺]_i by modulating cell’s calcium influx and/or calcium release leading to increased MAPK activity, both possibly playing a role in the game of observed pain reduction.