Pharmacological blockers of STIM1 inhibit increases in intracellular calcium in horse sweat gland cells (650.2)

Abstract

Calcium is a key second messenger in stimulus‐secretion coupling in human and Equidae sweat gland secretory cells. Upon stimulation, calcium is released from internal stores, facilitating the opening of membrane ion channels and the subsequent formation of secretion in the lumen of the gland. Sustained secretion requires an influx of calcium from the external milieu. This calcium influx is thought to enter the secretory cells via store operated calcium channels. Little is known about store‐operated calcium entry (SOCE) and so we studied its role in horse sweat gland cells from control animals and those that had developed anhidrosis, an inability to produce sweat.We had previously shown the presence of STIM and Orai proteins in cell lines derived from control and anhidrotic animals. The results also indicated a reduction in STIM1 mRNA and protein expression in anhidrotic sweat gland cells. The functionality of the SOCE pathway in both cell lines was investigated in response to agonist stimulation using FURA‐2AM calcium‐imaging techniques. Increases in [Ca2+]i could be abolished to varying degrees in control cells by a variety of known pharmacological blockers of SOCE. Additionally anhidrotic cells showed a significant decrease in [Ca2+]i FURA‐2 ratio in response to agonists when compared to control cells.The results suggest that a reduction of STIM1 expression in the SOCE pathway may play a role in anhidrosis in horses.Grant Funding Source: Supported by Glasgow Caledonian University.