Decreased calcium mobilisation and the lack of secretion in equine sweat gland cells

Abstract

Sweat secretion helps maintain skin surface ecosystems and allows humans and the Equidae to thermoregulate. A key component in sweat secretion is an increase in intracellular Ca2+ ([Ca2+])i from internal and external sources. Regulation of Ca2+ entry across the plasma membrane is initiated by emptying of the intracellular Ca2+stores and through a process known as store–operated Ca2+ entry (SOCE) via STIM and Orai proteins.We studied the role of SOCE in horse sweat gland cells from control animals and those that had developed anhidrosis, an inability to produce sweat.Western blot analysis and PCR confirmed the presence of STIM and Orai proteins in cell lines derived from control and anhidrotic animals. However, the results indicated a reduction in STIM1 mRNA and protein expression, as well as a decrease in the localisation of STIM1 in the ER of anhidrotic cells compared to control cells. The functionality of the SOCE pathway in both cell lines, in response to agonist stimulation was investigated using (FURA‐2AM) calcium imaging. Increases in [Ca2+]i could be abolished in the presence of pharmacological blockers of SOCE and that anhidrotic cells showed a significant decrease in the [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.Support provided by the Caledonian University.