Trp1, a candidate protein for the store-operated Ca2+ influx mechanism in salivary gland cells

Abstract

The trp gene family has been proposed to encode the store-operated Ca2+ influx (SOC) channel(s). This study examines the role of Trp1 in the SOC mechanism of salivary gland cells, htrp1, htrp3, and Trp1 were detected in the human submandibular gland cell line (HSG). HSG cells stably transfected with htrp1α cDNA displayed (i) a higher level of Trp1, (ii) a 3- 5-fold increase in SOC (thapsigargin-stimulated Ca2+ influx), determined by [Ca2+](i) and Ca2+-activated K+ channel current measurements, and (iii) similar basal Ca2+ permeability, and inhibition of sac by Gd3+ but not by Zn2+, as compared with control cells. Importantly, (i) transfection of HSG cells with antisense trp1α cDNA decreased endogenous Trp1 level and significantly attenuated SOC, and (ii) transfection of HSG cells with htrp3 cDNA did not increase SOC. These data demonstrate an association between Trp1 and SOC and strongly suggest that Trp1 is involved in this mechanism in HSG cells. Consistent with this suggestion, Trp1 was detected in the plasma membrane region, the proposed site of SOC, of acinar and ductal cells in intact rat submandibular glands. Based on these aggregate data, we propose Trp1 as a candidate protein for the sac mechanism in salivary gland cells.