Evidence that TRPC4 supports the calcium selective I(CRAC)-like current in human gingival keratinocytes.

We previously demonstrated that high external [Ca(2+)] activated two Ca(2+) currents in human gingival keratinocytes (HGKs): an initial small I(CRAC)-like current and a second large nonspecific cation current (Fatherazi S, Belton CM, Cai S, Zarif S, Goodwin PC, Lamont RJ, Izutsu KT; Pflugers Arch 448:93-104, 2004). It was recently shown that TRPC1, a member of the transient receptor potential protein family, is a component of the store-operated calcium entry mechanism in keratinocytes. To further elucidate the molecular identity of these channels, we investigated the expression of TRPC4 in gingival tissue and in cultured keratinocytes, and the effect of knockdown of TRPC4 expression on the Ca(2+) currents and influx.

Evidence that TRPC1 contributes to calcium-induced differentiation of human keratinocytes.

External calcium ion concentration is a major regulator of epidermal keratinocyte differentiation in vitro and probably also in vivo. Regulation of calcium-induced differentiation changes is proposed to occur via an external calcium-sensing, signaling pathway that utilizes increases in intracellular calcium ion concentration to activate differentiation-related gene expression. Calcium ion release from intracellular stores and calcium ion influx via store-operated calcium-permeable channels are key elements in this proposed signaling pathway; however, the channels involved have not yet been identified.

TRPC channel expression during calcium-induced differentiation of human gingival keratinocytes.

Background: Extracellular calcium is an important regulator of keratinocyte differentiation. An increase in intracellular calcium ion concentration is required for activation of calcium-induced keratinocyte differentiation. The signaling elements in this differentiation response include the calcium sensing receptor, phospholipase C, release of calcium ions from intracellular stores, and store-operated calcium channels.

Calcium oscillations in gingival epithelial cells infected with Porphyromonas gingivalis.

The periodontal pathogen Porphyromonas gingivalis modulates epithelial cell signal transduction pathways including Ca2+ signaling, and internalizes within the host cell cytoplasm. Since nuclear and cytoplasmic [Ca2+] increases can induce different host cell responses, P. gingivalis-related [Ca2+] changes in these compartments were measured by digital fluorescent imaging microscopy.

Calcium receptor message, expression and function decrease in differentiating keratinocytes.

Calcium-sensing receptor (CaSR) expression and function were studied in proliferating and differentiating cultured human gingival keratinocytes (HGKs). CaSR mRNA and protein were present in proliferating HGKs cultured in 0.03 mM [Ca(2+)] and decreased in cells induced to differentiate by culturing in 1.

Sequential activation of store-operated currents in human gingival keratinocytes.

Calcium ion store-activated currents in undifferentiated human gingival keratinocytes were measured with the whole cell patch clamp and fura techniques. Thapsigargin or intracellular inositol 1,4,5-trisphosphate and BAPTA rapidly induced an early transient current with I(CRAC) (calcium release activated calcium ion current) characteristics, and several later, larger sustained currents that depended on the mode of store depletion. Thapsigargin activated two currents within minutes of I(CRAC) activation.