Abstract. K + channels are key molecules in the progression of several cancer types and considered to be potential targets for cancer therapy. We examined the gene expressions of voltage-gated (K v ), Ca

Abstract. Ca2+ release from intracellular store sites via the ryanodine receptor (RyR) and hormonal regulation by flutamide, an androgen-receptor (AR) antagonist, on it were examined in vas deferens (VD) smooth muscle cells (SMCs). VD and VDSMCs were obtained from two groups of male rats that were treated p.o. with 100 mg/kg flutamide (Flu) or vehicle (Vehicle). Both spontaneous and caffeine-induced Ca 2+ releases were markedly smaller in single VDSMCs from Flu than in those from Vehicle. Interestingly, [Ca 2+ ] i rise by 100 μM norepinephrine in VDSMCs from Flu was larger than that in those from Vehicle. The contractions induced by direct electrical stimulation in tissue preparations from Flu showed lower susceptibility to 30 μM ryanodine than those from Vehicle. Real-time PCR analyses revealed that the transcripts of ryanodine receptor (RyR) type 2 and type 3 (RyR2 and RyR3) were expressed in VD and markedly reduced in Flu. The protein expression of total RyR was significantly reduced by flutamide treatment, but that of inositol 1,4,5-trisphosphate receptor (IP3R) was not affected. It can be strongly suggested that long term block of AR by flutamide reduced the expression of RyR and its contribution to the contraction, but not those of IP3R in VDSMCs.

These results suggest that KTF-374 possesses more potent hemostatic properties than FCCF for various patterns of bleeding. KTF-374 is a promising hemostat due to its potent efficacy and good visibility of the wound site through the patch.

No abstract

A-type K+ channels contribute to regulating the propagation and frequency of action potentials in smooth muscle cells (SMCs). The present study (i) identified the molecular components of A-type K+ channels in rat vas deferens SMs (VDSMs) and (ii) showed the long-term, genomic effects of testosterone on their expression in VDSMs. Transcripts of the A-type K+ channel α subunit, Kv4.3L and its regulatory β subunits, KChIP3, NCS1, and DPP6-S were predominantly expressed in rat VDSMs over the other related subtypes (Kv4.2, KChIP1, KChIP2, KChIP4, and DPP10). A-type K+ current (IA) density in VDSM cells (VDSMCs) was decreased by castration without changes in IA kinetics, and decreased IA density was compensated for by an oral treatment with 17α-methyltestosterone (MET). Correspondingly, in the VDSMs of castrated rats, Kv4.3L and KChIP3 were down-regulated at both the transcript and protein expression levels. Changes in Kv4.3L and KChIP3 expression levels were compensated for by the treatment with MET. These results suggest that testosterone level changes in testosterone disorders and growth processes control the functional expression of A-type K+ channels in VDSMCs.