Calcium and Vitamin D increase mRNA levels for the growth control hIK1 channel in human epidermal keratinocytes but functional channels are not observed

Manaves, Vlasios; Qin, Wuxuan; Bauer, Amy L.; Rossie, Sandra; Kobayashi, Masakazu; Rane, Stanley G.

doi:10.1186/1471-5945-4-7

Cited by 11 publications

(6 citation statements)

References 30 publications

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“…Furthermore, to elucidate the role of the BK channel in cell proliferation of ventricular fibroblasts, we carried out cell proliferation assay, and found that it was increased by clotrimazole (a specific IK channel blocker), but not by IBTX (a specific BK channel blocker) or apamin (a specific SK channel blocker) during 24 hr of incubation. Our results on IK channels are in good accordance with previous observation that 1-EBIO (a specific IK activator) suppresses mRNA expression of IK channels and cell proliferation in HaCaT kerationcytes (Koegel et al, 2003) and C6 glioma cell lines (Manaves et al, 2004). However, activation of IK channels with 1-EBIO increases T lymphocytes proliferations, whereas inhibition of the channel with clotrimazole decreases proliferation (Khanna et al, 1999).…”

Section: Discussionsupporting

confidence: 92%

Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

Choi

Lee

Yun

et al. 2008

Korean J Physiol Pharmacol

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Cardiac fibroblasts constitute one of the largest cell populations in the heart, and contribute to structural, biochemical, mechanical and electrical properties of the myocardium. Nonetheless, their cardiac functions, especially electrophysiological properties, have often been disregarded in studies. Ca 2+ -activated K + (KCa) channels can control Ca 2+ influx as well as a number of Ca 2+ -dependent physiological processes. W e, therefore, attempted to identify and characterize KCa channels in rat Cardiac fibroblasts. First, we showed that the cells cultured from the rat ventricle were cardiac fibroblasts by immunostaining for discoidin domain receptor 2 (DDR-2), a specific fibroblast marker. Secondly, we detected the expression of various KCa channels by reverse transcription polymerase chain reaction (RT-PCR), and found all three family members of KCa channels, including large conductance KCa (BK-α1-and -β1∼ 4 subunits), intermediate conductance KCa (IK), and small conductance KCa (SK1 ∼ 4 subunits) channels. Thirdly, we recorded BK, IK, and SK channels by whole cell mode patch clamp technique using their specific blockers. Finally, we performed cell proliferation assay to evaluate the effects of the channels on cell proliferation, and found that the inhibition of IK channel increased the cell proliferation. These results showed the existence of BK, IK, and SK channels in rat ventricular fibroblasts and involvement of IK channel in cell proliferation.

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Section: Discussionsupporting

confidence: 92%

Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

Choi

Lee

Yun

et al. 2008

Korean J Physiol Pharmacol

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“…EBIO activates K Ca 3.1 with an EC 50 of 24-80 μM, however, it also activates K Ca 2 channels with an EC 50 of 87 μM [5]. Non-specific effects of EBIO have also been reported by Manaves et al [17] who demonstrated that EBIO inhibited keratinocyte proliferation, suggesting that K Ca 3.1 could be anti-proliferative. However, this antiproliferative effect was not blocked by charybdotoxin, clotrimazole, or TRAM-34 leading the authors to conclude that EBIO inhibited proliferation by other mechanisms besides K Ca 3.1 activation, i.e.…”

Section: K Ca 31 Blockers and Activatorsmentioning

confidence: 80%

The Intermediate-Conductance Ca2+-Activated K+ Channel (KCa3.1) in Vascular Disease

Tharp

Bowles²

2009

CHAMC

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The intermediate-conductance Ca(2+)-activated K(+) channel (K(Ca)3.1) was first described by Gardos in erythrocytes and later confirmed to play a significant role in T-cell activation and the immune response. More recently, K(Ca)3.1 has been characterized in numerous cell types which contribute to the development of vascular disease, such as T-cells, B-cells, endothelial cells, fibroblasts, macrophages, and dedifferentiated smooth muscle cells (SMCs). Physiologically, K(Ca)3.1 has been demonstrated to play a role in acetylcholine and endothelium-derived hyperpolarizing factor (EDHF) induced hyperpolarization, and thus control of blood pressure. Pathophysiologically, K(Ca)3.1 contributes to proliferation of T-cells, B-cells, fibroblasts, and vascular SMCs, as well as the migration of SMCs and macrophages and platelet coagulation. Recent studies have indicated that blockade of K(Ca)3.1, by specific blockers such as TRAM-34, could prove to be an effective treatment for vascular disease by inhibiting T-cell activation as well as preventing proliferation and migration of macrophages, endothelial cells, and SMCs. This vasculoprotective potential of K(Ca)3.1 inhibition has been confirmed in both rodent and swine models of restenosis. In this review, we will discuss the physiological and pathophysiological role of K(Ca)3.1 in cells closely associated with vascular biology, and the effect of K(Ca)3.1 blockers on the initiation and progression of vascular disease.

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“…These results seem to suggest that the IK Ca channel expression is subject to the same (differentiation) signals controlling GFAP expression. Moreo- ver, a number of studies report that IK Ca channels are downregulated during differentiation in tumor and normal models (C6 rat glioma cells [23]; the keratinocyte cell line HaCaT [32]; myogenic cell lines [50,51]; promielocytes during granulocytic differentiation [21]), although in few cases an upregulation of the IK Ca channel expression has been observed following differentiation [52,53].…”

Section: Modulation Of the Ik Ca Channelsmentioning

confidence: 99%

Expression and Modulation of the Intermediate- Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel in Glioblastoma GL-15 Cells

Fioretti

Castigli

Micheli

et al. 2006

Cell Physiol Biochem

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We report here the expression and properties of the intermediate-conductance Ca²⁺-activated K⁺ (IK_Ca) channel in the GL-15 human glioblastoma cell line. Macroscopic IK_Ca currents on GL-15 cells displayed a mean amplitude of 7.2±0.8 pA/pF at 0 mV, at day 1 after plating. The current was inhibited by clotrimazole (CTL, IC₅₀=257 nM), TRAM-34 (IC₅₀=55 nM), and charybdotoxin (CTX, IC₅₀=10.3 nM). RT-PCR analysis demonstrated the expression of mRNA encoding the IK_Ca channel in GL-15 cells. Unitary currents recorded using the inside-out configuration had a conductance of 25 pS, a K_D for Ca²⁺ of 188 nM at -100 mV, and no voltage dependence. We tested whether the IKCa channel expression in GL-15 cells could be the result of an increased ERK activity. Inhibition of the ERK pathway with the MEK antagonist PD98059 (25 µM, for 5 days) virtually suppressed the IK_Ca current in GL-15 cells. PD98059 treatment also increased the length of cellular processes and up-regulated the astrocytic differentiative marker GFAP. A significant reduction of the IKCa current amplitude was also observed with time in culture, with mean currents of 7.17±0.75 pA/pF at 1-2 days, and 3.11±1.35 pA/pF at 5-6 days after plating. This time-dependent downregulation of the IK_Ca current was not accompanied by changes in the ERK activity, as assessed by immunoblot analysis. Semiquantitative RT-PCR analysis demonstrated a ~35% reduction of the IK_Ca channel mRNA resulting from ERK inhibition and a ~50% reduction with time in culture.

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Calcium and Vitamin D increase mRNA levels for the growth control hIK1 channel in human epidermal keratinocytes but functional channels are not observed

Cited by 11 publications

References 30 publications

Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

The Intermediate-Conductance Ca2+-Activated K+ Channel (KCa3.1) in Vascular Disease

Expression and Modulation of the Intermediate- Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel in Glioblastoma GL-15 Cells

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Calcium and Vitamin D increase mRNA levels for the growth control hIK1 channel in human epidermal keratinocytes but functional channels are not observed

Cited by 11 publications

References 30 publications

Expression of Ca2+-activated K+Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

Expression of Ca2+-activated K+Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

The Intermediate-Conductance Ca2+-Activated K+ Channel (KCa3.1) in Vascular Disease

Expression and Modulation of the Intermediate- Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel in Glioblastoma GL-15 Cells

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Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts

Expression of Ca²⁺-activated K₊Channels and Their Role in Proliferation of Rat Cardiac Fibroblasts