Effects of Serum Amyloid A and Lysophosphatidylcholine on Intracellular Calcium Concentration in Human Coronary Artery Smooth Muscle Cells

Tanaka, Tomofumi; Ikeda, Kenichi; Yamamoto, Yumiko; Iida, Hidehiro; Kikuchi, Hiromi; Morita, Toshihiro; Yamasoba, Tatsuya; Nagai, Ryozo; Nakajima, Toshiaki

doi:10.1536/ihj.52.185

Cited by 10 publications

(14 citation statements)

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“…A previous study demonstrated that lysoPC induced a sustained Ca 2+ i increase in human coronary artery SMCs, and the potential mediation of TRP channels was proposed [12]; however, the involvement of specific TRP channels was not understood. To specify which TRP channels mediate the lysoPC-induced Ca 2+ i increase and apoptosis, we determined the effect of lysoPC on cytosolic Ca 2+ by a confocal laser scanning technique in human coronary artery SMCs with different pharmacological tools.…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies reported that lysoPC induced an sustained increase in intracellular free Ca 2+ (Ca 2+ i ) in human [12] and rabbit [13] coronary artery SMCs and in human umbilical vein endothelial cells [14] and in cultured human corporal SMCs [15]. The participation of transient receptor potential (TRP) channels was proposed in these reports.…”

Section: Introductionmentioning

confidence: 99%

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TRPC1/TRPC3 channels mediate lysophosphatidylcholine-induced apoptosis in cultured human coronary artery smooth muscles cells

Wang

2016

Oncotarget

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The earlier study showed that lysophosphatidylcholine (lysoPC) induced apoptosis in human coronary artery smooth muscle cells (SMCs); however, the related molecular mechanisms are not fully understood. The present study investigated how lysoPC induces apoptosis in cultured human coronary artery SMCs using cell viability assay, flow cytometry, confocal microscopy, and molecular biological approaches. We found that lysoPC reduced cell viability in human coronary artery SMCs by eliciting a remarkable Ca2+ influx. The effect was antagonized by La3+, SKF-96365, or Pyr3 as well as by silencing TRPC1 or TRPC3. Co-immunoprecipitation revealed that TRPC1 and TRPC3 had protein-protein interaction. Silencing TRPC1 or TRPC3 countered the lysoPC-induced increase of Ca2+ influx and apoptosis, and the pro-apoptotic proteins Bax and cleaved caspase-3 and decrease of the anti-apoptotic protein Bcl-2 and the survival kinase pAkt. These results demonstrate the novel information that TRPC1/TRPC3 channels mediate lysoPC-induced Ca2+ influx and apoptosis via activating the pro-apoptotic proteins Bax and cleaved caspase-3 and inhibiting the anti-apoptotic protein Bcl-2 and the survival kinase pAkt in human coronary artery SMCs, which implies that TRPC1/TRC3 channels may be the therapeutic target of lysoPC-induced disorders such as atherosclerosis.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

TRPC1/TRPC3 channels mediate lysophosphatidylcholine-induced apoptosis in cultured human coronary artery smooth muscles cells

Wang

2016

Oncotarget

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“…Because TRP channels are known to be associated with atherosclerotic effects, such as inflammation and oxidative stress, [7][8][9][10][11][12][13] these results imply that these selective TRP channel gene products are those hat contribute to the atherosclerotic process. In line with these findings, Thilo et al 10,34 showed recently that TRP channels are regulated by oxidative and antioxidative substances.…”

Section: Perspectivesmentioning

confidence: 99%

“…Using the Transcriptor first-strand cDNA synthesis kit (Roche Diagnostics, Mannheim, Germany), cDNA was synthesized from 2 g of total RNA using oligo dT [12][13][14][15][16][17][18] and 5 U of Avian Myeloblastosis Virus reverse transcriptase at 50°C for 60 minutes, followed by heating to 85°C for 5 minutes.…”

Section: Rna Isolation and Reverse Transcriptionmentioning

confidence: 99%

“…6 Moreover, several subtypes of transient receptor potential (TRP) channels, including transient receptor potential cation channel, subfamily C, member 3 (TRPC3) TRPC6, TRPM7, and TRPV1, have been linked to cardiovascular disease, hypertension, and atherosclerosis. [7][8][9][10][11][12][13] TRP channels are activated by a variety of factors, including chemical stimuli and mechanical stimuli, like shear stress. TRP channels are known to be mechanosensitive, although the specific mechanisms still need to be elucidated.…”

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confidence: 99%

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Pulsatile Atheroprone Shear Stress Affects the Expression of Transient Receptor Potential Channels in Human Endothelial Cells

et al. 2012

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Abstract-The goal of the study was to assess whether pulsatile atheroprone shear stress modulates the expression of transient receptor potential (TRP) channels, TRPC3, TRPC6, TRPM7, and TRPV1 mRNA, in human umbilical vascular endothelial cells. Exposure of cultured vascular endothelial cells to defined shear stress, producing a constant laminar flow (generating a shear stress of 6 dyne/cm 2 ), laminar pulsatile atheroprotective flow (with a mean shear stress of 20 dyne/cm 2 ), or laminar atheroprone bidirectional flow (with a mean shear stress of 0 dyne/cm 2 ) differentially induced TRPC6 and TRPV1 mRNA as measured by quantitative real-time RT-PCR and normalized to GAPDH expression. Thereby, TRPC6 and TRPV1 mRNA expressions were significantly increased after 24 hours of exposure to an atheroprone flow profile compared with an atheroprotective flow profile. Furthermore, the expression of transcription factors GATA1 and GATA4 was significantly correlated with the expression of TRPC6 mRNA. In contrast, after 24 hours of constant laminar flow, the expression of TRPC6 and TRPV1 mRNA was unchanged, whereas the expression of TRPC3 and TRPM7 was significantly higher in endothelial cells exposed to shear stress in comparison with endothelial cells grown under static conditions. There was a significant association between the expression of TRPC6 and tumor necrosis factor-␣ mRNA in human vascular tissue. No-flow and atheroprone flow conditions are equally characterized by an increase in the expression of tumor necrosis factor-␣; however, inflammation-associated endothelial cell reactions may be further aggravated at atheroprone flow conditions by the increase of TRPV1 and TRPC6, as observed in our study. (Hypertension. 2012;59:1232-1240.)

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Suppression of Lysophosphatidylcholine‐Induced Human Aortic Smooth Muscle Cell Calcification by Protein Kinase A Inhibition

Toita

Asai

Otani

et al. 2019

Lipids

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Lysophosphatidylcholine (lysoPtdCho) is produced mainly by the phospholipase A2‐dependent hydrolysis of phosphatidylcholine (PtdCho) and can induce inflammatory activation and osteogenic gene expression in vascular smooth muscle cells. However, the mechanisms mediating these processes have not been fully elucidated. In this study, we investigated whether inhibition of protein kinase A (PKA) signaling suppressed lysoPtdCho‐induced calcification of human aortic smooth muscle cells (HASMC). Calcium levels and alkaline phosphatase activity were significantly increased in HASMC treated with lysoPtdCho, but not PtdCho, compared with those in phosphate‐buffered saline‐treated HASMC. However, the addition of a PKA inhibitor (H‐89) or PKA siRNA blocked lysoPtdCho‐induced HASMC calcification. These results showed that lysoPtdCho could activate PKA‐mediated HASMC calcification and that PKA may be a therapeutic target for lysoPtdCho‐mediated vascular smooth muscle cell calcification.

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Effects of Serum Amyloid A and Lysophosphatidylcholine on Intracellular Calcium Concentration in Human Coronary Artery Smooth Muscle Cells

Cited by 10 publications

References 65 publications

TRPC1/TRPC3 channels mediate lysophosphatidylcholine-induced apoptosis in cultured human coronary artery smooth muscles cells

TRPC1/TRPC3 channels mediate lysophosphatidylcholine-induced apoptosis in cultured human coronary artery smooth muscles cells

Pulsatile Atheroprone Shear Stress Affects the Expression of Transient Receptor Potential Channels in Human Endothelial Cells

Suppression of Lysophosphatidylcholine‐Induced Human Aortic Smooth Muscle Cell Calcification by Protein Kinase A Inhibition

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