Jie Pei

Luzhou Medical College, Lu-chou, Sichuan, China

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Publications (11)16.04 Total impact

  • World Congress of Cardiology Scientific Sessions; 05/2012
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    ABSTRACT: To compare the amplitude of the SK2 current (small conductance calcium-activated potassium channel) in human atrial myocytes with or without persistent atrial fibrillation (AF). Right atrial appendage was obtained from 15 patients with sinus rate (SR) and 7 patients with AF underwent surgical valve replacement. Single myocyte was isolated by enzymatic dissociation method and the SK2 channel current density was recorded using whole-cell patch clamp techniques to detect the changes. Immunofluorescence was used to observe SK2 channel protein distribution on right atrial appendage. Using the whole cell patch-clamp recording techniques, an inward rectifier K(+) mix currents could be obtained from both SR (n = 15) and AF (n = 7) samples, I(K1) mix currents density in single myocyte of AF group was significantly increased than in SR group [(-16.42 ± 5.32) pA/pF vs (-6.59 ± 2.24) pA/pF, P < 0.01], which could be partially inhibited by apamin (100 nmol/L). The apamin-sensitive current was obtained by subtraction of the currents before and after treatment with apamin. SK2 current density was significantly increased in AF group than that of SR group [(-9.81 ± 2.54) pA/pF vs (-3.67 ± 0.37) pA/pF, P < 0.01]. SK2 channel protein was evidenced with immunofluorescence method in right atrial appendage from AF group and SR group. SK2 channel protein and current were present in atrial myocytes. The SK2 current density was significantly increased in AF group than in SR group suggesting that the increase of SK2 current might contribute to the electrical remodeling in AF patients.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 02/2011; 39(2):147-51.
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    ABSTRACT: To detect the KChIP2 mRNA level in rheumatic heart disease patients with or without atrial fibrillation (AF) by real-time PCR. Right atrial appendage samples from rheumatic heart disease patients with (n = 17) or without AF (n = 13) were obtained during cardiac surgery. Total RNA was extracted from the atrial tissues, and the KChIP2 and Kv4.3 mRNA were detected by SYBR Green I real-time PCR with the GAPDH as the house keeping gene. The ratio of KChIP2/GAPDH (0.1468 +/- 0.0452 vs. 0.2200 +/- 0.0388, P<0.01) and the ratio of Kv4.3/GAPDH (0.3946 +/- 0.1826 vs. 0.5257 +/- 0.1427, P<0.05) were significantly lower in AF patients compared to non-AF patients. Down-regulated atrial KChIP2 and Kv4.3 mRNA expressions in rheumatic heart disease patients with chronic AF might be one of the molecular bases responsible for the down-regulation of the I(to) current density of AF.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 06/2009; 37(6):509-13.
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    ABSTRACT: The aim of the present study was to investigate the effects of inositol 1,4,5-trisphosphate (IP(3))-generating agonist UTP on spontaneous transient outward currents (STOCs), and explore the role of intracellular Ca(2+) release in the current response mediated by IP(3) in porcine coronary artery smooth muscle cells (CASMCs). The coronary artery was excised from the fresh porcine heart and cut into small segments (2 mm × 5 mm) and then transferred to enzymatic dissociation solution for incubation. Single CASMCs were obtained by two-step enzyme digestion at 37 °C. STOCs were recorded and characterized using the perforated whole-cell patch-clamp configuration in freshly isolated porcine CASMCs. The currents were amplified and filtered by patch-clamp amplifier (Axopatch 200B), and then the digitized data were recorded by pClamp 9.0 software and further analyzed by MiniAnalysis 6.0 program. The results were as follows: (1) UTP led to conspicuous increases in STOC amplitude by (57.54±5.34)% and in frequency by (77.46±8.42)% (P<0.01, n=38). (2) The specific blocker of phospholipase C (PLC) - U73122 (5 μmol/L) remarkably reduced STOC amplitude by (31.04±7.46)% and frequency by (41.65±16.59)%, respectively (P<0.05, n=10). In the presence of U73122, UTP failed to reactivate STOCs (n=7). (3) Verapamil (20 μmol/L) and CdCl2 (200 μmol/L), two blockers of L-type voltage-dependent Ca(2+) channels, had little effects on STOCs initiated by UTP (n=8). (4) 1 μmol/L bisindolylmaleimide I (BisI), a potent blocker of protein kinase C (PKC), significantly increased STOC amplitude by (65.44±24.66)% and frequency by (61.35±21.47)% (P<0.01, n=12); UTP (40 μmol/L), applied in the presence of 1 μmol/L BisI, could further increase STOC activity (P<0.05, P<0.01, n=12). Subsequent application of ryanodine (50 μmol/L) abolished STOC activity. (5) In the presence of UTP (40 μmol/L), inhibition of IP(3) receptors (IP(3)Rs) by 2-aminoethoxydiphenyl borate (2-APB, 40 μmol/L) reduced STOC amplitude by (24.08±3.97)% (P<0.05, n=8), but had little effect on STOC frequency (n=8). While application of 2-APB (80 μmol/L) significantly reduced STOC amplitude by (31.43±6.34)% and frequency by (40.59±19.01)%, respectively (P<0.05, P<0.01, n=6). Subsequent application of ryanodine (50 μmol/L) completely blocked STOC activity. Pretreatment of cells with 2-APB (40 μmol/L) or ryanodine (50 μmol/L), UTP (40 μmol/L) failed to reactivate STOCs. The results suggest that UTP activates STOCs mainly via PLC and IP(3)-dependent mechanisms. Complex Ca(2+)-mobilization pathways are involved in UTP-mediated STOC activation in porcine CASMCs.
    Sheng li xue bao: [Acta physiologica Sinica] 03/2008; 60(1):65-73.
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    ABSTRACT: To approach the method of isolation of tolerant human atrial myocytes, single myocytes were isolated by modified procedure of enzymatic dissociation with protease (type XXIV) and collagenase (type V). L-type calcium channel current (I(Ca-L)), sodium current (I(Na)), transient outward potassium current (I(to1)), and inward rectifier potassium current (I(K1)) in isolated atrial myocytes were recorded by using whole-cell patch-clamp techniques. Single cardiocytes isolated by this method were smooth, well-striated and rod-shaped. The yields of recordable myocytes, which viable and calcium-tolerant for electrophysiological studies, were 50%-60% of the total isolated cells. Compared with other isolation methods, this method was simple and steady, but with yield of a great number of qualified myocytes. The currents recorded in these cells were functional and active. Our research suggests that the myocytes isolated by the described method in this paper have normal electrophysiological function and are appropriate for patch-clamp experiments.
    Sheng li xue bao: [Acta physiologica Sinica] 01/2008; 59(6):858-64.
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    ABSTRACT: The purpose of the present study was to further study the characteristics and regulation of spontaneous transient outward currents (STOCs) in freshly isolated porcine coronary artery smooth muscle cells (ASMCs). STOCs were recorded using the perforated whole-cell patch-clamp configuration. STOCs were voltage-dependent and superimposed stochastically onto whole-cell Ca(2+)-activated-K(+) (BK(Ca)) currents. Charybdotoxin (ChTX, 200 nmol/L), a selective blocker of BK(Ca) channels, completely inhibited STOCs within 10 min. STOCs activity was greatly suppressed when extracellular Ca(2+) concentration decreased from 1.8 mmol/L to 200 nmol/L, further removal of Ca(2+) abolished STOCs activity. Ca(2+) ionophore A23187 (10 micromol/L) increased STOCs activity significantly. Verapamil (20 micromol/L) and CdCl(2) (200 micromol/L), two kinds of organic L-type voltage-dependent Ca(2+) channels (L-VDCCs) antagonists, had little effect on STOCs. In addition, the ryanodine receptors (RyRs) agonist caffeine (5 mmol/L) significantly activated STOCs. Application of ryanodine (50 micromol/L) to block RyRs abolished STOCs, subsequent washout of ryanodine or application of caffeine failed to reproduce STOCs activity. Inhibition of inositol 1,4,5-trisphosphate receptors (IP(3)Rs) by 2APB (40 micromol/L) greatly suppressed the activity of STOCs, application of caffeine (5 mmol/L) in the presence of 2APB caused a burst of outward currents followed by inhibition of STOCs. These results suggest that STOCs in porcine coronary ASMCs are mediated by BK(Ca) channels. Extracellular Ca(2+) is essential for STOCs activity, while Ca(2+) entry through L-VDCCs has little effect on STOCs. Intracellular Ca(2+) release induced by RyRs is responsible for the regulation of STOCs, whereas IP3Rs might also be involved.
    Science in China Series C Life Sciences 11/2007; 50(5):660-8. DOI:10.1007/s11427-007-0064-7 · 1.61 Impact Factor
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    ABSTRACT: Spontaneous transient outward currents (STOCs) play an important role in the myogenic regulation of small artery tone, such as coronary artery. In the present study, we investigated the electrophysiological properties and the regulation of STOCs in vascular smooth muscle cells (VSMCs) of porcine coronary artery by perforated patch-clamp technique. Our data showed that STOCs were dependent on voltage and extracellular calcium and they were highly variable in amplitudes and frequencies. STOCs superimposed stochastically onto whole-cell K(+) currents induced by step and ramp protocols. STOCs were completely abolished by ChTX [inhibitor of large-conductance Ca(2+)-activated potassium (BK(Ca)) channels], removal of extracellular Ca(2+), or addition of ryanodine (50 mumol/L) respectively. In contrast, CdCl2 and verapamil, inhibitors of voltage-dependent L-type Ca(2+) channels, had little effect on STOCs. Caffeine (5 mmol/L) transiently increased STOCs (hump), followed by a temporary inhibition. Ca(2+) ionophore A23187 increased both amplitude and frequency of STOCs. Na(+) ionophore monensin increased the frequency of STOCs. STOCs were strongly inhibited by KB-R7943, a selective inhibitor of the reverse mode of the Na(+)/Ca(2+) exchanger. Based on these observations, we conclude that STOCs are mediated by BK(Ca) channels. The generation and activation of STOCs depend upon Ca(2+) influx through Na(+)/Ca(2+) exchange and release of Ca(2+) from sarcoplasmic reticulum (SR) via ryanodine receptors. This suggests that Na(+)/Ca(2+) exchange determines calcium store refilling. Recycling of entering Ca(2+) from superficial SR may locally elevate Ca(2+) concentration at the plasma membrane, thereby activating BK(Ca) channels and then initiating STOCs.
    Sheng li xue bao: [Acta physiologica Sinica] 03/2007; 59(1):27-34.
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    ABSTRACT: To investigate the changes of L-type Ca(2+) channel current (I(Ca-L)) and its voltage-dependent activation and inactivation in atrial myocytes of patients with atrial fibrillation (AF). The specimens of right atrial appendage were obtained from 18 patients with normal sinus rhythm (NSR) and 12 patients with chronic atrial fibrillation (CAF). Single myocytes were isolated by enzymatic dissociation with two-step method and the ionic currents were recorded using whole-cell patch clamp techniques to detect the changes of I(Ca-L) density and kinetic properties. (1) I(Ca-L) density was (-1.32 +/- 0.19) pA/pF in CAF group (n = 12) and (-4.58 +/- 0.39) pA/pF in NSR group (n = 21) at the test potential from -40 mV to 0 mV. I(Ca-L) density of CAF group was significantly reduced (P < 0.01), compared with the NSR group. (2) No significant differences were noted between the two groups in the voltage-dependent activation parameters (V(1/2), K) and inactivation parameters (V(1/2), K). I(Ca-L) density of CAF group was significantly decreased whereas it's voltage-dependent kinetic properties had no change. This phenomenon may be one of the mechanisms of atrial electrophysiological remodeling in chronic atrial fibrillation.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 04/2006; 34(4):308-11.
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    ABSTRACT: The aim of the present study was to examine the effects of tetramethylpyrazine (TMP) on large-conductance Ca(2+)-activated potassium channels (BK(Ca) channels) in porcine coronary artery smooth muscle cells, in order to provide the experimental evidence for expounding the mechanism of TMP in dilating coronary artery. Cell-attached and inside-out single channel recording techniques were used to observe the effects of TMP on BK(Ca) channels as well as the effects after the cells were treated by protein kinase A (PKA) inhibitor or protein kinase G (PKG) inhibitor. In inside-out patch, TMP activated BK(Ca) channels by increasing open-state probability (N(Po)) and decreasing close time (Tc) in a concentration-dependent manner. TMP (0.73~8.07 mmol/L) in the bath solution increased N(Po) from (0.01+/-0.003) to (0.03+/-0.01)~(1.21+/-0.18) (P<0.01, n=10), and decreased Tc from (732.33+/-90.67) ms to (359.67+/-41.30) ~ (2.96+/-0.52) ms (P<0.01, n=10). These actions of TMP occurred even when the free Ca(2+) concentration in the bath was reduced to ~ 0 mmol/L. The specific inhibitors of PKA (H-89, 3 mumol/L) and PKG (KT-5823, 1 mumol/L) had no influence on the activation of TMP on BK(Ca) channels. These findings suggest that TMP can directly activate BK(Ca) channels in coronary artery smooth muscle, which probably is an important mechanism in dilating coronary artery.
    Sheng li xue bao: [Acta physiologica Sinica] 02/2006; 58(1):83-9.
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    ABSTRACT: To compare the changes of both inward rectifying K(+) (Kir) current(I(k1)) density and mRNA expression level of Kir2.1, a major subfamily of Kir in chronic human atrial fibrillation (CAF) with those in normal sinus rhythm (NSR). I(k1) density was measured with whole-cell patch clamp technique in single myocyte isolated by an enzymatic dissociation method from right atrial appendages in patients with CAF (n = 8) and those with NSR (n = 12). The mRNA expression levels of Kir2.1 was determined in right atrial appendages from CAF (n = 19) and NSR (n = 18) by semiquantitative reverse-transcription polymerase chain reaction (RT-PCR). The average resting membrane potentials were similar between CAF and NSR (-78.95 mV +/- 4.67 mV and -70.22 mV +/- 11.08 mV, P>0.05). I(k1) density in single myocyte significantly increased at hyperpolarized potential level (-100 mV) in CAF compared to that in NSR (-9.59 pA/pF +/- 2.47 pA/pF vs. -5.58 pA/pF +/- 2.52 pA/pF, P<0.01). The mRNA level of Kir2.1 was also significantly higher in CAF than that of NSR (0.50+/-0.16 vs. 0.34+/-0.09, P<0.05). The data suggest that Kir2.1 up-regulation and I(k1) current increase might contribute to the electrical remodeling in CAF patients.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 02/2006; 34(1):33-7.
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    ABSTRACT: D-myo-inositol 1,4,5-trisphosphate (IP(3)) plays an important role in signal transduction. It releases Ca(2+) from intracellular sites, which activates the Ca(2+)-dependent channels such as large-conductance Ca(2+)-activated potassium channels (BK channels). The present study was therefore designed to determine if the activity of BK channels in porcine coronary artery smooth muscle cells was increased by IP(3). Using the inside-out patch-clamp technique, the activity of single BK channels was recorded in porcine coronary artery smooth muscle cells. In excised inside-out membrane patches, IP(3) (10-50 micromol/L) enhanced the open probability (Po) of BK channels in a dose-dependent manner in the intracellular side of inside-out patches and its effect was almost completely abolished by washout. The open-state probability of the BK channels increased from a control level of 0.0402+/-0.0152 to 0.1365+/-0.0212 (20 micromol/L IP(3)) and 0.1865+/-0.0175 (30 micromol/L IP(3)). IP(3) decreased the mean close time markedly, but had no effect on the amplitude of BK channels. The activation of IP(3) on BK channels did not decline. The metabolite of IP(3) had no obvious effect on BK channels. This study provides evidence that IP(3) activates BK channels in porcine coronary artery smooth muscle cells in a dose-dependence manner.
    Sheng li xue bao: [Acta physiologica Sinica] 07/2005; 57(3):303-9.