Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces the change of calcium mobilization via TRPC ion channels in cultured human corporal smooth muscle cells

Insuk So, M. R. Chae, Sungjoon Kim, S. W. Lee

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Abstract

Hypercholesterolemia is a major risk factor for erectile dysfunction. To understand the mechanism(s) of hypercholesterolemia-induced erectile dysfunction, we studied the effect of lysophosphatidylcholine (LPC) on the membrane conductance of corporal smooth muscle cells. We used cultured human corporal smooth muscle cells. The intracelluar Ca2+ concentration ([Ca2+]i) and the influx of divalent cation was monitored by the ratio of fura-2 fluorescence (F340/380) and by the Mn 2+-induced quenching rate of fura-2, respectively. The LPC-induced membrane current was characterized by the whole-cell patch-clamp technique and the molecular identity of suspected channels was probed by RT-PCR. LPC (20 μM) induced a statistically significant increase in F340/380 to 119.9±3.9% of initial control (n=6) in corporal smooth muscle cells. The addition of 20 μM LPC accelerated the quenching rate of F360 by 59.5±11.8% (n=5). LPC activated nonselective cationic current (I LPC), similar to the known effects of phenylephrine in corporal myocytes. The size of ILPC at -60 mV was -55.3±6.3 pA (n=8). The transcript of transient receptor potential channel 6 (TRPC6) was detected in human corporal myocytes. We also found one splicing variant of TRPC6, TRPC6α. In conclusion, the present study suggests that the LPC, a major component of oxidized low-density lipoprotiens, increases calcium in corporal smooth muscle cells probably through activation of a TRPC6 channel and the increased [Ca2+]i by LPC via TRP channels is one of mechanisms for hypercholesterolemia-induced erectile dysfunction.

Original languageEnglish
Pages (from-to)475-483
Number of pages9
JournalInternational Journal of Impotence Research
Volume17
Issue number6
DOIs
StatePublished - 1 Dec 2005

Fingerprint

Lysophosphatidylcholines
Ion Channels
Lipoproteins
Smooth Muscle Myocytes
Calcium
Transient Receptor Potential Channels
Erectile Dysfunction
Hypercholesterolemia
Fura-2
Muscle Cells
Membranes
Divalent Cations
Phenylephrine
Patch-Clamp Techniques
Fluorescence
Polymerase Chain Reaction

Keywords

  • Corporal smooth muscle cells
  • Erectile dysfunction
  • Lysophosphatidylcholine
  • Transient receptor potential channel

Cite this

@article{5576edc3760347538332f579e4724680,
title = "Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces the change of calcium mobilization via TRPC ion channels in cultured human corporal smooth muscle cells",
abstract = "Hypercholesterolemia is a major risk factor for erectile dysfunction. To understand the mechanism(s) of hypercholesterolemia-induced erectile dysfunction, we studied the effect of lysophosphatidylcholine (LPC) on the membrane conductance of corporal smooth muscle cells. We used cultured human corporal smooth muscle cells. The intracelluar Ca2+ concentration ([Ca2+]i) and the influx of divalent cation was monitored by the ratio of fura-2 fluorescence (F340/380) and by the Mn 2+-induced quenching rate of fura-2, respectively. The LPC-induced membrane current was characterized by the whole-cell patch-clamp technique and the molecular identity of suspected channels was probed by RT-PCR. LPC (20 μM) induced a statistically significant increase in F340/380 to 119.9±3.9{\%} of initial control (n=6) in corporal smooth muscle cells. The addition of 20 μM LPC accelerated the quenching rate of F360 by 59.5±11.8{\%} (n=5). LPC activated nonselective cationic current (I LPC), similar to the known effects of phenylephrine in corporal myocytes. The size of ILPC at -60 mV was -55.3±6.3 pA (n=8). The transcript of transient receptor potential channel 6 (TRPC6) was detected in human corporal myocytes. We also found one splicing variant of TRPC6, TRPC6α. In conclusion, the present study suggests that the LPC, a major component of oxidized low-density lipoprotiens, increases calcium in corporal smooth muscle cells probably through activation of a TRPC6 channel and the increased [Ca2+]i by LPC via TRP channels is one of mechanisms for hypercholesterolemia-induced erectile dysfunction.",
keywords = "Corporal smooth muscle cells, Erectile dysfunction, Lysophosphatidylcholine, Transient receptor potential channel",
author = "Insuk So and Chae, {M. R.} and Sungjoon Kim and Lee, {S. W.}",
year = "2005",
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doi = "10.1038/sj.ijir.3901356",
language = "English",
volume = "17",
pages = "475--483",
journal = "International Journal of Impotence Research",
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TY - JOUR

T1 - Lysophosphatidylcholine, a component of atherogenic lipoproteins, induces the change of calcium mobilization via TRPC ion channels in cultured human corporal smooth muscle cells

AU - So, Insuk

AU - Chae, M. R.

AU - Kim, Sungjoon

AU - Lee, S. W.

PY - 2005/12/1

Y1 - 2005/12/1

N2 - Hypercholesterolemia is a major risk factor for erectile dysfunction. To understand the mechanism(s) of hypercholesterolemia-induced erectile dysfunction, we studied the effect of lysophosphatidylcholine (LPC) on the membrane conductance of corporal smooth muscle cells. We used cultured human corporal smooth muscle cells. The intracelluar Ca2+ concentration ([Ca2+]i) and the influx of divalent cation was monitored by the ratio of fura-2 fluorescence (F340/380) and by the Mn 2+-induced quenching rate of fura-2, respectively. The LPC-induced membrane current was characterized by the whole-cell patch-clamp technique and the molecular identity of suspected channels was probed by RT-PCR. LPC (20 μM) induced a statistically significant increase in F340/380 to 119.9±3.9% of initial control (n=6) in corporal smooth muscle cells. The addition of 20 μM LPC accelerated the quenching rate of F360 by 59.5±11.8% (n=5). LPC activated nonselective cationic current (I LPC), similar to the known effects of phenylephrine in corporal myocytes. The size of ILPC at -60 mV was -55.3±6.3 pA (n=8). The transcript of transient receptor potential channel 6 (TRPC6) was detected in human corporal myocytes. We also found one splicing variant of TRPC6, TRPC6α. In conclusion, the present study suggests that the LPC, a major component of oxidized low-density lipoprotiens, increases calcium in corporal smooth muscle cells probably through activation of a TRPC6 channel and the increased [Ca2+]i by LPC via TRP channels is one of mechanisms for hypercholesterolemia-induced erectile dysfunction.

AB - Hypercholesterolemia is a major risk factor for erectile dysfunction. To understand the mechanism(s) of hypercholesterolemia-induced erectile dysfunction, we studied the effect of lysophosphatidylcholine (LPC) on the membrane conductance of corporal smooth muscle cells. We used cultured human corporal smooth muscle cells. The intracelluar Ca2+ concentration ([Ca2+]i) and the influx of divalent cation was monitored by the ratio of fura-2 fluorescence (F340/380) and by the Mn 2+-induced quenching rate of fura-2, respectively. The LPC-induced membrane current was characterized by the whole-cell patch-clamp technique and the molecular identity of suspected channels was probed by RT-PCR. LPC (20 μM) induced a statistically significant increase in F340/380 to 119.9±3.9% of initial control (n=6) in corporal smooth muscle cells. The addition of 20 μM LPC accelerated the quenching rate of F360 by 59.5±11.8% (n=5). LPC activated nonselective cationic current (I LPC), similar to the known effects of phenylephrine in corporal myocytes. The size of ILPC at -60 mV was -55.3±6.3 pA (n=8). The transcript of transient receptor potential channel 6 (TRPC6) was detected in human corporal myocytes. We also found one splicing variant of TRPC6, TRPC6α. In conclusion, the present study suggests that the LPC, a major component of oxidized low-density lipoprotiens, increases calcium in corporal smooth muscle cells probably through activation of a TRPC6 channel and the increased [Ca2+]i by LPC via TRP channels is one of mechanisms for hypercholesterolemia-induced erectile dysfunction.

KW - Corporal smooth muscle cells

KW - Erectile dysfunction

KW - Lysophosphatidylcholine

KW - Transient receptor potential channel

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U2 - 10.1038/sj.ijir.3901356

DO - 10.1038/sj.ijir.3901356

M3 - Article

VL - 17

SP - 475

EP - 483

JO - International Journal of Impotence Research

JF - International Journal of Impotence Research

SN - 0955-9930

IS - 6

ER -