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Role of TRPC3 Channel in Human Internal Mammary Artery

Authorized Users Only
2012
Authors
Gao, Ge
Bai, Xiao-Yan
Xuan, Chao
Liu, Xiao-Cheng
Jing, Wen-Bin
Novaković, Aleksandra
Yang, Qin
He, Guo-Wei
Article (Published version)
Metadata
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Abstract
Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly a...ttenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p lt 0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p lt 0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.

Keywords:
TRPC3 / Ion channel / Vasorelaxation / Vasospasm
Source:
Archives of Medical Research, 2012, 43, 6, 431-437
Publisher:
  • Elsevier Science Inc, New York
Funding / projects:
  • International S & T Cooperation Program of China - 2009DFB30560

DOI: 10.1016/j.arcmed.2012.08.010

ISSN: 0188-4409

PubMed: 22960861

WoS: 000311766200003

Scopus: 2-s2.0-84867849716
[ Google Scholar ]
21
19
URI
https://farfar.pharmacy.bg.ac.rs/handle/123456789/1680
Collections
  • Radovi istraživača / Researchers’ publications
Institution/Community
Pharmacy
TY  - JOUR
AU  - Gao, Ge
AU  - Bai, Xiao-Yan
AU  - Xuan, Chao
AU  - Liu, Xiao-Cheng
AU  - Jing, Wen-Bin
AU  - Novaković, Aleksandra
AU  - Yang, Qin
AU  - He, Guo-Wei
PY  - 2012
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1680
AB  - Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly attenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p  lt  0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p  lt  0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.
PB  - Elsevier Science Inc, New York
T2  - Archives of Medical Research
T1  - Role of TRPC3 Channel in Human Internal Mammary Artery
VL  - 43
IS  - 6
SP  - 431
EP  - 437
DO  - 10.1016/j.arcmed.2012.08.010
ER  - 
@article{
author = "Gao, Ge and Bai, Xiao-Yan and Xuan, Chao and Liu, Xiao-Cheng and Jing, Wen-Bin and Novaković, Aleksandra and Yang, Qin and He, Guo-Wei",
year = "2012",
abstract = "Background and Aims. Intracellular calcium regulation in endothelial cells depends on transient receptor potential channels (TRPs). Canonical TRPs (TRPCs) are now recognized as the most important Ca2+-permeable cation channels in vascular endothelium and TRPC3 channel is reported to play a role in vasodilation in animal vessels. However, little is known about the role of TRPCs in human arteries. We therefore tested the hypothesis that TRPCs play a role in human arteries. Methods. Cumulative concentration-relaxation curves to acetylcholine (-11 to -4.5 log M) were established in the human internal mammary artery (IMA) rings (n = 42) taken from 28 patients undergoing coronary artery bypass grafting in precontraction induced by U46619 (-8 log M) in the absence or presence of SKF96365 (10 mu mol/L) or Pyr3 (3 mu mol/L). Protein expressions of TRPC3 were determined by Western blot and immunohistochemistry staining. Results. The maximal relaxation induced by acetylcholine was significantly attenuated by the nonspecific cation channels inhibitor, SKF96365 (48.2 +/- 3.7 vs. 66.0 +/- 0.9% in control, p  lt  0.01) or the selective TRPC3 blocker, Pyr3 (58.4 +/- 2.3% vs. 67.7 +/- 1.1% in control, p  lt  0.01). Protein expression of TRPC3 was detected in human 1MA. Conclusions. TRPC3 exists and plays a role in the acetylcholine-induced endothelium-dependent relaxation in the human IMA. This study suggests that TRPC3 may be a potential new target in endothelial protection in patients with endothelial dysfunction such as in patients with coronary artery disease in order to improve the long-term patency of the grafting vessels.",
publisher = "Elsevier Science Inc, New York",
journal = "Archives of Medical Research",
title = "Role of TRPC3 Channel in Human Internal Mammary Artery",
volume = "43",
number = "6",
pages = "431-437",
doi = "10.1016/j.arcmed.2012.08.010"
}
Gao, G., Bai, X., Xuan, C., Liu, X., Jing, W., Novaković, A., Yang, Q.,& He, G.. (2012). Role of TRPC3 Channel in Human Internal Mammary Artery. in Archives of Medical Research
Elsevier Science Inc, New York., 43(6), 431-437.
https://doi.org/10.1016/j.arcmed.2012.08.010
Gao G, Bai X, Xuan C, Liu X, Jing W, Novaković A, Yang Q, He G. Role of TRPC3 Channel in Human Internal Mammary Artery. in Archives of Medical Research. 2012;43(6):431-437.
doi:10.1016/j.arcmed.2012.08.010 .
Gao, Ge, Bai, Xiao-Yan, Xuan, Chao, Liu, Xiao-Cheng, Jing, Wen-Bin, Novaković, Aleksandra, Yang, Qin, He, Guo-Wei, "Role of TRPC3 Channel in Human Internal Mammary Artery" in Archives of Medical Research, 43, no. 6 (2012):431-437,
https://doi.org/10.1016/j.arcmed.2012.08.010 . .

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