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Mitochondrial regulation of arterial...
~
Narayanan, Damodaran.
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Mitochondrial regulation of arterial contractility.
紀錄類型:
書目-語言資料,印刷品 : Monograph/item
正題名/作者:
Mitochondrial regulation of arterial contractility./
作者:
Narayanan, Damodaran.
面頁冊數:
144 p.
附註:
Source: Dissertation Abstracts International, Volume: 71-11, Section: B, page: 6611.
Contained By:
Dissertation Abstracts International71-11B.
標題:
Biology, Cell. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3426051
ISBN:
9781124260617
Mitochondrial regulation of arterial contractility.
Narayanan, Damodaran.
Mitochondrial regulation of arterial contractility.
- 144 p.
Source: Dissertation Abstracts International, Volume: 71-11, Section: B, page: 6611.
Thesis (Ph.D.)--The University of Tennessee Health Science Center, 2010.
Rationale. Physiological functions of mitochondria in contractile arterial smooth muscle cells are poorly understood. Mitochondria can uptake calcium (Ca2+), but intracellular Ca2+ signals that regulate mitochondrial Ca2+ concentration ([Ca 2+]mito) and physiological functions of changes in [Ca 2+]mito in arterial smooth muscle cells are unclear.
ISBN: 9781124260617Subjects--Topical Terms:
1017686
Biology, Cell.
Mitochondrial regulation of arterial contractility.
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Source: Dissertation Abstracts International, Volume: 71-11, Section: B, page: 6611.
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Adviser: Jonathan H. Jaggar.
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Thesis (Ph.D.)--The University of Tennessee Health Science Center, 2010.
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Rationale. Physiological functions of mitochondria in contractile arterial smooth muscle cells are poorly understood. Mitochondria can uptake calcium (Ca2+), but intracellular Ca2+ signals that regulate mitochondrial Ca2+ concentration ([Ca 2+]mito) and physiological functions of changes in [Ca 2+]mito in arterial smooth muscle cells are unclear.
520
$a
Objective. Identify Ca2+ signals that regulate [Ca2+]mito, examine the significance of changes in [Ca2+]mito, and test the hypothesis that [Ca 2+]mito controls functional ion channel transcription in smooth muscle cells of resistance-size cerebral arteries.
520
$a
Methods and Results. Endothelin-1 (ET-1) activated Ca 2+ waves and elevated global Ca2+ concentration ([Ca 2+]i) via inositol 1,4,5-triphosphate receptor (IP 3R) activation. IP3R-mediated sarcoplasmic reticulum (SR) Ca2+ release increased [Ca2+]mito and induced mitochondrial depolarization, which stimulated mitochondrial reactive oxygen species (mitoROS) generation that elevated cytosolic ROS. In contrast, a global [Ca2+]i elevation did not alter [Ca2+] mito, mitochondrial potential, or mitoROS generation. ET-1 stimulated nuclear translocation of nuclear factor kappa B (NF-kappaB) p50 subunit and ET-1-induced IP3R-mediated mitoROS elevated NF-kappaB-dependent transcriptional activity. ET-1 elevated voltage-dependent Ca2+ (CaV1.2) channel expression, leading to an increase in both pressure (myogenic tone)- and depolarization-induced vasoconstriction. Baseline Ca V1.2 expression and the ET-1-induced elevation in CaV1.2 expression were both reduced by IP3R inhibition, mitochondrial electron transport chain block, antioxidant treatment, and NF-kappaB subunit knockdown, leading to vasodilation.
520
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Conclusions. IP3R-mediated SR Ca2+ release elevates [Ca2+]mito, which induces mitoROS generation. MitoROS activate NF-kappaB, which stimulates Ca V1.2 channel transcription. Thus, mitochondria sense IP3R-mediated SR Ca2+ release to control NF-kappaB-dependent CaV1.2 channel expression in arterial smooth muscle cells, thereby modulating arterial contractility.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3426051
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