Differential Regulation and Recovery of Intracellular Ca2+ in Cerebral and Small Mesenteric Arterial Smooth Muscle Cells of Simulated Microgravity Rat

Xue, Jun-Hui; Chen, Lianhong; Zhao, Hongyu; Pu, Yong; Feng, Han‐Zhong; Ma, Yihui; Ma, Jing; Chang, Yao-Ming; Zhang, Zuoming; Xie, Man‐Jiang

doi:10.1371/journal.pone.0019775

Cited by 23 publications

(37 citation statements)

References 30 publications

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“…In the presence of ryanodine, the KCl-induced Ca 2+ responses were still higher in HU conditions, confirming the increase in depolarization-induced Ca 2+ influx [50,51]. In our study, the increase in ST-bodipy(−)-DHP labeling further suggests that VDCC were expressed more and/or activated more in HU conditions, as previously observed in electrophysiology experiments [49,51].…”

Section: Discussionsupporting

confidence: 90%

“…The result of this up-regulation of VDCC was the increase in Ca 2+ influx activated by depolarization (present study) and potentially the enhancement of angiotensin-II responses, as previously described [30] and recently suggested in the HU model [50]. Whatever triggered the response, the result is an increase in calcium influx and mainly an increase in CICR.…”

Section: Discussionsupporting

confidence: 80%

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Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Morel

Dabertrand

Porte

et al. 2013

Pflugers Arch - Eur J Physiol

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Microgravity induces a redistribution of blood volume. Consequently, astronauts' body pressure is modified so that the upright blood pressure gradient is abolished, thereby inducing a modification in cerebral blood pressure. This effect is mimicked in the hindlimb unloaded rat model. After a duration of 8 days of unloading, Ca 2+ signals activated by depolarization and inositol-1,4,5-trisphosphate intracellular release were increased in cerebral arteries. In the presence of ryanodine and thapsigargin, the depolarization-induced Ca 2+ signals remained increased in hindlimb suspended animals, indicating that Ca 2+ influx and Ca 2+ -induced Ca 2+ release mechanism were both increased. Spontaneous Ca 2+ waves and localized Ca 2+ events were also investigated. Increases in both amplitude and frequency of spontaneous Ca 2+ waves were measured in hindlimb suspension conditions. After pharmacological segregation of Ca 2+ sparks and Ca 2+ sparklets, their kinetic parameters were characterized. Hindlimb suspension induced an increase in the frequencies of both Ca 2+ localized events, suggesting an increase of excitability. Labeling with bodipy compounds suggested that voltage-dependent Ca 2+ channels and ryanodine receptor expressions were increased. Finally, the expression of the ryanodine receptor subtype 1 (RyR1) was increased in hindlimb unloading conditions. Taken together, these results suggest that RyR1 expression and voltage-dependent Ca 2+ channels activity are the focal points of the regulation of Ca 2+ signals activated by vasoconstriction in rat cerebral arteries with an increase of the voltage-dependent Ca 2+ influx.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 80%

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Morel

Dabertrand

Porte

et al. 2013

Pflugers Arch - Eur J Physiol

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“…As for the mesenteric arteries, we did not found mitochondrial dysfunction in HU rats. Although the different changes in VSMCs ion channels (7–9) secondary to gravitational pressure gradient shifts in the circulation (4) have been indicated in differential vascular structural and functional remodeling during microgravity, the underlying mechanism remains to be established. Further studies are needed to investigate this question.…”

Section: Discussionmentioning

confidence: 99%

Simulated microgravity‐induced mitochondrial dysfunction in rat cerebral arteries

et al. 2014

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Exposure to microgravity results in cardiovascular deconditioning, and cerebrovascular oxidative stress injury has been suggested to occur. To elucidate the mechanism for this condition, we investigated whether simulated microgravity induces mitochondrial dysfunction in rat arteries. Four-week hindlimb unweighting (HU) was used to simulate microgravity in rats. Mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential (Δψm), mitochondrial permeability transition pore (mPTP) opening, mitochondrial respiratory control ratio (RCR), MnSOD/GPx activity and expression, and mitochondrial malondialdehyde (MDA) were examined in rat cerebral and mesenteric VSMCs. Compared with the control rats, mitochondrial ROS levels, mPTP opening, and MDA content increased significantly (P<0.001, P<0.01, and P<0.01, respectively), Δψm, RCR, MnSOD/GPx activity (P<0.001 for Δψm and RCR; P<0.05 for MnSOD; and P<0.001 for GPx activity) and protein abundance of mitochondrial MnSOD/GPx-1 decreased (P<0.001 for MnSOD and GPx-1) in HU rat cerebral but not mesenteric arteries. Chronic treatment with NADPH oxidase inhibitor apocynin and mitochondria-targeted antioxidant mitoTempol promoted recovery of mitochondrial function in HU rat cerebral arteries, but exerted no effects on HU rat mesenteric arteries. Therefore, simulated microgravity resulted in cerebrovascular mitochondrial dysfunction, and crosstalk between NADPH oxidase and mitochondria participated in the process.

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“…In mesenteric arteries, Colleran et al (12) demonstrated lower NE‐, KCl‐, and caffeine‐induced vasoconstriction, as well as decreased RyR‐2 mRNA and protein after 14 d of HU. In addition, ryanodinesensitive Ca 2+ release from the sarcoplasmic reticulum is decreased in vascular smooth muscle cells isolated from mesenteric arteries of HU rats (53). Thus, the mechanism of the microgravity‐induced impairment of mesenteric artery vasoconstrictor responsiveness in the present study appears to be consistent with that of ground‐based studies with HU rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of spaceflight and ground recovery on mesenteric artery and vein constrictor properties in mice

Behnke¹,

Stabley²,

McCullough³

et al. 2012

The FASEB Journal

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Following exposure to microgravity, there is a reduced ability of astronauts to augment peripheral vascular resistance, often resulting in orthostatic hypotension. The purpose of this study was to test the hypothesis that mesenteric arteries and veins will exhibit diminished vasoconstrictor responses after spaceflight. Mesenteric arteries and veins from female mice flown on the Space Transportation System (STS)-131 (n=11), STS-133 (n=6), and STS-135 (n=3) shuttle missions and respective ground-based control mice (n=30) were isolated for in vitro experimentation. Vasoconstrictor responses were evoked in arteries via norepinephrine (NE), potassium chloride (KCl), and caffeine, and in veins through NE across a range of intraluminal pressures (2-12 cmH(2)O). Vasoconstriction to NE was also determined in mesenteric arteries at 1, 5, and 7 d postlanding. In arteries, maximal constriction to NE, KCl, and caffeine were reduced immediately following spaceflight and 1 d postflight. Spaceflight also reduced arterial ryanodine receptor-3 mRNA levels. In mesenteric veins, there was diminished constriction to NE after flight. The results indicate that the impaired vasoconstriction following spaceflight occurs through the ryanodine receptor-mediated intracellular Ca(2+) release mechanism. Such vascular changes in astronauts could compromise the maintenance of arterial pressure during orthostatic stress.

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Differential Regulation and Recovery of Intracellular Ca2+ in Cerebral and Small Mesenteric Arterial Smooth Muscle Cells of Simulated Microgravity Rat

Cited by 23 publications

References 30 publications

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Up-regulation of ryanodine receptor expression increases the calcium-induced calcium release and spontaneous calcium signals in cerebral arteries from hindlimb unloaded rats

Simulated microgravity‐induced mitochondrial dysfunction in rat cerebral arteries

Effects of spaceflight and ground recovery on mesenteric artery and vein constrictor properties in mice

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