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  • 1
    Online Resource
    Online Resource
    Moesin is activated in cardiomyocytes in experimental autoimmune myocarditis and mediates cytoskeletal reorganization with protrusion formation
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 311, No. 2 ( 2016-08-01), p. H476-H486
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 311, No. 2 ( 2016-08-01), p. H476-H486
    Abstract: Acute myocarditis is a self-limiting disease. Most patients with myocarditis recover without cardiac dysfunction in spite of limited capacity of myocardial regeneration. Therefore, to address intrinsic reparative machinery of inflamed hearts, we investigated the cellular dynamics of cardiomyocytes in response to inflammation using experimental autoimmune myocarditis (EAM) model. EAM was induced by immunization of BALB/c mice with α-myosin heavy chain peptides twice. The inflammatory reaction was evoked with myocardial damage with the peak at 3 wk after the first immunization (EAM3w). Morphological and functional restoration started from EAM3w, when active protrusion formation, a critical process of myocardial healing, was observed in cardiomyocytes. Shotgun proteomics revealed that cytoskeletal proteins were preferentially increased in cardiomyocytes at EAM3w, compared with preimmunized (EAM0w) hearts, and that moesin was the most remarkably upregulated among them. Immunoblot analyses demonstrated that the expression of both total and phosphorylated moesin was upregulated in isolated cardiomyocytes from EAM3w hearts. Immunofluorescence staining showed that moesin was localized at cardiomyocyte protrusions at EAM3w. Adenoviral vectors expressing wild-type, constitutively active and inactive form of moesin (wtMoesin, caMoesin, and iaMoesin, respectively) were transfected in neonatal rat cardiomyocytes. The overexpression of wtMoesin and caMoesin resulted in protrusion formation, while not iaMoesin. Finally, we found that cardiomyocyte protrusions were accompanied by cell-cell contact formation. The expression of moesin was upregulated in cardiomyocytes under inflammation, inducing protrusion formation in a phosphorylation-dependent fashion. Moesin signal could be a novel therapeutic target that stimulates myocardial repair by promoting contact formation of cardiomyocytes.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00180.2016
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
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    Online Resource
    Effects of the motor cortical quadripulse transcranial magnetic stimulation (QPS) on the contralateral motor cortex and interhemispheric interactions
    American Physiological Society ; 2014
    In:  Journal of Neurophysiology Vol. 111, No. 1 ( 2014-01-01), p. 26-35
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 111, No. 1 ( 2014-01-01), p. 26-35
    Abstract: Corpus callosum connects the bilateral primary motor cortices (M1s) and plays an important role in motor control. Using the paired-pulse transcranial magnetic stimulation (TMS) paradigm, we can measure interhemispheric inhibition (IHI) and interhemispheric facilitation (IHF) as indexes of the interhemispheric interactions in humans. We investigated how quadripulse transcranial magnetic stimulation (QPS), one form of repetitive TMS (rTMS), on M1 affects the contralateral M1 and the interhemispheric interactions. QPS is able to induce bidirectional plastic changes in M1 depending on the interstimulus intervals (ISIs) of TMS pulses: long-term potentiation (LTP)-like effect by QPS-5 protocol, and long-term depression-like effect by QPS-50, whose numbers indicate the ISI (ms). Twelve healthy subjects were enrolled. We applied QPS over the left M1 and recorded several parameters before and 30 min after QPS. QPS-5, which increased motor-evoked potentials (MEPs) induced by left M1 activation, also increased MEPs induced by right M1 activation. Meanwhile, QPS-50, which decreased MEPs elicited by left M1 activation, did not induce any significant changes in MEPs elicited by right M1 activation. None of the resting motor threshold, active motor threshold, short-interval intracortical inhibition, long-interval intracortical inhibition, intracortical facilitation, and short-interval intracortical inhibition in right M1 were affected by QPS. IHI and IHF from left to right M1 significantly increased after left M1 QPS-5. The degree of left first dorsal interosseous MEP amplitude change by QPS-5 significantly correlated with the degree of IHF change. We suppose that the LTP-like effect on the contralateral M1 may be produced by some interhemispheric interactions through the corpus callosum.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00515.2013
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 3
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    Online Resource
    Role of 12-lipoxygenase in volatile anesthetic-induced delayed preconditioning in mice
    American Physiological Society ; 2006
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 291, No. 2 ( 2006-08), p. H979-H983
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 291, No. 2 ( 2006-08), p. H979-H983
    Abstract: Delayed cardiac protection mediated by 12-lipoxygenase (12-LO) expression and activity has been linked to opioid receptor stimulation. The role of 12-LO in volatile anesthetic-induced delayed cardiac protection has not been determined. We tested the hypothesis that expression and activity of 12-LO mediate delayed cardiac protection induced by isoflurane in the mouse heart in vivo. Mice were pretreated with 1.4% isoflurane for 30 min and allowed to recover for 1, 12, or 24 h. Immunoblot analysis showed isoflurane significantly enhanced 12-LO protein expression at 12 and 24 h after isoflurane exposure, and this induction of 12-LO was confirmed by immunohistochemistry of whole heart sections at 24 h. The induced protein expression appeared to be localized to intercalated disc regions adjoining adjacent cardiac myocytes. Additionally, mice ± isoflurane (24 h previously) were subjected to 30 min coronary artery occlusion followed by 2 h of reperfusion in the presence and absence of a 12-LO inhibitor. Isoflurane reduced infarct size (27.1 ± 2.2% of the area at risk; n = 8) compared with the control group (44.6 ± 3.6%, n = 8). Baicalein (3 mg/kg), a selective 12-LO inhibitor, blocked the delayed protective effects of isoflurane pretreatment on infarct size (40.6 ± 3.6%, n = 8). These data suggest that 12-LO is an important mediator of isoflurane-induced delayed preconditioning.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00266.2006
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Dark chocolate receptors: epicatechin-induced cardiac protection is dependent on δ-opioid receptor stimulation
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 299, No. 5 ( 2010-11), p. H1604-H1609
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 299, No. 5 ( 2010-11), p. H1604-H1609
    Abstract: Epicatechin, a flavonoid, is a well-known antioxidant linked to a variety of protective effects in both humans and animals. In particular, its role in protection against cardiovascular disease has been demonstrated by epidemiologic studies. Low-dose epicatechin, which does not have significant antioxidant activity, is also protective; however, the mechanism by which low-dose epicatechin induces this effect is unknown. Our laboratory tested the hypothesis that low-dose epicatechin mediates cardiac protection via opioid receptor activation. C57BL/6 mice were randomly assigned to 1 of 10 groups: control, epicatechin, naloxone (nonselective opioid receptor antagonist), epicatechin + naloxone, naltrindole (δ-specific opioid receptor antagonist), epicatechin + naltrindole, norbinaltorphimine (nor-BNI, κ-specific opioid receptor antagonist), epicatechin + nor-BNI, 5-hydroxydecanoic acid [5-HD, ATP-sensitive potassium channel antagonist], and epicatechin + 5-HD. Epicatechin (1 mg/kg) or other inhibitors (5 mg/kg) were administered by oral gavage or intraperitoneal injection, respectively, daily for 10 days. Mice were subjected to 30 min coronary artery occlusion followed by 2 h of reperfusion, and infarct size was determined via planimetry. Whole heart homogenates were assayed for downstream opioid receptor signaling targets. Infarct size was significantly reduced in epicatechin- and epicatechin + nor-BNI-treated mice compared with control mice. This protection was blocked by naloxone, naltrindole, and 5-HD. Epicatechin and epicatechin + nor-BNI increased the phosphorylation of Src, Akt, and IκBα, while simultaneously decreasing the expression of c-Jun NH 2 -terminal kinase and caspase-activated DNase. All signaling effects are consistent with opioid receptor stimulation and subsequent cardiac protection. Naloxone, naltrindole, and 5-HD attenuated these effects. In conclusion, epicatechin acts via opioid receptors and more specifically through the δ-opioid receptor to produce cardiac protection from ischemia-reperfusion injury.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00073.2010
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
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  • 5
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    Online Resource
    Conditioning intensity-dependent interaction between short-latency interhemispheric inhibition and short-latency afferent inhibition
    American Physiological Society ; 2012
    In:  Journal of Neurophysiology Vol. 108, No. 4 ( 2012-08-15), p. 1130-1137
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 108, No. 4 ( 2012-08-15), p. 1130-1137
    Abstract: The relationship between sensory and transcallosal inputs into the motor cortex may be important in motor performance, but it has not been well studied, especially in humans. The aim of this study was to reveal this relationship by investigating the interaction between short-latency interhemispheric inhibition (SIHI) and short-latency afferent inhibition (SAI) in humans with transcranial magnetic stimulation. SIHI is the inhibition of the primary motor cortex (M1) elicited by contralateral M1 stimulation given ∼10 ms before, and it reflects transcallosal inhibition. SAI is the inhibition of M1 elicited by contralateral median nerve stimulation preceding M1 stimulation by ∼20 ms. In this investigation, we studied the intensity dependence of SIHI and SAI and the interaction between SIHI and SAI in various conditioning intensities. Subjects were 11 normal volunteers. The degree of effects was evaluated by comparing motor evoked potential sizes recorded from the first dorsal interosseous muscle between a certain condition and control condition. Both SIHI and SAI were potentiated by increment of the conditioning stimulus intensity and saturated at 1.4 times resting motor threshold for SIHI and 3 times sensory threshold for SAI. No significant interaction was observed when either of their intensities was subthreshold for the inhibition on its own. Only when both intensities were strong enough for their inhibition did the presence of one inhibition lessen the other one. On the basis of these findings, we conclude that interneurons mediating SIHI and SAI have mutual, direct, and inhibitory interaction in a conditioning intensity-dependent manner.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00300.2012
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 6
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    Online Resource
    Modulation of error-sensitivity during a prism adaptation task in people with cerebellar degeneration
    American Physiological Society ; 2015
    In:  Journal of Neurophysiology Vol. 114, No. 4 ( 2015-10), p. 2460-2471
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 114, No. 4 ( 2015-10), p. 2460-2471
    Abstract: Cerebellar damage can profoundly impair human motor adaptation. For example, if reaching movements are perturbed abruptly, cerebellar damage impairs the ability to learn from the perturbation-induced errors. Interestingly, if the perturbation is imposed gradually over many trials, people with cerebellar damage may exhibit improved adaptation. However, this result is controversial, since the differential effects of gradual vs. abrupt protocols have not been observed in all studies. To examine this question, we recruited patients with pure cerebellar ataxia due to cerebellar cortical atrophy ( n = 13) and asked them to reach to a target while viewing the scene through wedge prisms. The prisms were computer controlled, making it possible to impose the full perturbation abruptly in one trial, or build up the perturbation gradually over many trials. To control visual feedback, we employed shutter glasses that removed visual feedback during the reach, allowing us to measure trial-by-trial learning from error (termed error-sensitivity), and trial-by-trial decay of motor memory (termed forgetting). We found that the patients benefited significantly from the gradual protocol, improving their performance with respect to the abrupt protocol by exhibiting smaller errors during the exposure block, and producing larger aftereffects during the postexposure block. Trial-by-trial analysis suggested that this improvement was due to increased error-sensitivity in the gradual protocol. Therefore, cerebellar patients exhibited an improved ability to learn from error if they experienced those errors gradually. This improvement coincided with increased error-sensitivity and was present in both groups of subjects, suggesting that control of error-sensitivity may be spared despite cerebellar damage.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00145.2015
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
    Location Call Number Limitation Availability
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