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Shengchen Tao Daiju Yamazaki Shinji Komazaki Chengzhu Zhao Tsunaki Iida Sho Kakizawa Yuji Imaizumi Hiroshi Takeshima 《The Journal of biological chemistry》2013,288(22):15581-15589
The TRIC channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation-specific channels and likely mediate counterion movements to support efficient Ca2+ release from the sarco/endoplasmic reticulum. Vascular smooth muscle cells (VSMCs) contain both TRIC subtypes and two Ca2+ release mechanisms; incidental opening of ryanodine receptors (RyRs) generates local Ca2+ sparks to induce hyperpolarization and relaxation, whereas agonist-induced activation of inositol trisphosphate receptors produces global Ca2+ transients causing contraction. Tric-a knock-out mice develop hypertension due to insufficient RyR-mediated Ca2+ sparks in VSMCs. Here we describe transgenic mice overexpressing TRIC-A channels under the control of a smooth muscle cell-specific promoter. The transgenic mice developed congenital hypotension. In Tric-a-overexpressing VSMCs from the transgenic mice, the resting membrane potential decreased because RyR-mediated Ca2+ sparks were facilitated and cell surface Ca2+-dependent K+ channels were hyperactivated. Under such hyperpolarized conditions, L-type Ca2+ channels were inactivated, and thus, the resting intracellular Ca2+ levels were reduced in Tric-a-overexpressing VSMCs. Moreover, Tric-a overexpression impaired inositol trisphosphate-sensitive stores to diminish agonist-induced Ca2+ signaling in VSMCs. These altered features likely reduced vascular tonus leading to the hypotensive phenotype. Our Tric-a-transgenic mice together with Tric-a knock-out mice indicate that TRIC-A channel density in VSMCs is responsible for controlling basal blood pressure at the whole-animal level. 相似文献
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Yoshiaki Suzuki Hisao Yamamura Susumu Ohya Yuji Imaizumi 《The Journal of biological chemistry》2013,288(51):36750-36761
L-type voltage-dependent Ca2+ channels (LVDCC) and large conductance Ca2+-activated K+ channels (BKCa) are the major factors defining membrane excitability in vascular smooth muscle cells (VSMCs). The Ca2+ release from sarcoplasmic reticulum through ryanodine receptor significantly contributes to BKCa activation in VSMCs. In this study direct coupling between LVDCC (Cav1.2) and BKCa and the role of caveoline-1 on their interaction in mouse mesenteric artery SMCs were examined. The direct activation of BKCa by Ca2+ influx through coupling LVDCC was demonstrated by patch clamp recordings in freshly isolated VSMCs. Using total internal reflection fluorescence microscopy, it was found that a large part of yellow fluorescent protein-tagged BKCa co-localized with the cyan fluorescent protein-tagged Cav1.2 expressed in the plasma membrane of primary cultured mouse VSMCs and that the two molecules often exhibited FRET. It is notable that each BKα subunit of a tetramer in BKCa can directly interact with Cav1.2 and promotes Cav1.2 cluster in the molecular complex. Furthermore, caveolin-1 deficiency in knock-out (KO) mice significantly reduced not only the direct coupling between BKCa and Cav1.2 but also the functional coupling between BKCa and ryanodine receptor in VSMCs. The measurement of single cell shortening by 40 mm K+ revealed enhanced contractility in VSMCs from KO mice than wild type. Taken together, caveolin-1 facilitates the accumulation/clustering of BKCa-LVDCC complex in caveolae, which effectively regulates spatiotemporal Ca2+ dynamics including the negative feedback, to control the arterial excitability and contractility. 相似文献
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Yukio Furuichi Takao Takahashi Katsumi Imaizumi Michihiro Sugano 《Bioscience, biotechnology, and biochemistry》2013,77(7):1777-1781
The absorbability of polyethylene glycol (PEG), a water-soluble nutritional marker, from the gastrointestinal tract of rat was examined using the [14C]-labeled compound ([14C]PEG) having a molecular weight of 4000. Intravenously injected [14C]PEG was readily excreted and recovered almost completely in the urine and neither hepatic nor renal uptake of the PEG was observed. Intragastrically administered [14C]PEG was eliminated in the urine with an average recovery of only 0.43 ± 0.13% (Mean ± S.D., n= 10) of the dose over 24 hr. From the gel column chromatographic profile of the radioactivity excreted in the urine after an oral dose, [14C]PEG was suggested to be absorbed in two forms, as an original form and as a low molecular weight component. The latter component might be the degraded product of PEG in the gastrointestinal tract. From these results it was confirmed that PEG with a molecular weight of 4000 is a satisfactory marker because of its low absorbability. 相似文献
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Analysis of terminal sugar moieties and species-specificities of acrosome reaction-inducing substance in Xenopus (ARISX) 总被引:1,自引:1,他引:0
Ueda Y Imaizumi C Kubo H Sato K Fukami Y Iwao Y 《Development, growth & differentiation》2007,49(7):591-601
The acrosome reaction of Xenopus sperm is triggered by the acrosome reaction-inducing substance in Xenopus (ARISX), an oviductal pars recta-derived, sugar-rich substance decorated on the entire surface of the vitelline envelope (VE) during ovulation. Here we addressed the functional importance of the sugar moiety in ARISX. Among various lectins examined, soybean agglutinin and Dolichos biflorus agglutinin were shown to abolish the acrosome reaction-inducing activity of ARISX present in pars recta extract or on the VE, indicating the importance of the terminal alpha-N-acetylgalactosamine residue for the function of ARISX. Consistently, the acrosome reaction-inducing activity was not affected by proteinase K digestion, in spite of the simultaneous shift of ARISX to a smaller molecular weight. Indirect immunofluorescence microscopic examinations showed that ARISX was distributed as two types of structures on VE; thick fiber-like materials and thin filamentous materials, and that a new structure appeared on the fertilization envelope instead of the thin filamentous materials. Sperm from several amphibian species were subjected to an in vitro assay during induction of the acrosome reaction with ARISX. The resulting limited population of sperm from a non-Xenopus species underwent acrosome reaction, implying a weak species-specificity of ARISX. 相似文献
20.
Disturbed activation of endoplasmic reticulum stress transducers by familial Alzheimer's disease-linked presenilin-1 mutations 总被引:8,自引:0,他引:8
Katayama T Imaizumi K Honda A Yoneda T Kudo T Takeda M Mori K Rozmahel R Fraser P George-Hyslop PS Tohyama M 《The Journal of biological chemistry》2001,276(46):43446-43454
Recent studies have shown independently that presenilin-1 (PS1) null mutants and familial Alzheimer's disease (FAD)-linked mutants should both down-regulate signaling of the unfolded protein response (UPR). However, it is difficult to accept that both mutants possess the same effects on the UPR. Furthermore, contrary to these observations, neither loss of PS1 and PS2 function nor expression of FAD-linked PS1 mutants were reported to have a discernable impact on the UPR. Therefore, re-examination and detailed analyses are needed to clarify the relationship between PS1 function and UPR signaling. Here, we report that PS1/PS2 null and dominant negative PS1 mutants, which are mutated at aspartate residue 257 or 385, did not affect signaling of the UPR. In contrast, FAD-linked PS1 mutants were confirmed to disturb UPR signaling by inhibiting activation of both Ire1alpha and ATF6, both of which are endoplasmic reticulum (ER) stress transducers in the UPR. Furthermore, PS1 mutants also disturbed activation of PERK (PKR-like ER kinase), which plays a crucial role in inhibiting translation during ER stress. Taken together, these observations suggested that PS1 mutations could affect signaling pathways controlled by each of the respective ER-stress transducers, possibly through a gain-of-function. 相似文献