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31.
Yosuke Omori Toshiaki Mano Tomohito Ohtani Yasushi Sakata Yasuharu Takeda Shunsuke Tamaki Yasumasa Tsukamoto Takeshi Miwa Kazuhiro Yamamoto Issei Komuro 《Yonago acta medica》2014,57(3):109-116
Background
Cardiac fibrosis is considered to be a crucial factor in the development of heart failure. Blockade of the mineralocorticoid receptor (MR) attenuated cardiac fibrosis and improved the prognosis of patients with chronic heart failure but the ligand for MR and the regulatory mechanism of MR pathway in the diseased heart are unclear. Here, we investigated whether glucocorticoids can promote cardiac fibrosis through MR in oxidative stress and the involvement of elongation factor eleven-nineteen lysine-rich leukemia (ELL), a co-activator of MR, in this pathway.Methods and Results
The MR antagonist eplerenone attenuated corticosterone-induced collagen synthesis assessed by [3H]proline incorporation in rat neonatal cultured cardiac fibroblasts in the presence of H2O2, as an oxidative stress but not in the absence of H2O2. H2O2 increased the ELL expression levels and MR-bound ELL. ELL expression levels and MR-bound ELL were also increased in the left ventricle of heart failure model rats with significant fibrosis and enhanced oxidative stress. Eplerenone did not attenuate corticosterone-induced increase of [3H]proline incorporation in the presence of H2O2 after knockdown of ELL expression using small interfering RNA in cardiac fibroblasts.Conclusion
Glucocorticoids can promote cardiac fibrosis via MR in oxidative stress, and oxidative stress modulates MR response to glucocorticoids through the interaction with ELL. Preventing cardiac fibrosis by modulating glucocorticoid-MR-ELL pathway may become a new therapeutic strategy for heart failure. 相似文献32.
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Tomoyuki Muto Takeshi Kokubu Yutaka Mifune Ryosuke Sakata Issei Nagura Hanako Nishimoto Yoshifumi Harada Kotaro Nishida Ryosuke Kuroda Masahiro Kurosaka 《Journal of orthopaedic research》2013,31(6):976-982
Triamcinolone acetonide (TA) injections are widely used to treat enthesopathy, but they may induce adverse effects such as tendon impairment and rupture. Platelet‐rich plasma (PRP) is a blood fraction containing high platelet concentrations and various growth factors that play a role in tissue repair processes. The purpose of this study is to investigate whether TA has deleterious effects on human rotator cuff‐derived cells, and if PRP can protect these cells from the effects of TA. Human rotator cuff‐derived cells were cultured with and without TA and PRP, and the culture without any additive served as the control. Cell morphology was assessed at days 7 and 21. Cell viability was evaluated at days 1, 7, 14, and 21 by a water‐soluble tetrazolium salt assay. Induction of apoptosis was measured by immunofluorescence staining and flow cytometry at day 7. Induction of cleaved caspase‐3 was measured by immunofluorescence staining at day 7. The cells cultured with TA had a flattened and polygonal shape at day 7. The cells cultured with both TA and PRP were similar in appearance to control cells. Exposure to TA also significantly decreased cell viability, but cell viability did not decrease when PRP was added along with TA. The number of apoptotic cells increased with TA exposure, while addition of PRP prevented cell apoptosis. In conclusion, the deleterious effect of TA was prevented by PRP, which can be used as a protective agent for patients receiving local TA injections. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 976–982, 2013 相似文献
36.
Nakamura Y Yasukochi M Kobayashi S Uehara K Honda A Inoue R Imanaga I Uehara A 《Pflügers Archiv : European journal of physiology》2007,453(4):455-462
Lysophosphatidylcholine (LPC) is metabolized from a membrane phospholipid and modulates a variety of channels in the plasma
membrane (PM). We examined LPC modulation of cardiac ryanodine receptor (RyR) channels in the sarcoplasmic reticulum (SR)
using the planar lipid bilayer method to measure the single-channel currents. Micromolar concentrations of LPC increased the
open probability of the reconstituted RyR channels irrespective of whether LPC was added to the cis or trans chamber. LPC
also increased the membrane capacitance of the bilayer. The effects of LPC contrasted well with those of sphingosylphosphorylcholine
(SPC). Taken together, these results suggest that amphipathic lipid LPC does not bind directly to the RyR channel protein,
but rather, is incorporated into the bilayer membrane and activates the channel. Thus, we consider cell membrane-derived LPC
to be a putative endogenous mediator that activates not only plasma membrane channels but also RyR channels and induces arrhythmogenic
Ca2+ mobilization in cardiomyocytes. 相似文献
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Noriko Nakanishi Ryohei Nomoto Kanako Sato Chihiro Koike Mari Kusuki Tatsuya Nakamura Katsumi Shigemura Toshiro Shirakawa Masato Fujisawa Issei Tokimatsu Kayo Osawa 《Journal of infection and chemotherapy》2019,25(2):154-156
Pseudomonas aeruginosa, responsible for serious nosocomial-acquired infections, possesses intrinsic antibiotic resistance mechanisms and commonly exhibits multidrug resistance. Here, we report the evolving resistance profiles of strains isolated from the sputum of a patient being treated for repeated P. aeruginosa infections following cancer resection. Whole genome sequencing of six isolates obtained over a 2-month period revealed two key single nucleotide polymorphisms in the mexR and gyrB genes that affected efflux pump expression and antimicrobial resistance. 相似文献