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Xiju He, Shoutian Li, Xiaoxia Fang, Yanhong Liao
TDCPP, Tris (1, 3-dichloro-2-propyl) phosphate belongs to a group of chemicals known as triester organophosphate flame retardants, It can alter calcium homeostasis at much lower concentrations in normal conditions, but the mechanism is unclear till now. Calcium overload is a leading cause of apoptosis in myocardial ischemia/reperfusion (I/R) injury, thus how to mitigate Ca(2+)-overload is deserved to be investigated. We therefore hypothesized that TDCPP could attenuate cardiomyocytes apoptosis in I/R injury...
November 9, 2017: Regulatory Toxicology and Pharmacology: RTP
Estella Zuccolo, Christian Andrea Di Buduo, Francesco Lodola, Stefania Orecchioni, Giorgia Scarpellino, Dlzar Ali Kheder, Valentina Poletto, Germano Guerra, Francesco Bertolini, Alessandra Balduini, Vittorio Rosti, Francesco Moccia
Stromal derived factor-1α (SDF-1α) drives endothelial colony forming cell (ECFC) homing and incorporation within neovessels, thereby restoring tissue perfusion in ischemic tissues and favouring tumor vascularization and metastasis. SDF-1α stimulates ECFC migration by activating the Gi-protein coupled receptor, CXCR4, and then engaging the phosphoinositide 3-kinase (PI3K)/AKT signalling pathway. Sporadic evidence showed that SDF-1α may also act through an increase in intracellular Ca2+ concentration ([Ca2+]i) in bone marrow-derived hematopoietic progenitor cells and fully differentiated endothelial cells...
November 9, 2017: Stem Cells and Development
Zhi-Hong Zhao, Jun Luo, Hai-Xia Li, Sai-Hua Wang, Xin-Ming Li
Stromal interaction molecule 1 (STIM1) is the key molecule responsible for store-operated Ca(2+) entry (SOCE). Numerous studies have demonstrated that STIM1 levels appeared to be enhanced during cardiac hypertrophy. However, the mechanism underlining this process remains to be clarified. In this study, phenylephrine (PE) was employed to establish a model of hypertrophic neonatal rat cardiomyocytes (HNRCs) in vitro, and low expression of primary and mature miR-223 was detected in PE-induced HNRCs. Our results have revealed that downregulation of miR-223 by PE contributed to the increase of STIM1, which in turn induced cardiac hypertrophy...
November 7, 2017: Molecular and Cellular Biochemistry
Bojun Zhang, Jay S Naik, Nikki L Jernigan, Benjimen R Walker, Thomas C Resta
Endothelial dysfunction in chronic hypoxia (CH)-induced pulmonary hypertension is characterized by reduced store-operated Ca(2+) entry (SOCE) and diminished Ca(2+)-dependent production of endothelium-derived vasodilators. We recently reported that SOCE in pulmonary arterial endothelial cells (PAEC) is tightly regulated by membrane cholesterol, and that decreased membrane cholesterol is responsible for impaired SOCE following CH. However, the ion channels involved in cholesterol-sensitive SOCE are unknown. We hypothesized that cholesterol facilitates SOCE in PAEC through the interaction of Orai1 and stromal interaction molecule 1 (STIM1)...
November 3, 2017: American Journal of Physiology. Heart and Circulatory Physiology
Vesna Bišof, Zoran Rakušić, Juraj Bibić, Timor Grego, Majana Soče
AIM: To compare intensity modulated radiotherapy with simultaneous integrated boost (IMRT-SIB) and a 3-dimensional conformal parotid gland-sparing radiotherapy (ConPas 3D-CRT) in treatment of nasopharyngeal carcinoma with regard to outcomes and dose distribution to the planning target volumes (PTVs) and to the organs at risk (OARs). METHODS: The treatment records of 24 patients with histologically proven carcinoma of the nasopharynx treated with ConPas 3D-CRT or IMRT-SIB technique between May 2009 and December 2016 were assessed...
November 1, 2017: La Radiologia Medica
Fei He, Qianfu Wu, Banglong Xu, Xiaocheng Wang, Jixiong Wu, Li Huang, Jing Cheng
Objective: Previous studies have demonstrated STIM1-mediated store-operated Ca(2+) entry(SOCE) contributes to intracellular Ca(2+) accumulation. The present study aimed to investigate the expression of STIM1 and Orai1/TRPC1 in the context of myocardial ischemia/reperfusion injury(MIRI) and the effect of STIM1 inhibition on Ca(2+) accumulation and apoptosis in H9c2 cardiomyocytes subjected to hypoxia/reoxygenation(H/R). Methods: Expression of STIM1/Orai1/TRPC1 was determined by RT-PCR and Western Blot in mice subjected to MIRI and H9C2 cardiomyocytes subjected to H/R...
October 31, 2017: Bioscience Reports
Simona Boncompagni, Antonio Michelucci, Laura Pietrangelo, Robert T Dirksen, Feliciano Protasi
Store-operated Ca(2+) entry (SOCE), a ubiquitous mechanism that allows recovery of Ca(2+) ions from the extracellular space, has been proposed to limit fatigue during repetitive skeletal muscle activity. However, the subcellular location for SOCE in muscle fibers has not been unequivocally identified. Here we show that exercise drives a significant remodeling of the sarcotubular system to form previously unidentified junctions between the sarcoplasmic reticulum (SR) and transverse-tubules (TTs). We also demonstrate that these new SR-TT junctions contain the molecular machinery that mediate SOCE: stromal interaction molecule-1 (STIM1), which functions as the SR Ca(2+) sensor, and Orai1, the Ca(2+)-permeable channel in the TT...
October 27, 2017: Scientific Reports
Xin Li, Guangyan Wu, Yin Yang, Shijuan Fu, Xiaofen Liu, Huimin Kang, Xue Yang, Xun-Cheng Su, Yuequan Shen
Store-operated calcium entry (SOCE) is a major pathway for calcium ions influx into cells and has a critical role in various cell functions. Here we demonstrate that calcium-bound calmodulin (Ca(2+)-CaM) binds to the core region of activated STIM1. This interaction facilitates slow Ca(2+)-dependent inactivation after Orai1 channel activation by wild-type STIM1 or a constitutively active STIM1 mutant. We define the CaM-binding site in STIM1, which is adjacent to the STIM1-Orai1 coupling region. The binding of Ca(2+)-CaM to activated STIM1 disrupts the STIM1-Orai1 complex and also disassembles STIM1 oligomer...
October 19, 2017: Nature Communications
Yibin Zhou, Peng Gu, Jian Li, Feng Li, Jin Zhu, Peng Gao, Yachen Zang, Yongchang Wang, Yuxi Shan, Dongrong Yang
Store-operated calcium entry (SOCE) plays an important role in the invasion and migration of cancer cells. Stromal-interacting molecule 1 (STIM1) is a critical component in the SOCE. STIM1 has been attracting more and more attention due to its oncogenic potential. STIM1 inhibition suppresses cell proliferation, migration and invasion in a variety of cancer models both in vitro and in vivo. However, the role of STIM1 in prostate carcinogenesis, in particular, in tumor migration and invasion is unclear. Herein, we downregulated STIM1 in prostate cancer cells by lentivirus-mediated short hairpin (shRNA), and then studied its impacts on cell migration and invasion...
September 18, 2017: Oncology Reports
Saifur Rahman, Taufiq Rahman
The store-operated calcium entry (SOCE) pathway is an important route for generating cytosolic Ca(2+) signals that regulate a diverse array of biological processes. Abnormal SOCE seem to underlie several diseases that notably include allergy, inflammation and cancer. Therefore, any modulator of this pathway is likely to have significant impact in cell biology under both normal and abnormal conditions. In this study, we screened the FDA-approved drug library for agents that share significant similarity in 3D shape and surface electrostatics with few, hitherto best known inhibitors of SOCE...
October 16, 2017: Scientific Reports
Martin Vaeth, Mate Maus, Stefan Klein-Hessling, Elizaveta Freinkman, Jun Yang, Miriam Eckstein, Scott Cameron, Stuart E Turvey, Edgar Serfling, Friederike Berberich-Siebelt, Richard Possemato, Stefan Feske
Store-operated Ca(2+) entry (SOCE) is the main Ca(2+) influx pathway in lymphocytes and is essential for T cell function and adaptive immunity. SOCE is mediated by Ca(2+) release-activated Ca(2+) (CRAC) channels that are activated by stromal interaction molecule (STIM) 1 and STIM2. SOCE regulates many Ca(2+)-dependent signaling molecules, including calcineurin, and inhibition of SOCE or calcineurin impairs antigen-dependent T cell proliferation. We here report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling glycolysis and oxidative phosphorylation...
October 17, 2017: Immunity
Ying-Chi Chen, Yu-Chung Chang, Heng-Ai Chang, Yu-Shan Lin, Chiung-Wen Tsao, Meng-Ru Shen, Wen-Tai Chiu
Mast cells play a primary role in allergic diseases. During an allergic reaction, mast cell activation is initiated by cross-linking IgE-FcεRI complex by multivalent antigen resulting in degranulation. Additionally, G protein-coupled receptors also induce degranulation upon activation. However, the spatio-temporal relationship between Ca(2+) mobilization and mast cell degranulation is not well understood. We investigated the relationship between oscillations in Ca(2+) level and mast cell degranulation upon stimulation in rat RBL-2H3 cells...
November 2017: Cell Calcium
Maria C Olianas, Simona Dedoni, Pierluigi Onali
The 5'-adenosine monophosphate-activated protein kinase (AMPK) is a key regulator of the cellular energy metabolism and may induce either cell survival or death. We previously reported that in SH-SY5Y human neuroblastoma cells stimulation of muscarinic acetylcholine receptors (mAChRs) activate AMPK by triggering store-operated Ca(2+) entry (SOCE). However, whether mAChRs may control AMPK activity by regulating additional mechanisms beyond SOCE remains to be investigated. In the present study we examined the effects of mAChRs on AMPK when SOCE was induced by the sarco-endoplasmic reticulum Ca(2+)-ATPase inhibitor thapsigargin...
October 9, 2017: Neurochemical Research
Kunkun Xia, Zegang Ma, Jianxin Shen, Menghan Li, Baoke Hou, Ming Gao, Shuijun Zhang, Jie Wu
Cellular Ca(2+) signals play a critical role in cell physiology and pathology. In most non-excitable cells, store-operated Ca(2+) entry (SOCE) is an important mechanism by which intracellular Ca(2+) signaling is regulated. However, few drugs can selectively modulate SOCE. 2-Aminoethoxydiphenyl borate (2APB) and its analogs (DPB162 and DPB163) have been reported to inhibit SOCE. Here, we examined the effects of another 2-APB analog, DPB161 on SOCE in acutely-isolated rat submandibular cells. Both patch-clamp recordings and Ca(2+) imaging showed that upon removal of extracellular Ca(2+) ([Ca(2+)]o=0), rat submandibular cells were unable to maintain ACh-induced Ca(2+) oscillations, but restoration of [Ca(2+)]o to refill Ca(2+) stores enable recovery of these Ca(2+) oscillations...
September 22, 2017: Oncotarget
Jia Song, Sisi Zheng, Nhung Nguyen, Youjun Wang, Yubin Zhou, Kui Lin
BACKGROUND: Because phylogenetic inference is an important basis for answering many evolutionary problems, a large number of algorithms have been developed. Some of these algorithms have been improved by integrating gene evolution models with the expectation of accommodating the hierarchy of evolutionary processes. To the best of our knowledge, however, there still is no single unifying model or algorithm that can take all evolutionary processes into account through a stepwise or simultaneous method...
October 3, 2017: BMC Bioinformatics
Pankaj Sehgal, Paula Szalai, Claus Olesen, Helle A Praetorius, Poul Nissen, Søren Brøgger Christensen, Nikolai Engedal, Jesper Vuust Møller
Calcium (Ca2+) is a fundamental regulator of cell signaling and function. Thapsigargin (Tg) blocks the sarco/endoplasmic reticulum (ER) Ca2+-ATPase (SERCA), disrupts Ca2+ homeostasis, and causes cell death. However, the exact mechanisms whereby SERCA-inhibition induces cell death are incompletely understood. Here, we report that low (0.1 μM) concentrations of Tg and Tg analogs with various long-chain substitutions at the O(8) position extensively inhibit SERCA1a-mediated Ca2+ transport. We also found that in both prostate and breast cancer cells, exposure to Tg or Tg analogs for 1 day caused extensive drainage of the ER Ca2+ stores...
September 29, 2017: Journal of Biological Chemistry
Yoshikazu Inoh, Aki Haneda, Satoshi Tadokoro, Satoru Yokawa, Tadahide Furuno
Cationic liposomes are commonly used as vectors to effectively introduce foreign genes (antisense DNA, plasmid DNA, siRNA, etc.) into target cells. Cationic liposomes are also known to affect cellular immunocompetences such as the mast cell function in allergic reactions. In particular, we previously showed that the cationic liposomes bound to the mast cell surface suppress the degranulation induced by cross-linking of high affinity IgE receptors in a time- and dose-dependent manner. This suppression is mediated by impairment of the sustained level of intracellular Ca(2+) concentration ([Ca(2+)]i) via inhibition of store-operated Ca(2+) entry (SOCE)...
December 2017: Biochimica et Biophysica Acta
Wei Hong, Gongyong Peng, Binwei Hao, Baoling Liao, Zhuxiang Zhao, Yumin Zhou, Fang Peng, Xiuqin Ye, Lingmei Huang, Mengning Zheng, Jinding Pu, Chunxiao Liang, Erkang Yi, Huanhuan Peng, Bing Li, Pixin Ran
BACKGROUND/AIMS: The proliferation of human bronchial smooth muscle cells (HBSMCs) is a key pathophysiological component of airway remodeling in chronic obstructive pulmonary disease (COPD) for which pharmacotherapy is limited, and only slight improvements in survival have been achieved in recent decades. Cigarette smoke is a well-recognized risk factor for COPD; however, the pathogenesis of cigarette smoke-induced COPD remains incompletely understood. This study aimed to investigate the mechanisms by which nicotine affects HBSMC proliferation...
September 29, 2017: Cellular Physiology and Biochemistry
Rui-Gang Zhang, Chung-Yin Yip, Wing-Hung Ko
BACKGROUND/AIMS: Carbon monoxide (CO) is an important autocrine/paracrine messenger involved in a variety of physiological and pathological processes. This study aimed to investigate the regulatory role of CO released by CO-releasing molecule-2 (CORM-2) in a P2Y receptor-mediated calcium-signaling pathway in the human bronchial epithelial cell line, 16HBE14o-. METHODS: Intracellular calcium ([Ca2+]i) was measured by fura-2 microspectrofluorimetry. D-myo-inositol-1-phosphate (IP1) levels and cGMP-dependent protein kinase activity (PKG) were also quantified...
2017: Cellular Physiology and Biochemistry
Lara E Terry, Mark VerMeer, Jennifer Giles, Quang-Kim Tran
The G protein-coupled estrogen receptor 1 (GPER, formerly also known as GPR30) modulates many Ca(2+)-dependent activities in endothelial cells. However, the underlying mechanisms are poorly understood. We recently reported that GPER acts to prolong cytoplasmic Ca(2+) signals by interacting with and promoting inhibitory phosphorylation of the plasma membrane Ca(2+)-ATPase. In the present study, we examined the role of GPER activation in modulating store-operated Ca(2+) entry (SOCE) via effects on the stromal interaction molecule 1 (STIM1)...
October 23, 2017: Biochemical Journal
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