Subjects: Biology >> Biophysics >> Integrative & Complementary Medicine submitted time 2016-05-12
Tan, Li
Chen, Weiwei
Wei, Ming-Yu
Shen, Jinhua
Yu, Meng-Fei
Liu, Qing-Hua
Tan, Li
Chen, Weiwei
Wei, Ming-Yu
Shen, Jinhua
Yu, Meng-Fei
Liu, Qing-Hua
Yang, Guangzhong
Guo, Donglin
Guo, Donglin
Qin, Gangjian
Ji, Guangju
Abstract： The traditional herb Plumula Nelumbinis is widely used in the world because it has many biological activities, such as anti-inflammation, antioxidant, antihypertension, and butyrylcholinesterase inhibition. However, the action of Plumula Nelumbinis on airway smooth muscle (ASM) relaxation has not been investigated. A chloroform extract of Plumula Nelumbinis (CEPN) was prepared, which completely inhibited precontraction induced by high K+ in a concentration-dependent manner in mouse tracheal rings, but it had no effect on resting tension. CEPN also blocked voltage-dependent L-type Ca2+ channel-(VDCC-) mediated currents. In addition, ACh-induced precontraction was also completely blocked by CEPN and partially inhibited by nifedipine or pyrazole 3. Besides, CEPN partially reduced ACh-activated nonselective cation channel (NSCC) currents. Taken together, our data demonstrate that CEPN blocked VDCC and NSCC to inhibit Ca2+ influx, resulting in relaxation of precontracted ASM. This finding indicates that CEPN would be a candidate of new potent bronchodilators.
Peer Review Status:
Awaiting Review
Subjects: Biology >> Biophysics >> Biochemistry & Molecular Biology submitted time 2016-05-11
Abstract： ERp44, an endoplasmic reticulum (ER) resident protein, regulates intracellular Ca2+ release and involves in the maturation of many proteins in mammalian cells. In this study, we investigated the effects and mechanism of ERp44 on cell apoptosis by using ERp44 knockdown stable HeLa cell lines. We found that ERp44 knockdown resulted in increases in cell apoptosis rate more than one fold higher than that of control; using serum starvation, caspase-3 protein level was significantly up-regulated in ERp44 knockdown cells compared to the control cells. Furthermore, we demonstrated that in response to serum starvation, the protein levels of CHOP and GRP78 were also largely raised in ERp44 knockdown cells. Moreover, caspase-12 was activated, which suggested cell apoptosis was induced by ER stress. Taken together, our results indicate that knockdown of ERp44 leads to cell apoptosis through the activation of ER stress. (C) 2015 Elsevier Inc. All rights reserved.
Peer Review Status:Awaiting Review
Subjects: Biology >> Biophysics >> Biochemistry & Molecular Biology submitted time 2016-05-11
Abstract： Calcium (Ca2+) oscillations play a central role in varieties of cellular processes including fertilization and immune response, but controversy over the regulation mechanisms still exists. It has been known that nitric oxide (NO) dependently regulates Ca2+ signaling in most physiopathological processes. Previous study indicated that eNOS translocation during some pathological process influences intracellular Ca2+ homeostasis. In this study, we investigated the role and mechanism of NO on Ca2+ release by overexpressing eNOS in cytoplasm (Cyto-eNOS) and endoplasmic reticulum (ER-eNOS) of HeLa cells. We found that the properties of Ca2+ release were altered by the overexpression of eNOS. The amplitude and frequency of extracellular ATP (eATP)-induced Ca2+ oscillation were enhanced in both Cyto-eNOS and ER-eNOS cells, respectively. Especially, the enhancement of the amplitude and frequency of the Ca2+ oscillation was much more significant in the ER-eNOS cells than that of Cyto-eNOS cells. Further study indicated that this effect was abrogated by NO inhibitor, 1..-NAME, suggesting it was not an artificial result induced by ER stress. Furthermore, an up-regulated phosphorylation of phospholamban (PLB) was observed and the sarco-endoplasmic reticulum Ca2tATPase (SERCA) function was activated followed by the significant increase in the ER Ca2+ load. Taken together, we revealed a novel regulatory mechanism of Ca2+ oscillation. (C) 2014 Elsevier Inc. All rights reserved.
Peer Review Status:Awaiting Review
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