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202 results on '"Chen, Shaorui"'

41. Electronic anti‐injection effect for carbonyl in anchor group based on diphenylacetylene D2‐π‐A sensitizer in dye‐sensitized solar cells.

Author

Chen, Shaorui, Pang, Zhihan, and Wu, Wenjun

Subjects
*PHOTOSENSITIZERS, *DYE-sensitized solar cells, *POLAR effects (Chemistry), *CARBONYL group, *INTRAMOLECULAR charge transfer, *ANCHORING effect, *DIPHENYLACETYLENE
Abstract

Summary: Up to now, in developing organic molecules for dye‐sensitized solar cells, the determining role of acceptors has not yet received enough attention. Herein, three novel sensitizers were prepared with D2‐π‐A structure, following cyanoacetic acid, acetic acid, and rhodanine‐3‐acetic acid as the acceptors, respectively. It was found that the thiocarbonyl and carbonyl groups, which are separated by two atoms with carboxyl group, effectively promoted molecular light harvesting, intramolecular charge transfer, and improved energy level matching, but a significant electron‐blocking effect occurred, which limited the enhancement of photoelectric conversion performance with rhodanine‐3‐acetic acid. From PT‐1 to PT‐3, the power conversion efficiency decreased sharply from 5.27% to 2.70%. As a result, an electronic anti‐injection effect of electron‐drawing unit in the anchor group compared with cyanoacetic acid was found for the development of organic sensitizer design. [ABSTRACT FROM AUTHOR]

Published
2021
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42. Store-Operated Ca2+Entry (SOCE) contributes to angiotensin II-induced cardiac fibrosis in cardiac fibroblasts

Author

Zhang, Boyu, Jiang, Jianmin, Yue, Zhongbao, Liu, Shenglan, Ma, Yunzi, Yu, Na, Gao, Ying, Sun, Shuya, Chen, Shaorui, and Liu, Peiqing

Abstract

Store-operated Ca2+entry (SOCE) is an important mechanism of extracellular Ca2+entry into cells. It has been proved that SOCE is involved in many pathologic and physiological processes. Two key participants of SOCE, stromal interaction molecule1 (STIM1) and Orai1, have been identified. But their function in cardiac fibroblasts remains elusive. In present study, our findings suggested the expression of STIM1 and Orai1 were increased followed by angiotensin II (Ang II) stimulation in vivoand in vitro. In cultured adult rat cardiac fibroblasts, Ang II led to STIM1 interact with Orai1 and Ca2+release from intracellular calcium store. In addition, the upregulation of fibronectin (FN), connective tissue growth factor (CTGF) and smooth muscle α-actin (α-SMA) induced by Ang II were attenuated by SOCE inhibitor SKF-96365, similar results were observed by knocking down STIM1 and Orai1. Furthermore, we found that silencing Orai1 by RNA interference also suppressed the translocation of Nuclear Factor of Activated T-cells (NFAT) Isoforms NFATc4 and decreased the phosphorylation of Smad2 and Smad3 induced by Ang II. These results unraveled a novel role of SOCE as a key modulator in the Ang II-induced cardiac fibrosis by mediating Ca2+influx.

Published
2024
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50. BIG1, a brefeldin A-inhibited guanine nucleotide-exchange protein modulates ABCA1 trafficking and function

Author

Lin, Sisi, Zhou, Chun, Neufeld, Edward, Wang, Yu-Hua, Xu, Suo-Wen, Lu, Liang, Wang, Ying, Liu, Zhi-Ping, Li, Dong, Li, Cuixian, Chen, Shaorui, Le, Kang, Huang, Heqing, Liu, Peiqing, Moss, Joel, Vaughan, Martha, and Shen, Xiaoyan

Subjects
Male, Time Factors, Apolipoprotein A-I, Cell Membrane, Hep G2 Cells, Transfection, Glutathione, Article, Rats, Lipoproteins, LDL, Rats, Sprague-Dawley, Protein Transport, Cholesterol, Liver, Animals, Guanine Nucleotide Exchange Factors, Humans, Immunoprecipitation, ADP-Ribosylation Factor 1, ATP-Binding Cassette Transporters, Biotinylation, RNA Interference, ATP Binding Cassette Transporter 1, HeLa Cells
Abstract

Cell-surface localization and intracellular trafficking are essential for the function of ATP-binding cassette transporter A-1 (ABCA1). However, regulation of these activities is still largely unknown. Brefeldin A, an uncompetitive inhibitor of brefeldin A-inhibited guanine nucleotide-exchange proteins (BIGs), disturbs the intracellular distribution of ABCA1, and thus inhibits cholesterol efflux. This study aimed to define the possible roles of BIGs in regulating ABCA1 trafficking and cholesterol efflux, and further to explore the potential mechanism.By vesicle immunoprecipitation, we found that BIG1 was associated with ABCA1 in vesicles preparation from rat liver. BIG1 depletion reduced surface ABCA1 on HepG2 cells, and inhibited by 60% cholesterol release. In contrast, BIG1 overexpression increased surface ABCA1 and cholesterol secretion. With partial restoration of BIG1 through overexpression in BIG1-depleted cells, surface ABCA1 was also restored. Biotinylation and glutathione cleavage revealed that BIG1 small interfering RNA dramatically decreased the internalization and recycling of ABCA1. This novel function of BIG1 was dependent on the guanine nucleotide-exchange activity and achieved through activation of ADP-ribosylation factor 1.BIG1, through its ability to activate ADP-ribosylation factor 1, regulates cell-surface levels and function of ABCA1, indicating a transcription-independent mechanism for controlling ABCA1 action.

Published
2012

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