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1,108 results on '"Zhang, Xiao Ling"'

167. Self‐Produced O2CNs‐Based Nanocarriers of DNA Hydrophobization Strategy Triggers Photodynamic and Mitochondrial‐Derived Ferroptosis for Hepatocellular Carcinoma Combined Treatment

Author

Liu, Ming‐Xuan, Liu, Yan‐Chao, Cai, Yu‐Ting, Gu, Ying‐Ying, Zhu, Ya‐Qi, Zhang, Nan, Zhu, Wei‐Zhong, Liu, Yong‐Hong, Yu, Lei, Zhang, Qi‐Tao, and Zhang, Xiao‐Ling

Abstract

Hypoxia can aggravate tumor occurrence, development, invasion, and metastasis, and greatly inhibit the photodynamic therapy (PDT) effect. Herein, carbon nitride (CNs)‐based DNA and photosensitizer co‐delivery systems (BPSCNs) with oxygen‐producing functions are developed to address this problem. Selenide glucose (Seglu) is used as the dopant to prepare red/NIR‐active CNs (SegluCNs). The tumor‐targeting unit Bio‐PEG2000is utilized to construct BPSCNs nanoparticles through esterification reactions. Furthermore, DNA hydrophobization is realized via mixing P53 gene with a positively charged mitochondrial‐targeted near‐infrared (NIR) emitting photosensitizer (MTTPY), which is encapsulated in non‐cationic BPSCNs for synergistic delivery. Ester bonds in BPSCNs@MTTPY‐P53 complexes can be disrupted by lipase in the liver to facilitate P53 release, upregulated P53 expression, and promoted HIF‐1α degradation in mitochondria. In addition, the oxygen produced by the complexes improved the hypoxic microenvironment of hepatocellular carcinoma (HCC), synergistically downregulated HIF‐1α expression in mitochondria, promoted mitochondrial‐derived ferroptosis and enhanced the PDT effect of the MTTPY unit. Both in vivo and in vitro experiments indicated that the transfected P53‐DNA, produced O2and ROS by these complexes synergistically led to mitochondrial‐derived ferroptosis in hepatoma cells through the HIF‐1α/SLC7A11 pathway, and completely avoiding PDT resistance caused by hypoxia, exerting a significant therapeutic role in HCC treatment. BPSCNs@MTTPY‐P53 complexes can be disrupted by lipase in the liver to facilitate P53 release, upregulated P53 expression, and promoted HIF‐1c degradation in mitochondria. After laser irradiation, the oxygen produced by the complexes improved the hypoxic microenvironment of HCC, synergistically downregulated HIF‐1α expression in mitochondria, promoted mitochondrial‐derived ferroptosis, and enhanced the PDT effect of tumors.

Published
2024
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178. Polarity of alveolar epithelial cell acid-base permeability

Author

Joseph, Dilip, Tirmizi, Omar, Zhang, Xiao-Ling, Crandall, Edward D., and Lubman, Richard L.

Subjects
Physiology -- Research, Epithelial cells -- Research, Acidosis -- Research, Biological sciences
Abstract

We investigated acid-base permeability properties of electrically resistive monolayers of alveolar epithelial cells (AEC) grown in primary culture. AEC monolayers were grown on tissue culture-treated polycarbonate filters. Filters were mounted in a partitioned cuvette containing two fluid compartments (apical and basolateral) separated by the adherent monolayer, cells were loaded with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein, and intracellular pH was determined. Monolayers in HC[O.sup.-.sub.3]-free [Na.sup.+] buffer (140 mM [Na.sup.+], 6 mM HEPES, pH 7.4) maintained a transepithelial pH gradient between the two fluid compartments over 30 min. Replacement of apical fluid by acidic (6.4) or basic (8.0) buffer resulted in minimal changes in intracellular pH. Replacement of basolateral fluid by acidic or basic buffer resulted in transmembrane proton fluxes and intracellular acidification or alkalinization. Intracellular alkalinization was blocked [greater than or equal to] 80% by 100 [micro]M dimethylamiloride, an inhibitor of [Na.sup.+]/[H.sup.+] exchange, whereas acidification was not affected by a series of acid/base transport inhibitors. Additional experiments in which AEC monolayers were grown in the presence of acidic (6.4) or basic (8.0) medium revealed differential effects on bioelectric properties depending on whether extracellular pH was altered in apical or basolateral fluid compartments bathing the cells. Acid exposure reduced (and base exposure increased) short-circuit current from the basolateral side; apical exposure did not affect short-circuit current in either case. We conclude that AEC monolayers are relatively impermeable to transepithelial acid/base fluxes, primarily because of impermeability of intercellular junctions and of the apical, rather than basolateral, cell membrane. The principal basolateral acid exit pathway observed under these experimental conditions is [Na.sup.+]/[H.sup.+] exchange, whereas proton uptake into cells occurs across the basolateral cell membrane by a different, undetermined mechanism. These results are consistent with the ability of the alveolar epithelium to maintain an apical-to-basolateral (air space-to-blood) pH gradient in situ. alveolar epithelium; 2',T-bis(2-carboxyethyl)-5(6)-carboxyfluorescein; 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid; sodium/hydrogen exchange; acidosis

Published
2002

183. MST4 negatively regulates the EMT, invasion and metastasis of HCC cells by inactivating PI3K/AKT/Snail1 axis

Author

Dian, Mei-Juan, primary, Li, Jing, additional, Zhang, Xiao-Ling, additional, Li, Zi-Jian, additional, Zhou, Ying, additional, Zhou, Wei, additional, Zhong, Qiu-Ling, additional, Pang, Wen-Qian, additional, Lin, Xiao-Lin, additional, Liu, Tao, additional, Liu, Yi-An, additional, Li, Yong-Long, additional, Han, Liu-Xin, additional, Zhao, Wen-Tao, additional, Jia, Jun-Shuang, additional, Xiao, Sheng-Jun, additional, Xiao, Dong, additional, Xia, Jia-Wei, additional, and Hao, Wei-Chao, additional

Published
2021
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