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22 results on '"Tang, Ming-Ming"'

10. Docosahexaenoic acid inhibits Ca2+ influx and downregulates CaSR by upregulating microRNA‐16 in pulmonary artery smooth muscle cells.

Author

Liu, Jin‐jun, Tang, Ming‐ming, Zhu, Ming‐li, Xie, Cai‐xia, Kang, Pin‐fang, Ling, Xuan, Zhang, Heng, Wang, Xiao‐jing, and Tang, Bi

Subjects
DOCOSAHEXAENOIC acid, PULMONARY artery, SMOOTH muscle, MUSCLE cells, CALCIUM-sensing receptors, OMEGA-6 fatty acids
Abstract

Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic‐free Ca2+ concentration ([Ca2+]cyt) was measured using Fluo‐3 AM method. Real‐time polymerase chain reaction was used to detect microRNA‐16 (miR‐16) and calcium‐sensing receptor (CaSR) messenger RNA expression levels. CCK‐8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR‐16 using dual‐luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca2+]cyt. After transfection of miR‐16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR‐16 inhibition. [Ca2+]cyt was also inhibited by miR‐16 transfection. DHA then promoted the expression of miR‐16, and the effects of DHA on PASMCs were annulled when miR‐16 was inhibited. CaSR was identified as a direct target of miR‐16. CaSR was inhibited directly by miR‐16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR‐16/CaSR axis. [ABSTRACT FROM AUTHOR]

Published
2020
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13. Fracture modelling based on the stochastic extended finite element method

Author

Tang Ming-ming, Lu Shuangfanga, Zhang Jinliang, and Ma Huifang

Subjects
Regional geology, Hydrogeology, Engineering geology, Geology, Fracture mechanics, Mechanics, Finite element method, Fuel Technology, Geochemistry and Petrology, Earth and Planetary Sciences (miscellaneous), Fracture (geology), Economic Geology, Petrology, Extended finite element method, Environmental geology
Abstract

Because a large number of oil and gas reservoirs are naturally fractured, they play an important role in hydrocarbon exploration and production. To fully extract and model the fracture system features of reservoirs, a new fracture modelling method, called the stochastic extended finite element (SEFE) method, is presented in this paper. This method couples fracture mechanics and the kriging method with a multi-field trend in an attempt to benefit from the advantages of each method: compliance with fracture mechanics equations and the reproduction of the fracture’s observed data, respectively. Based on the SEFE simulation method, we wrote a fracture modelling system software and built a fracture propagation model and a fracture distribution model of the Upper Cretaceous Formation in the Daqingzi region. A parallel study was performed to verify the fracture propagation pattern and boundary conditions in the proposed model based on a geomechanical analogue experiment. The results of these studies demonstrate that fracture modelling based on the SEFE method may improve the precise characterization of fractured reservoirs.

Published
2013
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22. Docosahexaenoic acid inhibits Ca 2+ influx and downregulates CaSR by upregulating microRNA-16 in pulmonary artery smooth muscle cells.

Author

Liu JJ, Tang MM, Zhu ML, Xie CX, Kang PF, Ling X, Zhang H, Wang XJ, and Tang B

Subjects
Binding Sites, Cells, Cultured, Docosahexaenoic Acids pharmacology, Humans, Ion Transport, Muscle, Smooth cytology, Muscle, Smooth metabolism, Pulmonary Artery cytology, Pulmonary Artery metabolism, Calcium metabolism, Down-Regulation drug effects, MicroRNAs metabolism, Muscle, Smooth drug effects, Pulmonary Artery drug effects, Receptors, Calcium-Sensing metabolism
Abstract

Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic-free Ca 2+ concentration ([Ca 2+ ]cyt) was measured using Fluo-3 AM method. Real-time polymerase chain reaction was used to detect microRNA-16 (miR-16) and calcium-sensing receptor (CaSR) messenger RNA expression levels. CCK-8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR-16 using dual-luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca 2+ ]cyt. After transfection of miR-16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR-16 inhibition. [Ca 2+ ]cyt was also inhibited by miR-16 transfection. DHA then promoted the expression of miR-16, and the effects of DHA on PASMCs were annulled when miR-16 was inhibited. CaSR was identified as a direct target of miR-16. CaSR was inhibited directly by miR-16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR-16/CaSR axis., (© 2020 Wiley Periodicals LLC.)

Published
2020
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