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Your search keyword '"Chen, Alex F."' showing total 29 results
Start Over Author "Chen, Alex F." Publisher wiley
29 results on '"Chen, Alex F."'

2. The beneficial effects of alpha‐tocopherol on intestinal function and the expression of tight junction proteins in differentiated segments of the intestine in piglets

Author

Huang, Yanjun, primary, He, Caimei, additional, Hu, Zheng, additional, Chu, Xuetong, additional, Zhou, Sichun, additional, Hu, Xin, additional, Deng, Jun, additional, Xiao, Di, additional, Tao, Ting, additional, Yang, Huansheng, additional, Chen, Alex F., additional, Yin, Yulong, additional, and Yang, Xiaoping, additional

Published
2022
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28. l-Homocysteine-induced cathepsin V mediates the vascular endothelial inflammation in hyperhomocysteinaemia.

Author

Leng YP, Ma YS, Li XG, Chen RF, Zeng PY, Li XH, Qiu CF, Li YP, Zhang Z, and Chen AF

Subjects
Animals, Aorta, Thoracic cytology, Cell Adhesion drug effects, Cells, Cultured, Endothelium, Vascular drug effects, Endothelium, Vascular metabolism, Homocysteine blood, Human Umbilical Vein Endothelial Cells drug effects, Human Umbilical Vein Endothelial Cells physiology, Humans, Male, Mice, Inbred C57BL, Mitogen-Activated Protein Kinases metabolism, THP-1 Cells, Cathepsins metabolism, Homocysteine pharmacology, Hyperhomocysteinemia metabolism, Vascular Diseases metabolism
Abstract

Background and Purpose: Vascular inflammation, including the expression of inflammatory cytokines in endothelial cells, plays a critical role in hyperhomocysteinaemia-associated vascular diseases. Cathepsin V, specifically expressed in humans, is involved in vascular diseases through its elastolytic and collagenolytic activities. The aim of this study was to determine the effects of cathepsin V on l-homocysteine-induced vascular inflammation., Experimental Approach: A high methionine diet-induced hyperhomocysteinaemic mouse model was used to assess cathepsin V expression and vascular inflammation. Cultures of HUVECs were challenged with l-homocysteine and the cathepsin L/V inhibitor SID to assess the pro-inflammatory effects of cathepsin V. Transfection and antisense techniques were utilized to investigate the effects of cathepsin V on the dual-specificity protein phosphatases (DUSPs) and MAPK pathways., Key Results: Cathepsin L (human cathepsin V homologous) was increased in the thoracic aorta endothelial cells of hyperhomocysteinaemic mice; l-homocysteine promoted cathepsin V expression in HUVECs. SID suppressed the activity of cathepsin V and reversed the up-regulation of inflammatory cytokines (IL-6, IL-8 and TNF-α), adhesion and chemotaxis of leukocytes and vascular inflammation induced by l-homocysteine in vivo and in vitro. Increased cathepsin V promoted the degradation of DUSP6 and DUSP7, phosphorylation and subsequent nuclear translocation of ERK1/2, phosphorylation of STAT1 and expression of IL-6, IL-8 and TNF-α., Conclusions and Implications: This study has identified a novel mechanism, which shows that l-homocysteine-induced upregulation of cathepsin V mediates vascular endothelial inflammation under high homocysteine condition partly via ERK 1/2 /STAT1 pathway. This mechanism could represent a potential therapeutic target in hyperaemia-associated vascular diseases., Linked Articles: This article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc., (© 2017 The British Pharmacological Society.)

Published
2018
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29. HIV protease inhibitors in pulmonary hypertension: rationale and design of a pilot trial in idiopathic pulmonary arterial hypertension.

Author

Li Y, Li XH, Yu ZX, Cai JJ, Billiar TR, Chen AF, Lv B, Chen ZY, Huang ZJ, Yang GP, Song J, Liu B, and Yuan H

Abstract

We propose an exploratory clinical study, the first of its kind to our knowledge, to determine the safety and potential clinical benefit of the combination of the HIV protease inhibitors (HIV-PIs) saquinavir and ritonavir (SQV+RIT) in patients with idiopathic pulmonary arterial hypertension (IPAH). This study is based on evidence that (1) HIV-PIs can improve pulmonary hemodynamics in experimental models; (2) both Toll-like receptor 4 and high-mobility group box 1 (HMGB1) participate in the pathogenesis of experimental pulmonary hypertension; and (3) a high-throughput screen for inhibitors of HMGB1-induced macrophage activation yielded HIV-PIs as potent inhibitors of HMGB1-induced cytokine production. In this proposed open-label, pre-post study, micro, low, and standard doses of SQV+RIT will be given to IPAH patients for 14 days. Patients will receive follow-up for the next 14 days. The primary outcome to be evaluated is change in HMGB1 level from baseline at 14 days. The secondary outcome is changes in tumor necrosis factor α, interleukin 1β, interleukin 6, C-reactive protein, pulmonary arterial pressure based on echocardiography parameters and New York Heart Association/World Health Organization functional class, and Brog dyspnea scale index from baseline at 14 days. Other secondary measurements will include N-terminal pro-brain natriuretic peptide, atrial natriuretic peptide, and 6-minute walk distance. We propose that SQV+RIT treatment will improve inflammatory disorders and pulmonary hemodynamics in IPAH patients. If the data support a potentially useful therapeutic effect and suggest that SQV+RIT is safe in IPAH patients, the study will warrant further investigation. (ClinicalTrials.gov identifier: NCT02023450.).

Published
2015
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