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3 results on '"Shiliang Xiao"'

1. The key role of apoptosis in the pathogenesis and treatment of pulmonary hypertension.

Author

Gurbanov E and Shiliang X

Subjects
Apoptosis drug effects, Dichloroacetic Acid therapeutic use, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use, Hypertension, Pulmonary drug therapy, Inhibitor of Apoptosis Proteins, Intracellular Signaling Peptides and Proteins therapeutic use, Lovastatin analogs & derivatives, Lovastatin therapeutic use, MAP Kinase Kinase Kinase 5 therapeutic use, Microtubule-Associated Proteins therapeutic use, Muscle, Smooth, Vascular physiopathology, Neoplasm Proteins therapeutic use, PPAR gamma therapeutic use, Pancreatic Elastase antagonists & inhibitors, Protein Serine-Threonine Kinases therapeutic use, Pulmonary Circulation physiology, Receptor, Bradykinin B2 agonists, Simvastatin therapeutic use, Survivin, Thrombosis physiopathology, Vasoconstriction physiology, rho-Associated Kinases, Apoptosis physiology, Hypertension, Pulmonary physiopathology
Abstract

In recent years, the process of the programmed cell death has gained much interest because it has important pathophysiological consequences contributing to the deletion of unwanted cells in the vessel wall, loss of pulmonary smooth muscle cells and therefore in reversing the pulmonary pressure. For the reason that most patients with pulmonary hypertension present with limited reversibility with vasodilators, antiremodeling approach for treatment appears to be feasible. Induction or enhancement of vascular smooth muscle cells apoptosis may be targeted to develop novel therapeutic approaches for pulmonary vascular remodeling in patients with pulmonary hypertension. This review summarizes the current mechanisms, investigate the roles and provide novel insights into the potential therapeutic value of apoptosis in the pulmonary artery remodeling of pulmonary hypertension.

Published
2006
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2. Fibroblast-like Synoviocytes-derived Exosomal PCGEM1 Accelerates IL-1β-induced Apoptosis and Cartilage Matrix Degradation by miR-142-5p/RUNX2 in Chondrocytes

Author

Shiliang Xiao, Guangxuan Zeng, Fei Li, and Gang Deng

Subjects
0301 basic medicine, Male, Immunology, Interleukin-1beta, Apoptosis, Core Binding Factor Alpha 1 Subunit, Exosomes, 03 medical and health sciences, 0302 clinical medicine, Chondrocytes, Downregulation and upregulation, Gene expression, Osteoarthritis, medicine, Humans, Fibroblast, Transcription factor, Chemistry, General Medicine, Fibroblasts, Synoviocytes, Microvesicles, Cell biology, Extracellular Matrix, RUNX2, Blot, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Cartilage, 030220 oncology & carcinogenesis, RNA, Long Noncoding
Abstract

Background: Long non-coding RNA (lncRNA) prostate cancer gene expression marker 1 (PCGEM1) has been revealed to participate in the pathogenesis of osteoarthritis (OA). However, the molecular mechanism of PCGEM1 regulating OA progression has not been fully elucidated.Methods: Fibroblast-like synoviocytes (FLSs) were isolated from synovium tissues of OA patients (OA-FLSs) and trauma donors (Normal-FLSs). The size and morphology of the isolated exosomes were analyzed by transmission electron microscopy and nanoparticle tracking analysis. Protein levels were analyzed by western blotting. Expression levels of PCGEM1, microRNA-142-5p (miR-142-5p), runt-related transcription factor 2 (RUNX2) mRNA, and OA related genes were assessed by qRT-PCR. Cell proliferation, viability, and apoptosis were evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide or flow cytometry assays. The relationship between miR-142-5p and PCGEM1 or RUNX2 was verified by dual-luciferase reporter and/or RNA pull down assays.Results: PCGEM1 was overexpressed in OA cartilages and exosomes from OA-FLSs. Exosomal PCGEM1 from OA-FLSs facilitated IL-1β-induced apoptosis and cartilage matrix degradation in chondrocytes. MiR-142-5p was downregulated while RUNX2 was upregulated in OA cartilages. Exosomal PCGEM1 from OA-FLSs regulated RUNX2 expression by sponging miR-142-5p in IL-1β-induced chondrocytes. MiR-142-5p inhibitor offset exosomal PCGEM1 knockdown-mediated effects on the apoptosis and cartilage matrix degradation of IL-1β-induced chondrocytes. RUNX2 overexpression counteracted the suppressive effect of miR-142-5p mimic on apoptosis and cartilage matrix degradation of IL-1β-induced chondrocytes.Conclusion: Exosomal PCGEM1 from OA-FLSs facilitated IL-1β-induced apoptosis and cartilage matrix degradation in chondrocytes by sequestering miR-142-5p and upregulating RUNX2, which offered new insights into the pathogenesis of OA.

Published
2021
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3. Feasibility of bone marrow stromal cells autologous transplantation for dilated cardiomyopathy

Author

Hongwen Fei, Shiliang Xiao, Cheng Zhou, and Chenyuan Yang

Subjects
Cardiomyopathy, Dilated, Cardiac function curve, Pathology, medicine.medical_specialty, Indoles, Time Factors, Stromal cell, Biomedical Engineering, Cardiomyopathy, Apoptosis, Cell Separation, Transplantation, Autologous, Biochemistry, Ventricular Function, Left, Biomaterials, Random Allocation, chemistry.chemical_compound, In Situ Nick-End Labeling, Genetics, medicine, Animals, Autologous transplantation, DAPI, Cells, Cultured, Bone Marrow Transplantation, Fluorescent Dyes, Earth-Surface Processes, Antibiotics, Antineoplastic, business.industry, Myocardium, Dilated cardiomyopathy, medicine.disease, Transplantation, medicine.anatomical_structure, Proto-Oncogene Proteins c-bcl-2, chemistry, Doxorubicin, Echocardiography, Feasibility Studies, Rabbits, Bone marrow, Stromal Cells, business
Abstract

The feasibility of bone marrow stromal cells autologous transplantation for rabbit model of dilated cardiomyopathy induced by adriamycin was studied. Twenty rabbits received 2 mg/kg of adriamycin intravenously once a week for 8 weeks (total dose, 16 mg/kg) to induce the cardiomyopathy model with the monitoring of cardiac function by transthoracic echocardiography. Marrow stromal cells were isolated from cell-transplanted group rabbits and were culture-expanded on the 8th week. On the 10th week, cells were labeled with 4,6-diamidino-2-phenylindole (DAPI), and then injected into the myocardium of the same rabbits. The results showed that viable cells labeled with DAPI could be identified in myocardium at 2nd week after transplantation. Histological findings showed the injury of the myocardium around the injection site was relieved with less apoptosis and more expression of bcl-2. The echocardiography found the improvement of local tissue movement from (2.12+/-0.51) cm/s to (3.81+/-0.47) cm/s (P0.05) around the inject site, but no improvement of heart function as whole. It was concluded bone marrow stromal cells transplantation for dilated cardiomyopathy was feasibe. The management of cells in vitro, the quantity and the pattern of the cells transplantation and the action mechanism still need further research.

Published
2007

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