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2 results on '"Tu, Man-Li"'

1. MiR-497∼195 cluster regulates angiogenesis during coupling with osteogenesis by maintaining endothelial Notch and HIF-1α activity.

Author

Yang M, Li CJ, Sun X, Guo Q, Xiao Y, Su T, Tu ML, Peng H, Lu Q, Liu Q, He HB, Jiang TJ, Lei MX, Wan M, Cao X, and Luo XH

Subjects
Animals, Antagomirs genetics, Antagomirs metabolism, Aptamers, Nucleotide genetics, Aptamers, Nucleotide metabolism, Bone Density, Bone and Bones blood supply, Bone and Bones metabolism, Bone and Bones pathology, F-Box-WD Repeat-Containing Protein 7 genetics, F-Box-WD Repeat-Containing Protein 7 metabolism, Gene Expression Regulation, Developmental, Humans, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Mice, Mice, Knockout, MicroRNAs agonists, MicroRNAs antagonists & inhibitors, MicroRNAs metabolism, Molecular Targeted Therapy, Neovascularization, Physiologic genetics, Osteogenesis genetics, Osteoporosis genetics, Osteoporosis metabolism, Osteoporosis pathology, Platelet Endothelial Cell Adhesion Molecule-1 agonists, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Prolyl Hydroxylases genetics, Prolyl Hydroxylases metabolism, Receptor, Notch1 metabolism, Sialoglycoproteins agonists, Sialoglycoproteins metabolism, Signal Transduction, Hypoxia-Inducible Factor 1, alpha Subunit genetics, MicroRNAs genetics, Osteoporosis therapy, Platelet Endothelial Cell Adhesion Molecule-1 genetics, Receptor, Notch1 genetics, Sialoglycoproteins genetics
Abstract

A specific bone vessel subtype, strongly positive for CD31 and endomucin (CD31 hi Emcn hi ), is identified as coupling angiogenesis and osteogenesis. The abundance of type CD31 hi Emcn hi vessels decrease during ageing. Here we show that expression of the miR-497∼195 cluster is high in CD31 hi Emcn hi endothelium but gradually decreases during ageing. Mice with depletion of miR-497∼195 in endothelial cells show fewer CD31 hi Emcn hi vessels and lower bone mass. Conversely, transgenic overexpression of miR-497∼195 in murine endothelium alleviates age-related reduction of type CD31 hi Emcn hi vessels and bone loss. miR-497∼195 cluster maintains the endothelial Notch activity and HIF-1α stability via targeting F-box and WD-40 domain protein (Fbxw7) and Prolyl 4-hydroxylase possessing a transmembrane domain (P4HTM) respectively. Notably, endothelialium-specific activation of miR-195 by intravenous injection of aptamer-agomiR-195 stimulates CD31 hi Emcn hi vessel and bone formation in aged mice. Together, our study indicates that miR-497∼195 regulates angiogenesis coupled with osteogenesis and may represent a potential therapeutic target for age-related osteoporosis.

Published
2017
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2. GDF11 Inhibits Bone Formation by Activating Smad2/3 in Bone Marrow Mesenchymal Stem Cells.

Author

Lu Q, Tu ML, Li CJ, Zhang L, Jiang TJ, Liu T, and Luo XH

Subjects
Animals, Bone Morphogenetic Proteins pharmacology, Cell Differentiation physiology, Female, Growth Differentiation Factors pharmacology, Mice, Mice, Inbred C57BL, Osteogenesis drug effects, Smad2 Protein metabolism, Smad3 Protein metabolism, Bone Marrow Cells metabolism, Bone Morphogenetic Proteins metabolism, Bone Resorption metabolism, Growth Differentiation Factors metabolism, Mesenchymal Stem Cells metabolism, Osteogenesis physiology
Abstract

Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor-β superfamily. Recent studies confirmed that GDF11 plays an important role in regulating the regeneration of brain, skeletal muscle, and heart during aging; however, its role in bone metabolism remains unclear. Thus, the aim of this study was to determine the effects of GDF11 on bone metabolism, including bone formation and bone resorption, both in vitro and in vivo. Our results showed that GDF11 inhibited osteoblastic differentiation of bone marrow mesenchymal stem cells in vitro. Mechanistically, GDF11 repressed Runx2 expression by inducing SMAD2/3 phosphorylation during osteoblast differentiation. Moreover, intraperitoneal injection of GDF11 inhibited bone formation and accelerated age-related bone loss in mice. Our results also showed that GDF11 had no effect on osteoclast differentiation or bone resorption both in vitro and in vivo. These results provide a further rationale for the therapeutic targeting of GDF11 for the treatment of age-related osteoporosis.

Published
2016
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