![]() ![]() Wright, Yan Zhang, Qin Huang, Dadong Wang, Naifeng Jing, Xiaoyao Liang, Fusong Jiang. Jing Ke, Yiqing Shen, Yizhou Lu, Junwei Deng, Jason D. Quantitative analysis of abnormalities in gynecologic cytopathology with deep learning. Representative Region Based Active Learning For Histological Classification Of Colorectal Cancer. International Symposium on Biomedical Imaging (ISBI), 2021. Style Normalization In Histology With Federated Learning. International Conference on Image Processing (ICIP), 2021. SU-Sampling Based Active Learning For Large-Scale Histopathology Image. International Conference on Medical Image Computing and Computer-Assisted Intervention (MICCAI), 2021. Jing Ke, Yiqing Shen *, Xiaoyao Liang, Dinggang Shen. Ĭontrastive Learning Based Stain Normalization Across Multiple Tumor in Histopathology. Jinghan Huang, Yiqing Shen, Dinggang Shen, Jing Ke. Publications 2021ĬA 2.5-Net Nuclei Segmentation Framework with a Microscopy Cell Benchmark Collection. My research interests span the fields of medical image analysis, computer vision, and particularly, their interdisciplinary direction. Investigations are expressed mean ± SEM calculated from three experiments.I am a senior undergraduate student at Shanghai Jiao Tong University. It increased H3K27ac occupancy in CXCL12 promoters and CXCL12 expression ( g) in bone marrow mesenchymal cells. Forced PCAF expression repressed the miR-29a downregulation of H3K27ac levels and RANKL expression ( f). miR-29a overexpression reduced PCAF and H3K27ac abundances ( d) and decreased H3K27ac enrichment in CXCL12 promoters ( e). Forced miR-29a expression decreased luciferase activity of 3′-UTR of RANKL mRNA ( b) and downregulated RANKL mRNA expression and protein abundances, whereas miR-29 interference upregulated RANKL expression ( c) of mesenchymal stem cell cultures. ![]() Asterisks * and hashtags # indicate significant difference from sham controls and OVX, respectively. The data are expressed mean ± SEM calculated from six mice. MiR-29a compromised the ovariectomy upregulation of RANKL and CXCL12 expression in bone marrow mesenchymal cells ( a). We also highlight that increasing miR-29a function in osteoblasts is beneficial for bone anabolism to fend off estrogen deficiency-induced excessive osteoclastic resorption and osteoporosis. Arrays of analyses shed new light on the miR-29a regulation of crosstalk between osteogenic and osteoclastogenic cells. Taken together, miR-29a signaling in osteogenic cells protects bone tissue from osteoporosis through repressing osteoclast regulators RANKL and CXCL12 to reduce osteoclastogenic differentiation. It also suppressed the histone acetyltransferase PCAF-mediated acetylation of lysine 27 in histone 3 (H3K27ac) and decreased the H3K27ac enrichment in CXCL12 promoters. Mechanistically, miR-29a inhibited RANKL secretion in osteoblasts through binding to 3'-UTR of RANKL. Treatment with miR-29a precursor improved the ovariectomy-mediated skeletal deterioration and biomechanical property loss. miR-29a overexpression also attenuated the estrogen loss-mediated excessive osteoclast surface histopathology, osteoclast formation of bone marrow macrophages, receptor activator nuclear factor-κ ligand (RANKL) and C-X-C motif chemokine ligand 12 (CXCL12) expression. The estrogen deficiency-induced loss of bone mass, trabecular morphometry, mechanical properties, mineral accretion and osteogenesis of bone marrow mesenchymal cells were compromised in miR-29aTg/OCN mice. Mice overexpressing miR-29a in osteoblasts driven by osteocalcin promoter (miR-29aTg/OCN) displayed higher bone mineral density, trabecular volume and mineral acquisition than wild-type mice. In vivo, decreased miR-29a expression occurred in ovariectomy-mediated osteoporotic skeletons. In this study, we uncovered that silencing miR-29a expression decreased mineralized matrix production in osteogenic cells, whereas osteoclast differentiation and pit formation were upregulated in bone marrow macrophages as co-incubated with the osteogenic cells in transwell plates. MicroRNA is known to regulate tissue remodeling however, its role in the development of osteoporosis remains elusive. Osteoporosis deteriorates bone mass and biomechanical strength, becoming a life-threatening cause to the elderly.
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