Publications by authors named "Manli Tu"

Article Synopsis
  • Excessive mechanical loading of cartilage is linked to the development of osteoarthritis (OA), but the specific molecular pathways involved are not fully understood.
  • In experiments, chondrocytes were subjected to mechanical strain to mimic OA conditions, and mice models were used to study the effect of the Rcn2 gene on OA progression.
  • The study identified reticulocalbin-2 (Rcn2) as a key factor that increases in response to mechanical strain, leading to changes in chondrocytes that worsen OA, while knocking down Rcn2 or inhibiting Piezo1 could help alleviate the condition.
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Osteoarthritis (OA) causes the destruction of joints. Its pathogenesis is still under investigation, and there is no effective disease-modifying therapy. Here, we report that elevated cyclooxygenase-2 (COX-2) expression in the osteocytes of subchondral bone causes both spontaneous OA and rheumatoid arthritis (RA).

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Acquired heterotopic ossification (HO) is a painful and debilitating disease characterized by extraskeletal bone formation after injury. The exact pathogenesis of HO remains unknown. Here we show that TGF-β initiates and promotes HO in mice.

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A specific bone vessel subtype, strongly positive for CD31 and endomucin (CD31Emcn), is identified as coupling angiogenesis and osteogenesis. The abundance of type CD31Emcn vessels decrease during ageing. Here we show that expression of the miR-497∼195 cluster is high in CD31Emcn endothelium but gradually decreases during ageing.

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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.

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MicroRNAs play important roles in regulating bone regeneration and remodeling. However, the pathophysiological roles of microRNAs in bone repair remain unclear. Here we identify a significant upregulation of miR-142-5p correlated with active osteoblastogenesis during the bone healing process.

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