EA Bowe's research while affiliated with University of Cambridge and other places

Publications (10)

Article
It has been shown by others that levels of matrix degrading enzymes are increased in osteoarthritis (OA) and so are proposed to be involved in the aetiopathogenesis of the disease, including exercise-associated OA. Therefore we hypothesised that cathepsin B and cathepsin D were increased in cartilage samples previously shown to have early stage OA...
Article
To identify the effect of fibroblastic growth factor-2 (FGF-2) on the intrinsic damage-repair response in articular cartilage in vitro. Articular equine cartilage explants, without subchondral bone, had a single impact load of 500 g applied from a height of 2.5 cm. Explants were then cultured in 0, 12, 25, 50 or 100 ng/ml FGF-2 for up to 28 days. U...
Article
The nature of the protein-mineral interface in bone was investigated by using solid-state nuclear magnetic resonance (NMR) spectroscopy. The non-dephased and dephased 13C-{31P} Rotational Echo DOuble Resonance (REDOR) spectra for the bone sample were shown for dephasing times of 4.8, 7.2, and 9.6 ms. The 13C-{31P} REDOR behavior of o-phospho-L-seri...

Citations

... Previous studies from our laboratory have focused specifically on the expression and role of cathepsins B and D in the horse 20 in the equine degenerative joint diseases osteochondrosis 21,22 and OA 23 and the in vitro effects of biomechanical trauma 24 . As a continuation of these studies the present project set out to address the question of the possible role of these enzymes in the onset of OA in horses following high intensity exercise. ...
... Cathepsin K and RANKL mRNA levels and RANKL to OPG ratios were reduced by NBQX. AMPA increases bone formation and mineralisation, 45 whereas AMPAR antagonists reduce bone mass, 55 inhibiting osteoblast activity and mineralisation. 45 Consistent with this, NBQX reduced cell number and prevented mineralisation in HOBs from OA patients. ...
... [16][17][18] However, no effective therapeutic intervention is yet available to prevent the progression of OA, reflecting our limited understanding of the exact pathways leading from impact to eventual cartilage degeneration. 19 We have recently qualitatively described the damage caused by a single-impact load applied using a simple drop tower device, [20][21][22] which was observed to be similar to that reported in clinical cases of OA. 2,9,15,23 The aim of this study was to quantify and compare histological osteoarthritislike changes in samples obtained from horses diagnosed with OA and in cartilage disks subjected to a single-impact load followed by recovery in culture. ...
... Discs were randomly divided into two groups – control (unimpacted) or impacted. Discs were impacted using a drop tower device following the method described previously [3,11,12]. Each disc, with the articular surface facing down was impacted from a height of 2.5 cm using a weight of 500 g. ...
... The combined electrostatic interactions between cationic and anionic sites, according to Walsh and Guzelsu [67], would be significant, and direct bond formation between the two kinds of materials may happen. Other bonding strategies were designed as well [68]. ...
... Chondrocytes, the sole cell type in cartilage, are responsible for maintaining the integrity of the cartilage matrix and secreting matrix-associated proteins [10]. Although the concept is still being debated, the movement of chondrocytes in vivo can be inferred from various findings based on in vitro cell cultures, ex vivo organ cultures and 3D human cartilage, and indications of mobile chondrocytes include the formation and extension of chondrocyte cell processes in the vicinity of cartilage damage and the outgrowth of chondrocytes at the wound margin [10][11][12][13]. Since chondrocytes in vivo are surrounded by a proteoglycan-rich pericellular matrix and an extensive collagen network, the migration of chondrocytes is a challenging process involving the deformation of the cell body and coordination of the binding and unbinding of the cell-extracellular matrix (ECM) adhesion. ...
... Similarly, the upregulation of aspartate protease cathepsin-D (predominantly intracellular) in the exosomes of hypoxic ADMSCs suggests its ECM remodeling function. Both the association of cathepsin-D expression with MMPs and its potential role in the inactivation of TIMP2 have already been established under physiological and pathological conditions [79,80]. Interestingly, we observed a concomitant increase of MMP2 along with cathepsin-D, signifying the potential role of ADMSCs in ECM regeneration. ...