M
Matthew T. Gillespie
Researcher at Monash University, Clayton campus
Publications - 174
Citations - 17150
Matthew T. Gillespie is an academic researcher from Monash University, Clayton campus. The author has contributed to research in topics: Osteoclast & RANKL. The author has an hindex of 62, co-authored 172 publications receiving 16443 citations. Previous affiliations of Matthew T. Gillespie include Prince Henry's Institute of Medical Research & University of Melbourne.
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Journal ArticleDOI
Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families.
TL;DR: Osteoblasts/stromal cells can now be replaced with RANKL and M-CSF in dealing with the whole life of osteoclasts, and new ways to treat several metabolic bone diseases caused by abnormal osteoclast recruitment and functions will be established.
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IL-17 in synovial fluids from patients with rheumatoid arthritis is a potent stimulator of osteoclastogenesis
Shigeru Kotake,Nobuyuki Udagawa,Naoyuki Takahashi,Kenichiro Matsuzaki,Kanami Itoh,Shigeru Ishiyama,Seiji Saito,Kazuhiko Inoue,Naoyuki Kamatani,Matthew T. Gillespie,T. John Martin,Tatsuo Suda +11 more
TL;DR: It is suggested that IL-17 first acts on osteoblasts, which stimulates both COX-2-dependent PGE2 synthesis and ODF gene expression, which in turn induce differentiation of osteoclast progenitors into mature osteoclasts, and that IL -17 is a crucial cytokine for osteoclastic bone resorption in RA patients.
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Breast cancer cells interact with osteoblasts to support osteoclast formation.
Rachel J. Thomas,Theresa A. Guise,J J Yin,J Elliott,Nicole J. Horwood,Thomas J. Martin,Matthew T. Gillespie +6 more
TL;DR: Using a murine model of breast cancer metastasis to bone, it is established that MCF-7 cells that overexpress PTHrP caused significantly more bone metastases, which were associated with increased osteoclast formation, elevated plasma P THrP concentrations and hypercalcaemia compared with parental or empty vector controls.
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Osteotropic Agents Regulate the Expression of Osteoclast Differentiation Factor and Osteoprotegerin in Osteoblastic Stromal Cells
TL;DR: It is established that osteoblastic cell lines incapable of supporting osteoclast formation have markedly reduced ODF expression and also illustrates the importance of the relative abundance of ODF compared with the levels of OPG for the induction of osteOClastogenesis.
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A combination of osteoclast differentiation factor and macrophage-colony stimulating factor is sufficient for both human and mouse osteoclast formation in vitro.
TL;DR: This study demonstrates that mouse spleen cells and monocytes form osteoclasts when cultured in the presence of macrophage-colony stimulating factor (M-CSF) and a soluble form of murine ODF (sODF), and shows that the same co-stimulation causes human osteoclast differentiation to occur.