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When compared to MTA cells, MTB-01 cells were susceptible to risedronateinduced apoptosis, had decreased ability to bind to risedronate-treated bone, and did not produce MMP-2 or MMP-9 proteases. MTA cells were less susceptible to risedronateinduced apoptosis and produced MMP-2. Additionally, adhesion of MTA cells to bone matrix was not diminished by risedronate treatment. Our results suggest that the nonresponsive nature of the MTA cell line may be due to MMP-2 production (possibly allowing ongoing destruction of risedronate-treated bone), continued adhesion to risedronate-treated bone…mehr

Produktbeschreibung
When compared to MTA cells, MTB-01 cells were susceptible to risedronateinduced apoptosis, had decreased ability to bind to risedronate-treated bone, and did not produce MMP-2 or MMP-9 proteases. MTA cells were less susceptible to risedronateinduced apoptosis and produced MMP-2. Additionally, adhesion of MTA cells to bone matrix was not diminished by risedronate treatment. Our results suggest that the nonresponsive nature of the MTA cell line may be due to MMP-2 production (possibly allowing ongoing destruction of risedronate-treated bone), continued adhesion to risedronate-treated bone matrix, and decreased susceptibility to risedronate-induced apoptosis.
Autorenporträt
Dr. Boyd received her undergraduate and DVM degrees from Mississippi State University. She completed a residency and PhD program at the University of Georgia. Her expertise is in comparative pathology with a special interest in pathology of genetically engineered mice and translational research.