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Biology Seminar: Tetraspanins in Bone Homeostasis: Defective Osteoclasts in CD82 Null Mice

  • Friday, February 20, 2015
  • 1:30 PM–2:20 PM
  • Science Building 010

Cindy Miranti, Ph.D. Associate Professor Laboratory of Integrin Signaling and Tumorigenesis Van Andel Research Institute

Bone is a dynamic tissue, striking a balance between degradation and re-synthesis. Osteoblasts are derived from mesenchymal stem cells and terminally differentiate to build calcified bone, whereas osteoclasts, derived from hematopoietic stem cells degrade bone. Soluble signals released from osteoblasts stimulate the differentiation of osteoclasts, and vice versa in a continuous cycle. Disruption of the cycle results in thinner or thicker bones which are more susceptible to fracture or improper healing. This seminar will describe experiments designed to study the signaling mechanisms that control bone degradation by osteoclasts.  Differential gene expression analysis identified several genes involved in this process, including tetraspanin CD82. It was hypothesized that mice deficient in CD82 expression would have bone abnormalities resembling those seen in mice with known defects in osteoclasts. The signaling pathways controlled by CD82 were studied using wild type mice and knock-out mice that do not express CD82.  Expression of enzymes known to be active in differentiated osteoclasts was reduced in knock-out mice, and there was a corresponding increase in bone mineral density in these mice.  It appears that CD82 loss blocks the function of intracellular signaling pathways, leading to reduced osteoclast-mediated bone degradation.

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