A Crucial Role for Mmp-2 in Osteocytic Canalicular Formation and Bone Metabolism
نویسندگان
چکیده
From the Laboratory for Behavioral Genetics 1 , RIKEN BSI, Wako, Saitama 351-0198, Japan; the Department of Molecular Pharmacology 2 , Medical Research Institute, and Center of Excellence Program for Molecular Destruction and Reconstruction of Tooth and Bone, Tokyo Medical & Dental University, Chiyoda, Tokyo 101-0062, Japan; the Department of Molecular Immunology 3 , Graduate School of Agricultural and Life Sciences, University of Tokyo, Bunkyo, Tokyo 113-8657, Japan; the Division of Biochemistry and Molecular Biology 4 , Department of Functional Biology, Kanagawa Dental College, Yokosuka, Kanagawa 238-8580, Japan; the Discovery Research Laboratories 5 , Shionogi & Co., Ltd., Toyonaka, Osaka 561-0825, Japan; and the Center for Immunology and Inflammatory Diseases 6 , Department of Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129 Running Title: MMP-2 in Bone Homeostasis Address correspondence to: Shigeyoshi Itohara, Laboratory for Behavioral Genetics, RIKEN BSI, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan, Tel. +81-48-467-9724; Fax. +81-48-467-9725; E-Mail: [email protected], and Masaki Noda, Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical & Dental University, 2-3-10 Kanda-Surugadai, Chiyoda, Tokyo 101-0062, Japan, Tel. +81-3-5280-8067; Fax. +81-3-5280-8067; E-Mail: [email protected]
منابع مشابه
Mitochondrial superoxide in osteocytes perturbs canalicular networks in the setting of age-related osteoporosis
Osteocytes are major bone cells that play a crucial role in maintaining the quality of and healing damage to bone tissue. The number of living osteocytes and canalicular networks declines in an age-dependent manner. However, the pathological effects of mitochondrial redox imbalances on osteocytes and bone metabolism have not been fully elucidated. We generated mice lacking mitochondrial superox...
متن کاملOsteocytic osteolysis: time for a second look?
Over 100 years ago it was suggested that osteocytes could remodel their surrounding environment by removing and replacing bone. In the 1960s and 1970s, many observations were made to suggest that osteocytes could resorb bone and increase the size of their lacunae. This concept became known as osteocytic osteolysis and studies suggested that it occurred in response to diverse stimuli such as par...
متن کاملTrabecular bone remodelling simulation considering osteocytic response to fluid-induced shear stress.
In bone functional adaptation by remodelling, osteocytes in the lacuno-canalicular system are believed to play important roles in the mechanosensory system. Under dynamic loading, bone matrix deformation generates an interstitial fluid flow in the lacuno-canalicular system; this flow induces shear stress on the osteocytic process membrane that is known to stimulate the osteocytes. In this sense...
متن کاملMicrogravity Induces Pelvic Bone Loss through Osteoclastic Activity, Osteocytic Osteolysis, and Osteoblastic Cell Cycle Inhibition by CDKN1a/p21
Bone is a dynamically remodeled tissue that requires gravity-mediated mechanical stimulation for maintenance of mineral content and structure. Homeostasis in bone occurs through a balance in the activities and signaling of osteoclasts, osteoblasts, and osteocytes, as well as proliferation and differentiation of their stem cell progenitors. Microgravity and unloading are known to cause osteoclas...
متن کاملPerlecan/Hspg2 Deficiency Alters the Pericellular Space of the Lacunocanalicular System Surrounding Osteocytic Processes in Cortical Bone
Osteocytes project long, slender processes throughout the mineralized matrix of bone, where they connect and communicate with effector cells. The interconnected cellular projections form the functional lacunocanalicular system, allowing fluid to pass for cell-to-cell communication and nutrient and waste exchange. Prevention of mineralization in the pericellular space of the lacunocanalicular pe...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2006