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Home  > Press Release  > “Identification of new molecular function that suppresses osteoporosis”

“Identification of new molecular function that suppresses osteoporosis”

Masaki Noda
Professor, Department of Molecular Pharmacology, Medical Research Institute (right)
Yoichi Ezura
Associate Professor, Department of Molecular Pharmacology, Medical Research Institute (center)
Chiho Watanabe
Assistant Professor, Department of Maxillofacial Orthognathics, Graduate School of Medical and Dental Sciences (left)

– Aging-induced osteopenia and Cnot3 –

Points

1.Identification of a new aspect of pathophysiology in osteoporosis that affects over 12 million patients in Japan.
2.We discovered a gene that plays a major role in aging-induced bone loss.
3.Our findings will contribute to understand the mechanism of osteoporosis development and to contemplate novel therapeutic measures.

 Professor Masaki Noda and Associate Professor Yoichi Ezura, Department of Molecular Pharmacology, Medical Research Institute, Tokyo Medical and Dental University in collaboration with Professor Keiji Moriyama, Department of Maxillofacial Orthognathics and Professor Tadashi Yamamoto, Okinawa Institute of Science and Technology have discovered the function of new gene, Cnot3.

Summary of the report

Aging causes loss of bone and resulting in osteoporosis that is a highly prevalent bone disease and affects about 12 million people in Japan. Osteoprosis is life-threatening in elderly patients. However, underlying pathophysiology including the posttranscriptional control of bone resorption is incompletely understood. CNOT3 is a member of the group of molecules that are involved in mRNA stability in yeast to mammalian cells, but its role in bone regulation is not known. Here, we report that Cnot3 deficiency specifically enhances receptor activator of NF-kappaB (RANK) mRNA stability and leads to osteopenia in healthy young adult animals. Importantly, Cnot3 levels are reduced in ageing-induced osteoporosis, and Cnot3 deficiency further exacerbates such osteoporosis. We examined and found as a mechanism that Cnot3 binds to RANK mRNA and its 3’-UTR. This fragment can render Cnot3-dependent instability to the reporter gene such as luciferase. Our results indicate that Cnot3 regulates aging-induced osteoporosis as an endogenous suppressor of RANK.

Contact

Masaki Noda, MD, PhD
Professor
Dept Molecular Pharmacology, Medical Research Institute
Tokyo Medical and Dental University
MD Tower 24th Floor, Room 2401
5-45 Yushima 1-Chome, Bunkyo-Ku, Tokyo, Japan 113-5810
Tel/Fax 81-3-5803-4061
E-mail: noda.mph(at)mri.tmd.ac.jp

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