Home ENGLISH MAGAZINE Bones, cartilages and fat: a common protein rules them all

Bones, cartilages and fat: a common protein rules them all

Osteoporosis is a disease in which the bones become weak and brittle, increasing the risk of fracture. Bone is a living tissue that constantly regenerates and the body maintains a balance between the creation of new bone cells and the removal of old cells. As we age, the rate at which the new bone replaces the old or damaged bone slows and the bone density gradually decreases. But if this frequency slows too much, it can lead to osteoporosis. Osteoporosis is a major public health problem and is more common in women than in men. Estimates suggest that around 1 in 3 women and 1 in 5 men over age 50 suffer from bone fractures due to osteoporosis. In women over the age of 45, the disease represents more days spent in hospital than diabetes, heart attack and breast cancer. In the United States, osteopenia and osteoporosis are believed to affect over half (55%) of people aged 50 and over. The progenitor cells are immature cells that are in reserve until they receive genetic instructions from the transcription factors, that indicate to them what type of cell it must become. In the case of bone tissue, progenitor cells are mesenchymal stem cells of the bone marrow.

Depending on the instructions they receive, mesenchymal stem cells can mature into: bone-producing cells called osteoblasts; cells producing cartilage or chondrocytes; and adipocytes or fat cells. Until now it was not clear what controlled the direction of maturity of the progenitor cells, so as to maintain the delicate balance or homeostasis of bone formation. In the journal PNAS, scientists at the University of Alabama in Birmingham and Zhejiang University in China explain how a nuclear protein called CBF-beta is important for controlling the speed at which new bone cells replace old ones. When they studied the transcription factors that control the direction of maturity, the team found that a protein called the beta-binding subunit of the core binding factor (CBF-beta) was vital for the change of targets between bone-producing cells and fat cells. To undertake the study, the team engineered three groups of mice by eliminating CBF-beta at three different stages in the maturation of progenitor cells. The team found that all three groups of mice developed severe osteoporosis, having accumulated fat cells in their bone marrow.

The pattern was similar to that observed in age-related bone loss. They also found an increase in the expression of fat cell genes in bone marrow mesenchymal stem cells, and in bone cells in the skulls of mice lacking CBF-beta. When CBF-beta activates a signal within a cell type known as Wnt10b / beta-catenin, it blocks the expression of the gene that directs progenitor cells to mature into fat cells. The team also found that CBF-beta drives progenitor cells to become bone-producing cells through another type of signal sent to neighboring cells: the Wnt paracrine pathway. The researchers hope that their mapping will improve the understanding of the role that CBF-beta plays in maintaining bone, especially with age. The investigations of this study will fill an important gap in knowledge and could facilitate the development of new therapies for bone loss, which are devoid of negative side effects from current osteoporosis therapy.

  • edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Pubblicazioni scientifiche

Wu M et al. PNAS U S A. 2017 Sep 19;114(38):10119-124.

Thiel VN et al. Leukemia. 2017 Nov; 31(11):2491-2502. 

Park NR et al. J Cell Physiol. 2016 Jan; 231(1):162-71.

Lim KE et al. J Bone Miner Res. 2015 Apr;30(4):715-22.

Chen W et al. PNAS U S A. 2014 Jun 10;111(23):8482-87.

Dott. Gianfrancesco Cormaci
- Laurea in Medicina e Chirurgia nel 1998 (MD Degree in 1998) - Specialista in Biochimica Clinica nel 2002 (Clinical Biochemistry specialty in 2002) - Dottorato in Neurobiologia nel 2006 (Neurobiology PhD in 2006) - Ha soggiornato negli Stati Uniti, Baltimora (MD) come ricercatore alle dipendenze del National Institute on Drug Abuse (NIDA/NIH) e poi alla Johns Hopkins University, dal 2004 al 2008. - Dal 2009 si occupa di Medicina personalizzata. - Guardia medica presso strutture private dal 2010 - Detentore di un brevetto sulla preparazione di prodotti gluten-free a partire da regolare farina di frumento immunologicamente neutralizzata (owner of a patent concerning the production of bakery gluten-free products, starting from regular wheat flour). - Responsabile del reparto Ricerca e Sviluppo per la società CoFood s.r.l. (leader of the R&D for the partnership CoFood s.r.l.) - Autore di un libro riguardante la salute e l'alimentazione, con approfondimenti su come questa condizioni tutti i sistemi corporei. - Autore di articoli su informazione medica, salute e benessere sui siti web salutesicilia.com e medicomunicare.it