As everyone has been able to experience, cartilage injuries to the joints such as knees, shoulders and hips can prove to be extremely painful and debilitating. Conditions that cause cartilage degeneration, such as arthritis, affect 350 million people in the world and cost the US public health system more than 300 billion dollars every year. Patients suffering from these conditions experience an increase in pain and discomfort over time. However, an exciting study conducted by the Faculty of the Forsyth Institute suggests new strategies to produce cartilage cells with enormous implications in regenerative medicine for future cartilage injuries and degenerative treatments. Recent progress in stem cells research also offer new generation therapies for large craniophalical defects caused by various conditions, including trauma, tumors, congenital disorders and progressive deforming diseases. A correct determination of cell destiny can further facilitate the effectiveness of cellular therapies based on stem cells.
Previously, it was thought that the transduction route of the WNT signal was the decisive factor if a cell became bone or cartilage. The main factor that transdes the WNT signals is β-catenin. The basis of this belief was the result that when the β-catenin was interrupted, the bone became cartilage. However, β-catenin also acts as a cellular adhesion molecule to facilitate cell-cell interaction, the original function identified first. Scientists know that this cellular protein is important for the determination of cell destiny, but the complete mechanisms of its molecular interactions remain open to the study. The team tested what would happen when β-catenin was only partially compromised for reporting, discovering that, in that case, the cells were unable to form bones or cartilage. After these tests, scientists concluded that WNT reporting is a decisive factor for bone formation, but that it is not enough for the generation of cartilage.
So they wanted to know what the factor was for the determination of cell destiny; So, the question was what a cell is reprogrammed to become cartilage if it is not reporting WNT? This question led to a second important discovery: the intervention of the GATA-3 protein, an alternative action of the β-catenine responsible for the change of the fate of the skeletal cells. GATA-3 is a nuclear transcription factor and a single gene regulator, which activates the specific gene expression of cartilage in the cells. Basically, GATA-3 is linked to the sequences of the genome necessary for reprogramming. Being able to control cell destiny in this way makes it possible to direct a cell to become bone, cartilage or fat, which has enormous implications for the creation of new treatments for 1 in 4 people who live with cartilage injuries and cartilage degeneration. Currently there is no treatment capable of regenerating the cartilage; and the current treatments are unable to improve joint function.
Not only that, there are thousands of cases every year of children who are born with deformity of the skull or face, palatoschisi and other bone anomalies of the head and neck. Understanding how to adjust the WNT – Beta catenin – GATA3 signaling and manipulate it by pharmacological basis could revolutionize the therapy of these conditions, in addition to the regular and only outfit of care, i.e surgical. This study provides proof that reporting β-catenine regardless of its transcriptional function specifies the fate of skeletal cells. The loss of the transcription dependent on β-catenin does not alter the commitment of the skeletal lineage, arguing against the previous knowledge in which canonical WNT signaling is required for the determination of skeletal fate. This research opens up new paths to explore for scientists and is an enthusiasm for research on the regeneration of fabrics with the promise of significant relief for thousands of patients, who must resort to surgery to solve aesthetic problems, but above all of comfort and quality of life.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
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Pubblicazioni scientifiche
Maruyama T et al. Sci Advances 2022; 8(48):eadd6172.
Doumpas N, Lampart F et al. EMBO J. 2019; 38:e98873.
Meyers C, Lisiecki J et al. JBMR Plus 2019; 3:e10172.
Zaidan N, Ottersbach K. Open Biology 2018; 8:180152.
Dott. Gianfrancesco Cormaci
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