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Hair follicle-resident progenitor cells are a major cellular contributor to heterotopic subcutaneous ossifications in a mouse model of Albright hereditary osteodystrophy. | LitMetric

AI Article Synopsis

  • Heterotopic ossifications (HOs) occur when bone forms abnormally outside the skeletal system, leading to ongoing clinical issues but lacking effective prevention and treatment strategies due to insufficient understanding of their development.
  • Albright hereditary osteodystrophy (AHO), a condition caused by mutations in a specific gene, is linked to the formation of painful subcutaneous ossifications (SCOs) that affect patients.
  • Research using an AHO mouse model shows that these SCOs arise from the abnormal growth of hair follicle stem cells into bone-forming cells, revealing potential new pathways for developing therapies for AHO and similar conditions involving HOs.

Article Abstract

Heterotopic ossifications (HOs) are the pathologic process by which bone inappropriately forms outside of the skeletal system. Despite HOs being a persistent clinical problem in the general population, there are no definitive strategies for their prevention and treatment due to a limited understanding of the cellular and molecular mechanisms contributing to lesion development. One disease in which the development of heterotopic subcutaneous ossifications (SCOs) leads to morbidity is Albright hereditary osteodystrophy (AHO). AHO is caused by heterozygous inactivation of , the gene that encodes the α-stimulatory subunit (Gα) of G proteins. Previously, we had shown using our laboratory's AHO mouse model that SCOs develop around hair follicles (HFs). Here we show that SCO formation occurs due to inappropriate expansion and differentiation of HF-resident stem cells into osteoblasts. We also show in AHO patients and mice that ( expression is upregulated in regions of SCO formation and that elimination of in male AHO mice exacerbates SCO development. These studies provide key insights into the cellular and molecular mechanisms contributing to SCO development and have implications for potential therapeutic modalities not only for AHO patients but also for patients suffering from HOs with other etiologies.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11213030PMC
http://dx.doi.org/10.1101/2024.06.18.599506DOI Listing

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