Sexually dimorphic estrogen sensing in skeletal stem cells controls skeletal regeneration

Tom W. Andrew, Lauren S. Koepke, Yuting Wang, Michael Lopez, Holly Steininger, Danielle Struck, Tatiana Boyko, Thomas H. Ambrosi, Xinming Tong, Yuxi Sun, Gunsagar S. Gulati, Matthew P. Murphy, Owen Marecic, Ruth Tevlin, Katharina Schallmoser, Dirk Strunk, Jun Seita, Stuart B. Goodman, Fan Yang, Michael T. Longaker, George P. Yang () and Charles K. F. Chan ()
Additional contact information
Tom W. Andrew: Stanford University School of Medicine
Lauren S. Koepke: Stanford University School of Medicine
Yuting Wang: Stanford University School of Medicine
Michael Lopez: Stanford University School of Medicine
Holly Steininger: Stanford University School of Medicine
Danielle Struck: Stanford University School of Medicine
Tatiana Boyko: Stanford University School of Medicine
Thomas H. Ambrosi: Stanford University School of Medicine
Xinming Tong: Stanford University
Yuxi Sun: University of Alabama at Birmingham
Gunsagar S. Gulati: Stanford University School of Medicine
Matthew P. Murphy: Stanford University School of Medicine
Owen Marecic: Stanford University School of Medicine
Ruth Tevlin: Stanford Hospital and Clinics
Katharina Schallmoser: Paracelsus Medical University of Salzburg
Dirk Strunk: Paracelsus Medical University of Salzburg
Jun Seita: RIKEN
Stuart B. Goodman: Stanford University
Fan Yang: Stanford University
Michael T. Longaker: Stanford University School of Medicine
George P. Yang: University of Alabama at Birmingham
Charles K. F. Chan: Stanford University School of Medicine

Nature Communications, 2022, vol. 13, issue 1, 1-13

Abstract: Abstract Sexually dimorphic tissues are formed by cells that are regulated by sex hormones. While a number of systemic hormones and transcription factors are known to regulate proliferation and differentiation of osteoblasts and osteoclasts, the mechanisms that determine sexually dimorphic differences in bone regeneration are unclear. To explore how sex hormones regulate bone regeneration, we compared bone fracture repair between adult male and female mice. We found that skeletal stem cell (SSC) mediated regeneration in female mice is dependent on estrogen signaling but SSCs from male mice do not exhibit similar estrogen responsiveness. Mechanistically, we found that estrogen acts directly on the SSC lineage in mice and humans by up-regulating multiple skeletogenic pathways and is necessary for the stem cell’s ability to self- renew and differentiate. Our results also suggest a clinically applicable strategy to accelerate bone healing using localized estrogen hormone therapy.

Date: 2022
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DOI: 10.1038/s41467-022-34063-5

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