Deletion of Fibroblast growth factor 9 globally and in skeletal muscle results in enlarged tuberosities at sites of deltoid tendon attachments
| Autor: | Connor C Leek, David M. Ornitz, Jaysheel Bhavsar, Megan C Smith, Jaclyn M. Soulas, Shawn W. Polson, Ryan C. Locke, Elahe Ganji, Megan L. Killian, Iman Bhattacharya |
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| Rok vydání: | 2021 |
| Předmět: |
Fibroblast Growth Factor 9
Male 0301 basic medicine Mice Transgenic Chondrocyte hypertrophy Biology Fibroblast growth factor Article Muscle hypertrophy Tendons Mice 03 medical and health sciences 0302 clinical medicine FGF9 Osteogenesis Pregnancy medicine Animals Muscle Skeletal Endochondral ossification Bone Development Cell growth Deltoid tuberosity Skeletal muscle Hypertrophy Embryo Mammalian Cell biology Mice Inbred C57BL stomatognathic diseases 030104 developmental biology medicine.anatomical_structure Animals Newborn Organ Specificity Female Bone Diseases Chondrogenesis Gene Deletion 030217 neurology & neurosurgery Developmental Biology |
| Zdroj: | Dev Dyn |
| ISSN: | 1097-0177 1058-8388 |
| DOI: | 10.1002/dvdy.383 |
| Popis: | Background The growth of most bony tuberosities, like the deltoid tuberosity (DT), rely on the transmission of muscle forces at the tendon-bone attachment during skeletal growth. Tuberosities distribute muscle forces and provide mechanical leverage at attachment sites for joint stability and mobility. The genetic factors that regulate tuberosity growth remain largely unknown. In mouse embryos with global deletion of fibroblast growth factor 9 (Fgf9), the DT size is notably enlarged. In this study, we explored the tissue-specific regulation of DT size using both global and targeted deletion of Fgf9. Results We showed that cell hypertrophy and mineralization dynamics of the DT, as well as transcriptional signatures from skeletal muscle but not bone, were influenced by the global loss of Fgf9. Loss of Fgf9 during embryonic growth led to increased chondrocyte hypertrophy and reduced cell proliferation at the DT attachment site. This endured hypertrophy and limited proliferation may explain the abnormal mineralization patterns and locally dysregulated expression of markers of endochondral development in Fgf9null attachments. We then showed that targeted deletion of Fgf9 in skeletal muscle leads to postnatal enlargement of the DT. Conclusion Taken together, we discovered that Fgf9 may play an influential role in muscle-bone crosstalk during embryonic and postnatal development. This article is protected by copyright. All rights reserved. |
| Databáze: | OpenAIRE |
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