ArticleApplied microbiology and biotechnology2019
PLGA-based control release of Noggin blocks the premature fusion of cranial sutures caused by retinoic acid.
Article in Applied microbiology and biotechnology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Temporally regulated FGFR2-retinoic acid signaling mediates dura mater-suture mesenchyme interactions to prevent craniosynostosis in mice.International journal of oral science · 2026Article
- Clinical and genetic features of syndromic craniosynostosis in 18 Chinese probands: novel candidate genes and phenotypes of known pathogenic genes.Frontiers in genetics · 2026Article
- Lhx6 deficiency causes human embryonic palatal mesenchymal cell mitophagy dysfunction in cleft palate.Molecular medicine (Cambridge, Mass.) · 2024Article
- Targeting of C-ROS-1 Activity Using a Controlled Release Carrier to Treat Craniosynostosis in a Preclinical Model of Saethre-Chotzen Syndrome.Journal of tissue engineering and regenerative medicine · 2024Article
- Direct BMP signaling to chordoblasts is required for the initiation of segmented notochord sheath mineralization in zebrafish vertebral column development.Frontiers in endocrinology · 2023Article
- Altered BMP-Smad4 signaling causes complete cleft palate by disturbing osteogenesis in palatal mesenchyme.Journal of molecular histology · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Craniosynostosis (CS), the premature and pathological fusion of cranial sutures, is a relatively common developmental disorder. Elucidation of the pathways involved and thus therapeutically targeting it would be promising for the prevention of CS. In the present study, we examined the role of BMP pathway in the all-trans retinoic acid (atRA)-induced CS model and tried to target the pathway in vivo via PLGA-based control release. As expected, the posterior frontal suture was found to fuse prematurely in the atRA subcutaneous injection mouse model. Further mechanism study revealed that atRA could repress the proliferation while promote the osteogenic differentiation of suture-derived mesenchymal cells (SMCs). Moreover, BMP signal pathway was found to be activated by atRA, as seen from increased expression of BMPR-2 and pSMAD1/5/9. Recombinant mouse Noggin blocked the atRA-induced enhancement of osteogenesis of SMCs in vitro. In vivo, PLGA microsphere encapsulated with Noggin significantly prevented the atRA-induced suture fusion. Collectively, these data support the hypothesis that BMP signaling is involved in retinoic acid-induced premature fusion of cranial sutures, while PLGA microsphere-based control release of Noggin emerges as a promising strategy for prevention of atRA-induced suture fusion.
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