Version 1
: Received: 17 May 2024 / Approved: 21 May 2024 / Online: 23 May 2024 (11:38:09 CEST)
How to cite:
Stanwick, M.; Fenesha, F.; Hamid, A.; Kang, K.; Kanniard, D.; Kim, I.; Mandarano, N.; Schumacher, F. L.; Peters, S. B. Impaired Tertiary Dentin Secretion After Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling. Preprints2024, 2024051398. https://doi.org/10.20944/preprints202405.1398.v1
Stanwick, M.; Fenesha, F.; Hamid, A.; Kang, K.; Kanniard, D.; Kim, I.; Mandarano, N.; Schumacher, F. L.; Peters, S. B. Impaired Tertiary Dentin Secretion After Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling. Preprints 2024, 2024051398. https://doi.org/10.20944/preprints202405.1398.v1
Stanwick, M.; Fenesha, F.; Hamid, A.; Kang, K.; Kanniard, D.; Kim, I.; Mandarano, N.; Schumacher, F. L.; Peters, S. B. Impaired Tertiary Dentin Secretion After Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling. Preprints2024, 2024051398. https://doi.org/10.20944/preprints202405.1398.v1
APA Style
Stanwick, M., Fenesha, F., Hamid, A., Kang, K., Kanniard, D., Kim, I., Mandarano, N., Schumacher, F. L., & Peters, S. B. (2024). Impaired Tertiary Dentin Secretion After Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling. Preprints. https://doi.org/10.20944/preprints202405.1398.v1
Chicago/Turabian Style
Stanwick, M., Fernanda L Schumacher and Sarah B. Peters. 2024 "Impaired Tertiary Dentin Secretion After Shallow Injury in Tgfbr2-Deficient Dental Pulp Cells Is Rescued by Extended CGRP Signaling" Preprints. https://doi.org/10.20944/preprints202405.1398.v1
Abstract
Introduction: Transforming growth factor beta receptor 2 (Tgfbr2) signaling regulates odontoblast differentiation, dentin mineralization, and the paracrine signaling that guides sensory innervation in developing mouse molars. We hypothesized that Tgfbr2 also regulates the neuro-pulpal responses to injury to activate axon sprouting and tertiary dentin secretion. Methods: We per-formed a timed deletion of Tgfbr2 using tetracycline-responsive Osterix-Cre;Tgfbr2f/f (Tgfbr2^cko) mice, which allowed them to develop normally. At 3 months, we drilled a shallow hole on the mesial side of the first mandibular molar (M1) in both control and Tgfbr2^cko mice. Hemi-mandibles were collected 4, 8, 21, and 56 days post-injury (dpi). In situ hybridization (ISH) for Sp7 was performed to confirm Osterix-Cre transcription. Microcomputed tomography (micro-CT) imaging and histology were used to examine the tertiary dentin, and immunofluorescence was used to visualize CGRP+ axons following the injury. Results: Tgfbr2 deletion was inferred by Sp7 ISH. Micro-CT and histology indicated a lower dentin volume in 21 dpi Tgfbr2^cko M1s compared to WT M1s, but the volume was comparable by 56 dpi. The duration of axon sprouting was longer in injured Tgfbr2^cko M1s compared to WT M1s. Conclusions: These results suggest that sensory afferents may support dentin repair in Tgfbr2-deficient odontoblasts.
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
