980 nm Photobiomodulation Promotes Osteo/Odontogenic Differentiation of the Stem Cells from Human Exfoliated Deciduous Teeth Via the Cross talk Between BMP/Smad and Wnt/β‐Catenin Signaling Pathways

Abstract

Increasing evidence suggests stem cells from human exfoliated deciduous teeth (SHEDs) serve as desirable sources of dentin regeneration. Photobiomodulation (PBM) has shown great potential in enhancing the proliferation and osteogenesis of human bone marrow mesenchymal stem cells (hBMMSCs). However, the specific role of PBM in odontogenic differentiation of SHEDs is little know, and we further investigated potential mechanism of PBM osteo/odontogenisis. A 980 nm diode laser with different energy densities of (0.5, 5, 10 J cm−2) in a 100‐mW continuous wave was used for irradiation every 24 h. Osteo/odontogenic differentiation of SHEDs was achieved by performing alkaline phosphatase (ALP) and alizarin red staining (ARS) and osteo/odontogenic markers were also evaluated by qRT‐PCR and western blotting. Additionally, western blot and immunohistochemical staining were performed to evaluate the levels of BMP/Smad and Wnt/β‐catenin signaling‐related proteins. We found that PBM at 5 J cm−1 increased mineral deposition and upregulated the expression of related osteo/odontogenic markers along with the elevated expression of β‐catenin and phosphorylation level of Smad1/5/9. Furthermore, Wnt signaling inhibition using DKK1 and BMP signaling inhibition using noggin inhibited PBM‐induced osteo/odontogenic marker expression when used individually or jointly. In conclusion, PBM induces the osteo/odontogenic differentiation of SHEDs through cross talk between BMP/Smad and Wnt/β‐catenin signaling pathways.

Overexpression of long noncoding RNA 4933425B07Rik leads to renal hypoplasia by inactivating Wnt/β-catenin signaling pathway

“…According to reports, the antagonist gremlin 1 reduces BMP4 activity in the mesenchyme, allowing outgrowth of UBs and creation of autoregulatory GDNF/WNT11 feedback signaling, which is necessary for the start of metanephric kidney development ( Michos et al, 2007 ). Moreover, it has been reported that there may be crosstalk between BMP/SMAD and Wnt/β-catenin signaling pathways during the differentiation of the stem cells ( Wang et al, 2022 ). Therefore, we propose the idea that renal hypoplasia may not only be caused by the inactivation of Wnt/β-catenin signaling pathway in Rik PB/PB ; Hoxb7 mice, but also by AhR and TGF-β/BMP/SMAD signaling pathway.…”