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LncRNA CARMN facilitates odontogenic differentiation of dental pulp cells by impairing EZH2.
Oral Diseases 2023 May 25
OBJECTIVE: This study aimed to reveal the potential role of CARMN in odontogenic differentiation of dental pulp cells (DPCs).
METHODS: Laser capture microdissection was used to detect Carmn in DPCs and odontoblasts in P0 mice. After manipulating CARMN expression in odontogenic differentiation induced hDPCs, the state of odontogenic differentiation was evaluated by ALP staining, ARS, and related marker expression in qRT-PCR and western blotting. The subcutaneous transplantation of HA/β-TCP loaded with hDPCs was performed to verify CARMN's role in promoting odontogenic differentiation in vivo. RNAplex and RIP were employed to reveal potential mechanism of CARMN in hDPCs.
RESULTS: CARMN expressed more abundantly in odontoblasts than DPCs in P0 mice. CARMN expression boosted during in vitro odontogenic differentiation of hDPCs. CARMN overexpression enhanced odontogenic differentiation of hDPCs in vitro, while inhibition impaired the process. CARMN overexpression in HA/β-TCP composites promoted more mineralized nodule formation in vivo. CARMN knockdown led to soared EZH2, while CARMN overexpression brought about EZH2 inhibition. CARMN functioned via direct interaction with EZH2.
CONCLUSIONS: The results uncovered CARMN as a modulator during the odontogenic differentiation of DPCs. CARMN promoted odontogenic differentiation of DPCs by impairing EZH2.
METHODS: Laser capture microdissection was used to detect Carmn in DPCs and odontoblasts in P0 mice. After manipulating CARMN expression in odontogenic differentiation induced hDPCs, the state of odontogenic differentiation was evaluated by ALP staining, ARS, and related marker expression in qRT-PCR and western blotting. The subcutaneous transplantation of HA/β-TCP loaded with hDPCs was performed to verify CARMN's role in promoting odontogenic differentiation in vivo. RNAplex and RIP were employed to reveal potential mechanism of CARMN in hDPCs.
RESULTS: CARMN expressed more abundantly in odontoblasts than DPCs in P0 mice. CARMN expression boosted during in vitro odontogenic differentiation of hDPCs. CARMN overexpression enhanced odontogenic differentiation of hDPCs in vitro, while inhibition impaired the process. CARMN overexpression in HA/β-TCP composites promoted more mineralized nodule formation in vivo. CARMN knockdown led to soared EZH2, while CARMN overexpression brought about EZH2 inhibition. CARMN functioned via direct interaction with EZH2.
CONCLUSIONS: The results uncovered CARMN as a modulator during the odontogenic differentiation of DPCs. CARMN promoted odontogenic differentiation of DPCs by impairing EZH2.
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