Cementogenesis is inhibited under a mechanical static compressive force via Piezo1

Author:

Zhang Ying-ying1,Huang Yi-ping2,Zhao Hua-xiang2,Zhang Ting3,Chen Feng4,Liu Yan5

Affiliation:

1. MS Student, Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China.

2. PhD Student, Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China.

3. Research Assistant, Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China.

4. Research Associate, Central Laboratory, Peking University School and Hospital of Stomatology, Beijing, China.

5. Associate Professor, Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China.

Abstract

ABSTRACT Objective: To investigate whether Piezo1, a mechanotransduction gene mediates the cementogenic activity of cementoblasts under a static mechanical compressive force. Materials and Methods: Murine cementoblasts (OCCM-30) were exposed to a 2.0 g/cm2 static compressive force for 3, 6, 12, and 24 hours. Then the expression profile of Piezo1 and the cementogenic activity markers osteoprotegerin (Opg), osteopontin (Opn), osteocalcin (Oc), and protein tyrosine phosphataselike member A (Ptpla) were analyzed. Opg, Opn, Oc, and Ptpla expression was further measured after using siRNA to knock down Piezo1. Real-time PCR, Western blot, and cell proliferation assays were performed according to standard procedures. Results: After mechanical stimulation, cell morphology and proliferation did not change significantly. The expression of Piezo1, Opg, Opn, Oc, and Ptpla was significantly decreased, with a high positive correlation between Opg and Piezo1 expression. After Piezo1 knockdown, the expression of Opg, Opn, Oc, and Ptpla was further decreased under mechanical stimulation. Conclusions: Cementogenic activity was inhibited in OCCM-30 cells under static mechanical force, a process that was partially mediated by the decrease of Piezo1. This study provides a new viewpoint of the pathogenesis mechanism of orthodontically induced root resorption and repair.

Publisher

The Angle Orthodontist (EH Angle Education & Research Foundation)

Subject

Orthodontics

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