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Updated: Aug 17, 2026

Isolation, Characterization and MicroRNA-based Genetic Modification of Human Dental Follicle Stem Cells
Published on: November 16, 2018
TRPM7 is Involved in the Regulation of Proliferation, Migration and Osteogenic Differentiation of Human Dental
Dongchuan Zuo1,2, Jiali Li3,4, Yueyue Huang3,4
1The Key Laboratory of Medical Electrophysiology, Ministry of Education, Collaborative Innovation Center for Prevention and Treatment of Cardiovascular Disease, Institute of Cardiovascular Research, Southwest Medical University, 646000 Luzhou, Sichuan, China.
Background:
Dental follicle cells (DFCs) are promising candidates for tissue engineering. However, the molecular mechanisms that regulate the biological characteristics of DFCs are still unclear. Transient receptor potential melastatin 7 (TRPM7) is a Ca2+- and Mg2+-permeable cation channel. The aim of this study was to determine the impact of TRPM7 on the proliferation, migration and osteogenic differentiation of DFCs.
Methods:
PCR, Western blotting, Immunocytochemical staining and Patch clamp methods were used to identify the gene and protein expression of TRPM7 in DFCs. DFCs were infected with lentiviruses that expressed either TRPM7 specific shRNA or scrambled non-effective shRNA to investigate its functional role. Cell proliferation and migration were assessed using Cell Counting Kit-8 assays and transwell cell culture chambers separately. Cell osteogenic differentiation were determined by ALP assay kit and Alizarin Red staining.
Results:
Gene and protein expression of TRPM7 were detected in DFCs, but not of TRPM6, which is a closely related channel with similar function. In the absence of Mg2+, typical whole cell TRPM7-like currents were recorded by patch clamp. These were inhibited by low concentrations of 2-APB, but activated by high concentrations of 2-APB. Functional studies demonstrated that suppression of TRPM7 expression inhibited the proliferation and migration of DFCs, and promoted their osteogenic differentiation. Furthermore, Mg2+ deficiency mimicked the effects of TRPM7 knockdown in terms of osteogenic differentiation of DFCs.
Conclusions:
These results demonstrate that TRPM7 is involved in regulating the proliferation, migration and osteogenic differentiation of DFCs.
Insights
Transient receptor potential melastatin 7 (TRPM7) regulates dental follicle cell functions. Suppressing TRPM7 inhibits proliferation and migration but enhances osteogenic differentiation, crucial for tissue engineering.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Ion Channel Physiology
Background:
- Dental follicle cells (DFCs) show potential for tissue engineering applications.
- The molecular regulators of DFC biological characteristics remain largely unelucidated.
- Transient receptor potential melastatin 7 (TRPM7) is a cation channel permeable to Ca2+ and Mg2+.
Purpose of the Study:
- To investigate the role of TRPM7 in DFC proliferation, migration, and osteogenic differentiation.
- To determine the impact of TRPM7 expression levels on DFC behavior.
Main Methods:
- TRPM7 gene and protein expression analyzed using PCR, Western blotting, and immunocytochemistry.
- TRPM7 function studied via lentiviral-mediated shRNA knockdown and patch-clamp electrophysiology.
- Cell proliferation, migration, and osteogenic differentiation assessed via CCK-8, Transwell assays, ALP activity, and Alizarin Red staining.
Main Results:
- TRPM7 expression was detected in DFCs, unlike TRPM6.
- TRPM7-like currents were recorded and modulated by 2-APB.
- TRPM7 knockdown inhibited DFC proliferation and migration while promoting osteogenic differentiation.
- Mg2+ deficiency mimicked TRPM7 knockdown effects on osteogenic differentiation.
Conclusions:
- TRPM7 plays a significant role in regulating DFC proliferation, migration, and osteogenic differentiation.
- TRPM7 is a potential therapeutic target for enhancing DFC-based tissue engineering strategies.
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