Department of Stomatology, Chinese PLA General Hospital, 28th Fuxing Road, Beijing, 100853, People's Republic of China.
BMC Oral Health. 2018 Nov 21;18(1):190. doi: 10.1186/s12903-018-0624-1.
Dental and periodontal tissue development is a complicated process involving a finely regulated network of communication among various cell types. Understanding the mechanisms involved in regulating dental mesenchymal stem cells (MSCs) and osteoclast cell differentiation is critical. However, it is still unclear whether histone deacetylase HDAC6 is involved in dental MSCs fate determination and osteoclast differentiation.
We used shRNA and siRNA knockdown to explore the role of HDAC6 in dental MSCs odontogenic differentiation and osteoclasts maturation.
Based on HDAC6 knockdown dental MSCs, our data suggest that HDAC6 knockdown significantly increases alkaline phosphate activity and mineralized nodules formation. Additionally, mRNA expression of odontogenic marker genes (OSX, OCN, and OPN) was induced by HDAC6 knockdown. By using HDAC6 siRNA, we knocked down HDAC6 in osteoclast precursor RAW 264.7 cells. Our data suggests that HDAC6 knockdown significantly inhibited osteoclasts differentiation. Additionally, mRNA expression of osteoclast marker genes Trap, Mmp9, and Ctsk was decreased by HDAC6 knockdown.
Our study demonstrated that HDAC6 plays an important role in regulating dental MSCs and osteoclasts differentiation.
牙齿和牙周组织的发育是一个复杂的过程，涉及到各种细胞类型之间精细调节的通讯网络。了解调节牙齿间充质干细胞（MSCs）和破骨细胞分化的机制至关重要。然而，目前尚不清楚组蛋白去乙酰化酶 HDAC6 是否参与牙齿 MSCs 命运的决定和破骨细胞的分化。
我们使用 shRNA 和 siRNA 敲低来探索 HDAC6 在牙齿 MSCs 成牙分化和破骨细胞成熟中的作用。
基于 HDAC6 敲低的牙齿 MSCs，我们的数据表明，HDAC6 敲低显著增加碱性磷酸酶活性和矿化结节形成。此外，HDAC6 敲低诱导了成牙标志基因（OSX、OCN 和 OPN）的 mRNA 表达。通过使用 HDAC6 siRNA，我们在破骨细胞前体细胞 RAW 264.7 中敲低了 HDAC6。我们的数据表明，HDAC6 敲低显著抑制了破骨细胞的分化。此外，破骨细胞标志基因 Trap、Mmp9 和 Ctsk 的 mRNA 表达也被 HDAC6 敲低所抑制。
我们的研究表明，HDAC6 在调节牙齿 MSCs 和破骨细胞分化中发挥着重要作用。
