Mechanical stress-activated immune response genes via Sirtuin 1 expression in human periodontal ligament cells

Lee, S.-I.; Park, K.-H.; Kim, S.-J.; Kang, Yoon‐Goo; Lee, Y.-M.; Kim, E.-C.

doi:10.1111/j.1365-2249.2011.04549.x

Cited by 58 publications

(45 citation statements)

References 48 publications

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“…Mechanical stress (MS) can activate the expression of immune/defense genes encoding defensins, chemokines, cytokines, and toll‐like receptors in PDLSC via the SIRT1 pathway (Lee et al, ). Since the cytokines IL‐1, IL‐6, IL‐11, IL‐17, and TNF‐α promote the expression of RANKL in the bone marrow stromal cells and osteoblasts, they are collectively referred to as osteoclastogenesis factors (Hofbauer et al, ; Kobayashi et al, ).…”

Section: Discussionmentioning

confidence: 99%

Nicotinamide‐induced silencing of SIRT1 by miR‐22‐3p increases periodontal ligament stem cell proliferation and differentiation

Zheng

Guo

2019

Cell Biology International

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Dental stem cell proliferation and osteoblast differentiation are key cellular processes involved in periodontitis diseases. Researchers have found that SIRT1 (sirtuin 1, silent mating type information regulation 2 homolog 1) and microRNAs play a pivotal role in the process, but a clear underlying mechanism has not been determined. In this study, the has‐miR‐22‐3p that target SIRT1 was predicted by TargetScan. Luciferase reporter assay was used to confirm that SIRT1 is the direct target of miR‐22‐3p. Importantly, miR‐22‐3p was revealed to control SIRT1 in periodontal ligament stem cell (PDLSC) and to regulate the proliferation and differentiation of PDLSC by SIRT1 silencing. Furthermore, we detected the induction of miR‐22‐3p expression by nicotinamide treatment on PDLSC. Induction of PDLSC proliferation and differentiation by nicotinamide treatment was blocked by miR‐22‐3p knockdown. These results suggested that the effect of nicotinamide on PDLSC is through miR‐22‐3p. In addition, miR‐22‐3p also upregulated the expression levels of the inflammatory cytokines tumor necrosis factor‐α, interleukin‐1β (IL‐1β), and IL‐8 in PDLSC through SIRT1 pathway and downregulated the expression of TLR‐2 and TLR‐4. miR‐22‐3p is a new target either for the treatment of periodontitis or the improvement of inflammation caused by orthodontics.

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Section: Discussionmentioning

confidence: 99%

Nicotinamide‐induced silencing of SIRT1 by miR‐22‐3p increases periodontal ligament stem cell proliferation and differentiation

Zheng

Guo

2019

Cell Biology International

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“…Many reports have described the intracellular accumulation of ROS and calcium in response to mechanical forces in many types of cells [37–39] and the close relationship between ROS and calcium with the intrinsic apoptosis [40, 41]. Researchers demonstrated that the level of ROS significantly increased in PDL fibroblasts exposed to mechanical compression [38, 41]. What’s more, it has been reported that excess endoplasmic reticulum stress, induced by unfolded and malfolded proteins, mediated another apoptotic pathway [42,43].…”

Section: Discussionmentioning

confidence: 99%

Caspase-8 and Caspase-9 Functioned Differently at Different Stages of the Cyclic Stretch-Induced Apoptosis in Human Periodontal Ligament Cells

Zhao

Zhuang

et al. 2016

PLoS ONE

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BackgroundHuman periodontal ligament (PDL) cells underwent apoptosis after mechanical stretch loading. However, the exact signalling pathway remains unknown. This study aimed to elucidate how the apoptotic caspases functioned in the cyclic stretch-induced apoptosis in human PDL cells.Materials and MethodsIn the present study, 20% cyclic stretch was selected to load the cells for 6 or 24 h. The following parameters were analyzed: apoptotic rates, the protein levels of caspase-3, -7, -8 and -9 and the activities of caspase-8 and -9. Subsequently, the influences of caspase-8 and caspase-9 inhibitors on the apoptotic rate and the protein level of the activated caspase-3 were assessed as well.ResultsThe apoptotic rates increased in response to cyclic stretch, but the cells entered different apoptotic stages after 6 and 24 h stretches. Caspase-3, -7, -8 and -9 were all activated after stretch loading. The stretch-induced apoptosis and the protein level of the activated caspase-3 were inhibited after inhibiting both caspase-8 and caspase-9 in both 6 and 24 h stretched cells and after inhibiting caspase-9 in 24 h stretched cells.ConclusionCaspase-8 and -9 functioned differently at different apoptotic stages in human PDL cells after cyclic stretch.

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“…Stem cells from exfoliated deciduous teeth also express PECAM-1 and vascular endothelial cadherin, suggesting that stem cells from exfoliated deciduous teeth progressively acquire an endothelial phenotype when exposed to VEGF (4). SIRT1, a nicotinamide adenosine dinucleotide-dependent deacetylase and a class III histone deacetylase, plays a critical role in aging, cell cycle regulation, apoptosis, and inflammation (9)(10)(11). However, the effects of SIRT1 overexpression or activation on differentiation remain unclear.…”

mentioning

confidence: 98%

The Role of SIRT1 on Angiogenic and Odontogenic Potential in Human Dental Pulp Cells

Kim¹,

Kim²,

Kim³

et al. 2012

Journal of Endodontics

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Mechanical stress-activated immune response genes via Sirtuin 1 expression in human periodontal ligament cells

Cited by 58 publications

References 48 publications

Nicotinamide‐induced silencing of SIRT1 by miR‐22‐3p increases periodontal ligament stem cell proliferation and differentiation

Nicotinamide‐induced silencing of SIRT1 by miR‐22‐3p increases periodontal ligament stem cell proliferation and differentiation

Caspase-8 and Caspase-9 Functioned Differently at Different Stages of the Cyclic Stretch-Induced Apoptosis in Human Periodontal Ligament Cells

The Role of SIRT1 on Angiogenic and Odontogenic Potential in Human Dental Pulp Cells

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