Cyclic stretching force‐induced early apoptosis in human periodontal ligament cells

Zhong, Weijie; Xu, Chun; Zhang, Fan; Xue, Jiang; Zhang, X; Ye, D

doi:10.1111/j.1601-0825.2007.01375.x

Cited by 34 publications

(36 citation statements)

References 43 publications

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“…The fraction of apoptotic hPDL cells was significantly upregulated, in comparison to the control, following exposure to 6 or 24 h. Figure. 4b showed that the rate of apoptosis reached a peak when the cells were compressed for 24 h. These results are supported by those previously reported in other models namely the stretching force model in hPDL cells 32) and the compression force model in osteoblast 33) . Furthermore, after staining with Hoechst 33258, the PDL cells which were subjected to a compression force exhibited the typical morphological features of apoptosis (Fig.…”

Section: Discussionsupporting

confidence: 81%

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Funakoshi

Yamaguchi

Asano

et al. 2013

J. Hard Tissue Biology.

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The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygen species (ROS)-induced apoptosis in PDL cells. Following the application of orthodontic force to maxillary first molars, the molars were investigated using immunohistochemical analysis. The cell cycle and apoptosis were assessed in compression force-treated PDL cells using flow cytometry. Furthermore, we assayed the effect on ROS generation by DCFDA fluorescence. In vivo study revealed an increased number of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. Taken together, these results provide new information on compression force-induced G1 arrest and apoptosis in hPDL cells.

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Section: Discussionsupporting

confidence: 81%

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Funakoshi

Yamaguchi

Asano

et al. 2013

J. Hard Tissue Biology.

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“…Caspase-3 is considered to be a central mediator of apoptosis and is one of the major activated cysteine proteases in the caspase family that is pivotal in apoptosis[41]. It was reported that cyclic stretch-induced apoptosis was controlled by caspase-3[42]. Considering its importance in apoptosis, we observed cleaved caspase-3 protein levels in the current study, indicating an association with increased apoptosis in osteoblasts responding to large-magnitude mechanical stress.…”

Section: Discussionsupporting

confidence: 64%

Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K/Akt and JNK MAPK Signaling Pathways

et al. 2016

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It is widely accepted that physiological mechanical stimulation suppresses apoptosis and induces synthesis of extracellular matrix by osteoblasts; however, the effect of stress overloading on osteoblasts has not been fully illustrated. In the present study, we investigated the effect of cyclic compressive stress on rat osteoblasts apoptosis, using a novel liquid drop method to generate mechanical stress on osteoblast monolayers. After treatment with different levels of mechanical stress, apoptosis of osteoblasts and activations of mitogen-activated protein kinases (MAPKs) and PI3-kinase (PI3K)/Akt signaling pathways were investigated. Osteoblasts apoptosis was observed after treated with specific inhibitors prior to mechanical stimulation. Protein levels of Bax/Bcl-2/caspase-3 signaling were determined using western blot with or without inhibitors of PI3K/Akt and phosphorylation of c-jun N-terminal kinase (JNK) MAPK. Results showed that mechanical stimulation led to osteoblasts apoptosis in a dose-dependent manner and a remarkable activation of MAPKs and PI3K/Akt signaling pathways. Activation of PI3K/Akt protected against apoptosis, whereas JNK MAPK increased apoptosis via regulation of Bax/Bcl-2/caspase-3 activation. In summary, the PI3K/Akt and JNK MAPK signaling pathways played opposing roles in osteoblasts apoptosis, resulting in inhibition of apoptosis upon small-magnitude stress and increased apoptosis upon large-magnitude stress.

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“…Cells reached confluence following 3 d of culture and then were subjected to cyclic stretch using a Flexcell Tension Plus system (FX-5000T, Flexcell International) with a 20% elongation magnitude for 6 or 24 h. Cells cultured on the same kind of plates but without stretch loading were used as time-matched control cells. The loading frequency of 6 cycles/min (5 s stretch and 5 s relaxation) was the same to that in our previous studies [17, 18]. Three independent loading experiments were carried out in every group.…”

Section: Methodsmentioning

confidence: 99%

Activation of NLRP1 and NLRP3 inflammasomes contributed to cyclic stretch-induced pyroptosis and release of IL-1β in human periodontal ligament cells

Zhao

Zhuang

et al. 2016

Oncotarget

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Inflammasomes have been reported to be present in periodontal inflammatory tissue, but the exact role of inflammasomes in periodontal inflammatory reactions especially those related to mechanical stimulations has not been clarified. In this study, it was shown that cyclic stretch activated the nucleotide-binding oligomerization domain-like receptor containing pyrin domain 1 and 3 (NLRP1 and NLRP3) inflammasomes and induced the release of IL-1β and pyroptosis via a caspase-1-related mechanism in human periodontal ligament cells (HPDLCs). This study firstly demonstrated that activation of NLRP inflammasomes contributed to the stretch-induced inflammatory response in HPDLCs. As inflammasomes have been reported to be involved in both programmed cell death and inflammation, further studies are required to elucidate the exact roles and signaling pathway of inflammasomes in stretch-induced periodontal inflammation.

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Cyclic stretching force‐induced early apoptosis in human periodontal ligament cells

Abstract: The overall results suggested that stretching force not only influenced morphology but also induced early apoptosis in human PDL cells.

Cited by 34 publications

References 43 publications

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Effect of Compression Force on Apoptosis in Human Periodontal Ligament Cells

Cyclic Compressive Stress Regulates Apoptosis in Rat Osteoblasts: Involvement of PI3K/Akt and JNK MAPK Signaling Pathways

Activation of NLRP1 and NLRP3 inflammasomes contributed to cyclic stretch-induced pyroptosis and release of IL-1β in human periodontal ligament cells

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