Pericytes in the Periodontal Ligament

Komaki, Motohiro

doi:10.1007/978-3-030-11093-2_10

Cited by 14 publications

(10 citation statements)

References 83 publications

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“…Stem cells in periodontal tissues are considered a group of heterogeneous cells. To date, there is no single specific biomarker for isolation and identification of stem cells in periodontal ligament [16]. It is reported that STRO-1, SSEA-4, CD271, and CD146 are used as indicators for the enrichment of periodontal ligament cells [17] that possess the ability of self-renewal and multiple differentiation potential.…”

Section: Discussionmentioning

confidence: 99%

High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1

Zhu

Qiu

Luo

et al. 2020

Stem Cells International

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Objective. This research is aimed at investigating how high glucose affects the proliferation and apoptosis in periodontal ligament stem cells (PDLSCs) in the presence of TNF-α. Methods. PDLSCs obtained from periodontal healthy permanent teeth were treated under either high-glucose condition (30 mmol/L, G30 group) or normal glucose condition (5.6 mmol/L, G5.6 group) in the presence or absence of TNF-α (10 ng/ml) for 2 to 6 days. Cell proliferation and cell cycle were evaluated by CCK-8, EdU incorporation assay, and flow cytometry. Cell apoptosis was assessed by annexin V/PI staining. Protein expression was detected by western blotting. Cellular ROS expression was evaluated by CellROX labeling and flow cytometry. Specific antibodies targeting TNFR1 and TNFR2 were used to block TNF-α signaling. Vitamin C was also used to verify if the blockage of ROS can rescue PDLSCs in the presence of high glucose and TNF-α. Results. CCK-8 assay showed that high glucose exacerbated TNF-α-induced cell viability inhibition (57.0%, 85.2%, and 100% for the G30+TNF-α group, G5.6+TNF-α group, and control group, respectively) on day 6. High glucose increased protein expression of TNFR1 compared with the control group on day 2 (1.24-fold) and day 6 (1.26-fold). Blocking TNFR1 totally reversed the proliferative inhibition in G30+TNF-α group. The addition of vitamin C or TNFR1 antibody totally reversed the elevation of intracellular ROS expression caused by high glucose and TNF-α. Vitamin C partially restored cell proliferation in the presence of high glucose and TNF-α. Conclusion. High glucose exacerbates TNF-α-induced proliferative inhibition in human periodontal ligament stem cells through the upregulation and activation of TNF receptor 1. Inhibition of intracellular ROS expression by vitamin C partially rescues PDLSCs in terms of cell proliferation.

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Section: Discussionmentioning

confidence: 99%

High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1

Zhu

Qiu

Luo

et al. 2020

Stem Cells International

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“…Infections and the subsequent host immune responses have remodeled an aberrant microenvironment, which generally lead to the dysfunction of PDLSCs, which are the potential “seed cells” for periodontal regeneration applications and bone tissues engineering [ 16 , 17 ]. Interestingly, recent studies have reported that scathing PDLSCs may conduce to the perturbation of periodontal homeostasis [ 18 – 20 ].…”

Section: Discussionmentioning

confidence: 99%

EZH2 Regulates Lipopolysaccharide-Induced Periodontal Ligament Stem Cell Proliferation and Osteogenesis through TLR4/MyD88/NF-κB Pathway

Wang

Tian

Zhang

et al. 2021

Stem Cells International

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Background. Periodontitis induced by bacteria especially Gram-negative bacteria is the most prevalent chronic inflammatory disease worldwide. Emerging evidence supported that EZH2 plays a significant role in the inflammatory response of periodontal tissues. However, little information is available regarding the underlying mechanism of EZH2 in periodontitis. This study is aimed at determining the potential role and underlying mechanism of EZH2 in periodontitis. Methods. The protein levels of EZH2, H3K27ME, p-p65, p-IKB, TLR4, MyD88, Runx2, and OCN were examined by western blot assay. Proliferation was evaluated by CCK8 assay. The levels of TNFα, IL1β, and IL6 were detected by ELISA assay. Migration was detected by wound healing assay. The distribution of p65 was detected by immunofluorescence. The formation of mineralized nodules was analyzed using alizarin red staining. Results. LPS stimulation significantly promoted EZH2 and H3K27me3 expression in primary human periodontal ligament stem cells (PDLSCs). Targeting EZH2 prevented LPS-induced upregulation of the inflammatory cytokines and inhibition of cell proliferation and migration. Furthermore, EZH2 knockdown attenuated the TLR4/MyD88/NF-κB signaling to facilitate PDLSC osteogenesis. Conclusions. Modulation of the NF-κB pathway through the inhibition of EZH2 may offer a new perspective on the treatment of chronic apical periodontitis.

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“…hPDLSCs have vascular potential, they are able to produce high levels of VEGF and FGF [13]. hPDLSCs share some cell surface markers with pericytes [20]. Similar to pericytes, hPDLSCs keep themselves stay near the endothelial cell networks and help stabilize and supply nutrients to these cell networks [20].…”

Section: Discussionmentioning

confidence: 99%

“…hPDLSCs share some cell surface markers with pericytes [20]. Similar to pericytes, hPDLSCs keep themselves stay near the endothelial cell networks and help stabilize and supply nutrients to these cell networks [20]. In particular, as a type of MSCs with neural crest origin, hPDLSCs are capable of generating endothelial tissues and possess a robust angiogenic potential [21].…”

Section: Discussionmentioning

confidence: 99%

Human Periodontal Ligament Stem Cell and Umbilical Vein Endothelial Cell Co-Culture to Prevascularize Scaffolds for Angiogenic and Osteogenic Tissue Engineering

Zhao

Sun

Qiao

et al. 2021

IJMS

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(1) Background: Vascularization remains a critical challenge in bone tissue engineering. The objective of this study was to prevascularize calcium phosphate cement (CPC) scaffold by co-culturing human periodontal ligament stem cells (hPDLSCs) and human umbilical vein endothelial cells (hUVECs) for the first time; (2) Methods: hPDLSCs and/or hUVECs were seeded on CPC scaffolds. Three groups were tested: (i) hUVEC group (hUVECs on CPC); (ii) hPDLSC group (hPDLSCs on CPC); (iii) co-culture group (hPDLSCs + hUVECs on CPC). Osteogenic differentiation, bone mineral synthesis, and microcapillary-like structures were evaluated; (3) Results: Angiogenic gene expressions of co-culture group were 6–9 fold those of monoculture. vWF expression of co-culture group was 3 times lower than hUVEC-monoculture group. Osteogenic expressions of co-culture group were 2–3 folds those of the hPDLSC-monoculture group. ALP activity and bone mineral synthesis of co-culture were much higher than hPDLSC-monoculture group. Co-culture group formed capillary-like structures at 14–21 days. Vessel length and junction numbers increased with time; (4) Conclusions: The hUVECs + hPDLSCs co-culture on CPC scaffold achieved excellent osteogenic and angiogenic capability in vitro for the first time, generating prevascularized networks. The hPDLSCs + hUVECs co-culture had much better osteogenesis and angiogenesis than monoculture. CPC scaffolds prevacularized via hPDLSCs + hUVECs are promising for dental, craniofacial, and orthopedic applications.

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Pericytes in the Periodontal Ligament

Cited by 14 publications

References 83 publications

High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1

High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1

EZH2 Regulates Lipopolysaccharide-Induced Periodontal Ligament Stem Cell Proliferation and Osteogenesis through TLR4/MyD88/NF-κB Pathway

Human Periodontal Ligament Stem Cell and Umbilical Vein Endothelial Cell Co-Culture to Prevascularize Scaffolds for Angiogenic and Osteogenic Tissue Engineering

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