Shear Stress Enhances the Paracrine-Mediated Immunoregulatory Function of Human Periodontal Ligament Stem Cells via the ERK Signalling Pathway

Suwittayarak, Ravipha; Klincumhom, Nuttha; Ngaokrajang, Utapin; Namangkalakul, Worachat; Ferreira, João N.; Pavasant, Prasit; Osathanon, Thanaphum

doi:10.3390/ijms23137119

Cited by 10 publications

(7 citation statements)

References 71 publications

(107 reference statements)

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“…In this study, we con rmed that OSS promotes the formation of early and lately AS plaques in ApoE-/-mice by oil red staining analysis and immunohistochemical and immuno uorescence staining found that OSS activates the EndMT process and regulates ID1 protein expression. Multiple studies have shown that TGF-β signalling is enriched in the OSS region (Deng et al, 2021), (Suwittayarak et al, 2022), which is consistent with our immunohistochemical results. We used TGF-β1 to act on HAECs to simulate a low oscillating shear stress environment in vitro.…”

Section: Discussionsupporting

confidence: 93%

ID1 protein inhibitor depresses low-oscillating shear stress-mediated EndMT and atherosclerosis by Snail and Wnt/β-catenin signalling pathways

Jun,

Yang,

Wang

et al. 2024

Preprint

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The lateral pressure exerted by blood on the vessel wall, called low oscillating shear stress(OSS), destroys the endothelial cell barrier function through a process called EndMT and promotes the occurrence of atherosclerosis. The specific mechanism by which OSS regulates EndMT is still unclear. Inhibitor of differentiation 1 (ID1) is controlled by shear stress as an essential force-sensitive factor, and little is known about the effect of ID1 on EndMT in OSS-mediated atherosclerosis. This study investigated the impact of ID1 inhibitors on OSS-mediated EndMT in ApoE−/− mice and TGF-β1-induced human aortic endothelial cells (HAECs). First, we found that the expression of ID1 was down-regulated. At the same time, EndMT and plaque formation occurred in the ligated left common carotid artery (OSS) compared with the unligated right common carotid artery. Then, our results showed that the ID1 inhibitor AGX51 attenuated EndMT in atherosclerosis plaques in OSS mice. However, in vitro studies show that ID1 is upregulated in TGF-β1-treated HAECs and induces EndMT.sh-ID1 or AGX51 to inhibit the EndMT process and restore the migratory ability of endothelial cells. Furthermore, ID1 overexpression promoted the occurrence of EndMT.In addition, inhibition of ID1 may inhibit OSS-induced EndMT by regulating EndMT-specific transcription factors Snail and Wnt/β-catenin signalling pathway in vivo and in vitro by Immunohistochemistry and Western blot. These results suggest that ID1 inhibitors regulate the occurrence and development of low oscillating shear stress-mediated EndMT and atherosclerosis by Ctrlling Snail and Wnt/β-catenin signalling pathways.

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Section: Discussionsupporting

confidence: 93%

ID1 protein inhibitor depresses low-oscillating shear stress-mediated EndMT and atherosclerosis by Snail and Wnt/β-catenin signalling pathways

Jun,

Yang,

Wang

et al. 2024

Preprint

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“…All experiments were repeated using the cells derived from at least four different donors (n = 4; Manokawinchoke et al, 2019Manokawinchoke et al, , 2020Suwittayarak et al, 2022). The statistical analysis was performed using Prism 8 (GraphPad Software).…”

Section: Discussionmentioning

confidence: 99%

Tideglusib enhances odontogenic differentiation in human dental pulp stem cellsin vitro

2022

Self Cite

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Aim Tideglusib is a small molecule agonist of the canonical Wnt pathway. The present study investigated the influence of Tideglusib on human dental pulp stem cell (hDPSC) proliferation, apoptosis, migration and odonto/osteogenic differentiation. Methodology hDPSCs were treated with 50, 100 nM or 200 nM Tideglusib. β‐catenin accumulation was detected by immunofluorescence staining. Colony‐forming unit ability was assessed by staining with Coomassie blue. Cell cycle progression and cell apoptosis were investigated using flow cytometry. Cell migration was examined using an in vitro wound‐healing assay. Osteogenic differentiation was examined using alkaline phosphatase (ALP) staining, alizarin red S staining and osteogenic‐related gene expression. The gene expression profile was examined using a high‐throughput RNA sequencing technique. All experiments were repeated using cells derived from at least four different donors (n = 4). The Mann–Whitney U‐test was used to identify significant differences between two independent group comparisons. For three or more group comparisons, statistical differences were assessed using the Kruskal–Wallis test followed by pairwise comparison. The significance level was set at 5% (p < .05). Results Tideglusib activated the Wnt signalling pathway in hDPSCs as demonstrated by an increase in cytoplasmic β‐catenin accumulation and nuclear translocation. Tideglusib did not affect hDPSC proliferation, cell cycle progression, cell apoptosis or cell migration. In contrast, 50 and 100 nM Tideglusib significantly enhanced mineralization and osteogenic marker gene expression (RUNX2, ALP, BMP2 and DSPP; p < .05). Conclusions Tideglusib enhanced the odonto/osteogenic differentiation of hDPSCs. Therefore, incorporating this bioactive molecule in a pulp‐capping material could be a promising strategy to promote dentine repair.

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“…Naringin, at a dose of 1 µM, can promote the proliferation and differentiation of hPDLSCs into osteoblasts, as indicated by upregulating bone-related factors, such as RUNX2, COL1A2, OPN, and OCN [38]. However, the limited lifespan of hPDLSCs restricts their application [39]. The knock-in of Bmil may enhance the cell cycle, cell replication, and stemness of hPDLSCs.…”

Section: Osteogenic Differentiation Inductionmentioning

confidence: 99%

The Development of Naringin for Use against Bone and Cartilage Disorders

Gan

Deng

et al. 2023

Molecules

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Bone and cartilage disorders are the leading causes of musculoskeletal disability. There is no absolute cure for all bone and cartilage disorders. The exploration of natural compounds for the potential therapeutic use against bone and cartilage disorders is proving promising. Among these natural chemicals, naringin, a flavanone glycoside, is a potential candidate due to its multifaceted pharmacological activities in bone and cartilage tissues. Emerging studies indicate that naringin may promote osteogenic differentiation, inhibit osteoclast formation, and exhibit protective effects against osteoporosis in vivo and in vitro. Many signaling pathways, such as BMP-2, Wnt/β-catenin, and VEGF/VEGFR, participate in the biological actions of naringin in mediating the pathological development of osteoporosis. In addition, the anti-inflammatory, anti-oxidative stress, and anti-apoptosis abilities of naringin also demonstrate its beneficial effects against bone and cartilage disorders, including intervertebral disc degeneration, osteoarthritis, rheumatoid arthritis, bone and cartilage tumors, and tibial dyschondroplasia. Naringin exhibits protective effects against bone and cartilage disorders. However, more efforts are still needed due to, at least in part, the uncertainty of drug targets. Further biological and pharmacological evaluations of naringin and its applications in bone tissue engineering, particularly its therapeutic effects against osteoporosis, might result in developing potential drug candidates.

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Shear Stress Enhances the Paracrine-Mediated Immunoregulatory Function of Human Periodontal Ligament Stem Cells via the ERK Signalling Pathway

Cited by 10 publications

References 71 publications

ID1 protein inhibitor depresses low-oscillating shear stress-mediated EndMT and atherosclerosis by Snail and Wnt/β-catenin signalling pathways

ID1 protein inhibitor depresses low-oscillating shear stress-mediated EndMT and atherosclerosis by Snail and Wnt/β-catenin signalling pathways

Tideglusib enhances odontogenic differentiation in human dental pulp stem cellsin vitro

The Development of Naringin for Use against Bone and Cartilage Disorders

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