Endoplasmic reticulum stress remodels alveolar bone formation after tooth extraction

Chen, Yun; Guo, Yue; Li, Jun; Chen, Yingyi; Liu, Qiong; Tan, Li; Gao, Zhengrong; Zhang, Shaohui; Zhou, Yinghui; Feng, Yun‐Zhi

doi:10.1111/jcmm.15753

Cited by 17 publications

(17 citation statements)

References 43 publications

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“…28 Animal study reported that reducing ER stress was conducive to cell differentiation and proliferation, and controlling ER stress at a reduced level would promote osteogenesis. 29 Protein kinase RNA (PKR)-like ER kinase is essential for regulating the collagen and growth factors secreted by osteoblasts to maintain the normal growth and development of bone tissue. PERK is also closely related to bone remodeling.…”

Section: Physiological Role Of Er Stress In Periodontal Tissuementioning

confidence: 99%

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The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Jiang

Zhu

2022

J of Periodontal Research

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The endoplasmic reticulum (ER) is a principal organelle for folding, post‐translational modifications and transport of secretory, luminal, and membrane proteins. ER stress is a condition induced by the accumulation of unfolded or misfolded proteins owing to a variety of physiological and pathological phenomena. To overcome the deleterious effects of ER stress, unfolded protein response (UPR) is initiated to translocate and remove the misfolded and accumulated proteins. Plenty of evidence shows the correlation between ER stress/UPR and the pathology of inflammatory disease. Periodontal disease is a chronic inflammatory disease characterized by the irreversible destruction of periodontal tissues, which associates with the onset and progress of several systemic diseases. Periodontopathic bacterium and pro‐inflammatory mediators play a pivotal role in the progress of periodontal disease. Besides, cigarette smoke has long been associated with periodontal disease. As an inflammatory disorder of the periodontium, periodontal disease is highly related to ER stress. In this review, we provide an overview of the pathophysiological effect of ER stress on periodontal disease through five aspects as follow: ER stress and periodontal tissue remodeling, including both soft tissue and hard tissue; ER stress and the inflammation; ER stress and systematic effect during the periodontal disease; last but not least, ER stress and the autophagic apoptosis in cells.

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Section: Physiological Role Of Er Stress In Periodontal Tissuementioning

confidence: 99%

“…Osteoblasts in the periodontal ligament and alveolar bone are replaced every few months 28 . Animal study reported that reducing ER stress was conducive to cell differentiation and proliferation, and controlling ER stress at a reduced level would promote osteogenesis 29 …”

Section: Introductionmentioning

confidence: 99%

The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

Jiang

Zhu

2022

J of Periodontal Research

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“…Total protein was lysed in RIPA lysis buffer (Thermo Scientific, Rockford, IL, USA) containing protease and phosphatase inhibitors. Western blot was then performed as described previously ( 22 ). Primary antibodies were used at the manufacturer’s suggested concentrations: CTSG (1:500; 23840-1-AP; Proteintech), TNFRSF4 (1:500; 20006-1-AP; Proteintech) or β-actin (1:5000; Proteintech).…”

Section: Methodsmentioning

confidence: 99%

A Novel Immune-Related Gene Signature to Identify the Tumor Microenvironment and Prognose Disease Among Patients With Oral Squamous Cell Carcinoma Patients Using ssGSEA: A Bioinformatics and Biological Validation Study

et al. 2022

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Oral squamous cell carcinoma (OSCC) is the most invasive oral malignancy in adults and is associated with a poor prognosis. Accurate prognostic models are urgently needed, however, knowledge of the probable mechanisms behind OSCC tumorigenesis and prognosis remain limited. The clinical importance of the interplay between the immune system and tumor microenvironment has become increasingly evident. This study explored immune-related alterations at the multi-omics level to extract accurate prognostic markers linked to the immune response and presents a more accurate landscape of the immune genomic map during OSCC. The Cancer Genome Atlas (TCGA) OSCC cohort (n = 329) was used to detect the immune infiltration pattern of OSCC and categorize patients into two immunity groups using single-sample gene set enrichment analysis (ssGSEA) and hierarchical clustering analysis. Multiple strategies, including lasso regression (LASSO), Cox proportional hazards regression, and principal component analysis (PCA) were used to screen clinically significant signatures and identify an incorporated prognosis model with robust discriminative power on the survival status of both the training and testing set. We identified two OSCC subtypes based on immunological characteristics: Immunity-high and immunity low, and verified that the categorization was accurate and repeatable. Immunity_ high cluster with a higher immunological and stromal score. 1047 differential genes (DEGs) integrate with immune genes to obtain 319 immue-related DEGs. A robust model with five signatures for OSCC patient prognosis was established. The GEO cohort (n = 97) were used to validate the risk model’s predictive value. The low-risk group had a better overall survival (OS) than the high-risk group. Significant prognostic potential for OSCC patients was found using ROC analysis and immune checkpoint gene expression was lower in the low-risk group. We also investigated at the therapeutic sensitivity of a number of frequently used chemotherapeutic drugs in patients with various risk factors. The underlying biological behavior of the OSCC cell line was preliminarily validated. This study characterizes a reliable marker of OSCC disease progression and provides a new potential target for immunotherapy against this disease.

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“…Meanwhile, we also found that autophagosomes gathered around trabecular bone after GlcN activated autophagy. While osteoblasts were attached around bone trabeculae [26,27]. In addition, our previous in vitro studies reported that GlcN increased the level of osteoblast autophagy.…”

Section: Glcn Delays Osteoporosis By Promoting Osteoblast Autophagymentioning

confidence: 99%

Glucosamine Delays the Progression of Osteoporosis in Senile Mice by Promoting Osteoblast Autophagy

Huang

Zheng

et al. 2022

Preprint

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Background: Senile osteoporosis (SOP) is one of the most prevalent diseases that afflict the elderly population, which characterized by decreased osteogenic ability. Glucosamine (GlcN) is an over-the-counter dietary supplement. Our previous study reported that GlcN promotes osteoblast proliferation by activating autophagy in vitro. The purpose of this study is to determine the effects and mechanisms of GlcN on senile osteoporosis and osteogenic differentiation in vivo.Methods: Aging was induced by subcutaneous injection of D-Galactose (D-Gal), and treated with GlcN or vehicle. The anti-senile-osteoporosis effect of GlcN was explored by examining changes in micro-CT, serum indicators, body weight, protein and gene expression of aging and apoptosis. Additionally, the effects of GlcN on protein and gene expression of osteogenesis and autophagy were observed by inhibiting autophagy with 3-Methyladenine (3-MA).Results: GlcN significantly improved bone mineral density (BMD) and bone micro-architecture, decreased skeletal senescence and apoptosis and increased osteogenesis in D-Gal induced osteoporotic mice. While all effect was reversed with 3-MA.Conclusion: GlcN effectively delayed the progression of osteoporosis in senile osteoporotic mice by promoting osteoblast autophagy. This study suggested that GlcN may be a prospective candidate drug for the treatment of SOP.

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Endoplasmic reticulum stress remodels alveolar bone formation after tooth extraction

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 17 publications

References 43 publications

The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

The role of endoplasmic reticulum stress in the pathophysiology of periodontal disease

A Novel Immune-Related Gene Signature to Identify the Tumor Microenvironment and Prognose Disease Among Patients With Oral Squamous Cell Carcinoma Patients Using ssGSEA: A Bioinformatics and Biological Validation Study

Glucosamine Delays the Progression of Osteoporosis in Senile Mice by Promoting Osteoblast Autophagy

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