Blockade of receptors of advanced glycation end products ameliorates diabetic osteogenesis of adipose‐derived stem cells through <scp>DNA</scp> methylation and Wnt signalling pathway

Zhang, Maorui; Li, Yong; Rao, Pengcheng; Huang, Kui; Luo, Daowen; Cai, Xiaoxiao; Xiao, Jingang

doi:10.1111/cpr.12471

Cited by 45 publications

(69 citation statements)

References 46 publications

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“…Additionally, by testing ST2 cells and human MSCs, it was shown that AGEs interact with RAGE and increase expression and secretion of TGF- β , which can suppress stromal cell mineralization [60]. The interaction of AGE–RAGE seems to be the dominant way, as their inhibitory effects on Wnt signaling pathway is reversible with the RAGE receptor antagonist FPS-ZM1 [72]. RAGE suppresses cell proliferation through suppression of Wnt, PI3K, and ERK signaling pathways [73].…”

Section: Age/rage and The Bone Remodeling Processmentioning

confidence: 99%

Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature

Asadipooya

2019

Journal of the Endocrine Society

160

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Diabetes compromises bone cell metabolism and function, resulting in increased risk of fragility fracture. Advanced glycation end products (AGEs) interact with the receptor for AGEs (RAGE) and can make a meaningful contribution to bone cell metabolism and/or alter function. Searches in PubMed using the key words “advanced glycation end-product,” “RAGE,” “sRAGE,” “bone,” and “diabetes” were made to explain some of the clinical outcomes of diabetes in bone metabolism through the AGE–RAGE signaling pathway. All published clinical studies were included in tables. The AGE–RAGE signaling pathway participates in diabetic complications, including diabetic osteopathy. Some clinical results in diabetic patients, such as reduced bone density, suppressed bone turnover markers, and bone quality impairment, could be potentially due to AGE–RAGE signaling consequences. However, the AGE–RAGE signaling pathway has some helpful roles in the bone, including an increase in osteogenic function. Soluble RAGE (sRAGE), as a ligand decoy, may increase in either conditions of RAGE production or destruction, and then it cannot always reflect the AGE–RAGE signaling. Recombinant sRAGE can block the AGE–RAGE signaling pathway but is associated with some limitations, such as accessibility to AGEs, an increase in other RAGE ligands, and a long half-life (24 hours), which is associated with losing the beneficial effect of AGE/RAGE. As a result, sRAGE is not a helpful marker to assess activity of the RAGE signaling pathway. The recombinant sRAGE cannot be translated into clinical practice due to its limitations.

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Section: Age/rage and The Bone Remodeling Processmentioning

confidence: 99%

Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature

Asadipooya

2019

Journal of the Endocrine Society

160

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“…FPS-ZM1 rescues AGE-induced loss of the osteogenic potential of adipose-derived stem cells (ASCs) in a diabetic environment [41]. Irbesartan, an agiotensin II type 1 receptor blocker, has anabolic bone effects in diabetes, inhibiting the deleterious effects of oxidative stress mediated by AGEs/RAGE [42].…”

Section: Ragementioning

confidence: 99%

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

et al. 2020

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Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiological processes and inflammatory diseases including osteoporosis. The aim of the review was to evaluate the role of alarmins in osteoporosis. A bibliographic search of the published scientific literature regarding the role of alarmins in osteoporosis was organized independently by two researchers in the following scientific databases: Pubmed, Scopus, and Web of Science. The keywords used were combined as follows: “alarmins and osteoporosis”, “RAGE and osteoporosis”, “HMGB1 and osteoporosis”, “IL-1 and osteoporosis”, “IL 33 and osteopororsis”, “S100s protein and osteoporosis”. The information was summarized and organized in the present review. We highlight the emerging roles of alarmins in various bone remodeling processes involved in the onset and development of osteoporosis, as well as their potential role as biomarkers of osteoporosis severity and progression. Findings of the research suggest a potential use of alarmins as pharmacological targets in future therapeutic strategies aimed at preventing bone loss and fragility fractures induced by aging and inflammatory diseases.

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“…Axin2 negatively regulates β-catenin and is a target of Wnt/β-catenin signaling ( Bernkopf et al, 2019 ). LEF1, binding to Wnt response elements to provide docking sites for β-catenin is a Wnt signaling pathway marker ( Zhang M. et al, 2018 ). A growing body of evidence suggests that susceptibility genes of Parkinson’s disease are associated with Wnt signaling regulation ( Berwick and Harvey, 2014 ; L’Episcopo et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Parkin Accelerates Osteoblastic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells and Bone Regeneration by Enhancing Autophagy and β-Catenin Signaling

Zhang

Hou

Chen

et al. 2020

Front. Cell Dev. Biol.

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Osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) plays a key role in bone formation. Parkin, an E3 ubiquitin ligase, related to Parkinson's disease and aging. Previous studies have indicated that Parkinson's disease have a higher risk of osteoporotic fracture. To investigate the effects and underlying mechanism of Parkin in the osteogenic differentiation of BMSCs, osteogenic differentiation was analyzed following upregulation or downregulation of Parkin. We found that Parkin was increased during differentiation. Parkin overexpression enhanced osteo-specific markers, and downregulation of Parkin mitigated osteo-specific markers. Moreover, upregulation of Parkin promoted β-catenin expression and autophagy and vice versa. The upregulation of β-catenin enhanced autophagy, and the activation of autophagy also increased the expression of β-catenin in Parkin-downregulated BMSCs. Parkinoverexpressed cell sheets accelerated bone healing in a tibial fracture model. Based on these results, we concluded that Parkin meditates osteoblastic differentiation of BMSCs via β-catenin and autophagy signaling.

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Blockade of receptors of advanced glycation end products ameliorates diabetic osteogenesis of adipose‐derived stem cells through DNA methylation and Wnt signalling pathway

Cited by 45 publications

References 46 publications

Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature

Advanced Glycation End Products (AGEs), Receptor for AGEs, Diabetes, and Bone: Review of the Literature

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

Upregulation of Parkin Accelerates Osteoblastic Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells and Bone Regeneration by Enhancing Autophagy and β-Catenin Signaling

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