High Glucose Suppresses Osteogenic Differentiation and Induces Mitochondrial Dysfunction in Osteoblasts via SIRT1/RECQL4 Axis&#894; A Laboratory Study Using Mouse Cells

Xiahui Zhou; Weixiong Peng; Shenglian Pan; Zhe Lin; Rongrong Pan; Qinglai Wang

doi:10.23812/j.biol.regul.homeost.agents.20223604.99

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Macrophages in the pathogenesis of psoriasis and anti-psoriatic nanotherapies

Psoriasis is a common, chronic, and inflammatory skin disease. Macrophages account for about 61.3% of the inflammatory cells infiltrating psoriatic lesions. Modulating macrophage polarization, inhibiting their infiltration, and targeting the secretion of inflammatory factors and associated inflammatory pathways by these cells can alleviate psoriasis symptoms and inflammation. Moreover, nanomaterials as novel drug carriers, offer unique advantages such as large surface area, easy modification, high biocompatibility, good biodegradability, enhanced systemic adsorption, etc. Nanomaterials have great potential for efficient drug delivery and release, as well as improving therapeutic efficacy while reducing adverse effects. By systematically addressing the role of macrophages in psoriasis pathogenesis and the potential of nanomaterials in treating psoriasis through modulating macrophages, this review enhances our understanding of the disease mechanism and holds promise for novel therapeutic breakthroughs and advancements in the future treatment of psoriasis.

High Glucose Suppresses Osteogenic Differentiation and Induces Mitochondrial Dysfunction in Osteoblasts via SIRT1/RECQL4 Axis; A Laboratory Study Using Mouse Cells

Xiahui Zhou, Weixiong Peng, Shenglian Pan, Zhe Lin, Rongrong Pan, Qinglai Wang

Article ID: 6945
Vol 36, Issue 4, 2022

DOI: https://doi.org/10.23812/j.biol.regul.homeost.agents.20223604.99

Received: 8 September 2022; Accepted: 8 September 2022; Available online: 8 September 2022; Issue release: 8 September 2022

Abstract

Background: Diabetes mellitus has an adverse effect on human bones, which is a risk factor for osteoporosis. The aim of this study was to explore the mechanism of the effects of high glucose (HG) on the osteogenic differentiation of osteoblasts. Methods: In this study, mouse MC3T3-E1 cells were cultured in high glucose level at 30 mM with 24.5 mM mannitol and 5.5 mM glucose as control. Plasmid circular deoxyribonucleic acids (pcDNAs) and small interference ribonucleic acids (RNAs) were transfected for functional analysis of RecQ helicase-like 4 (RECQL4) and sirtuin 1 (SIRT1). The viability, alkaline phosphatase (ALP) activity, and OCN (provide in full) concentration was measured via methyl thiazolyl tetrazolium (MTT), colorimetric, enzyme-linked immunosorbent assay (ELISA) assays. Mitochondrial functions were assessed by mitochondrial membrane potential (MMP) and the levels of adenosine triphosphate (ATP), glutathione (GSH), and malondialdehyde (MDA). Quantitative reverse-transcription polymerase chain reaction or western blot were conducted to detect the gene or protein expression. RECQL4 acetylation assay was performed and the interaction between RECQL4 and SIRT1 was detected via co-immunoprecipitation assay. Results: The effects of HG on downregulating cell viability, the levels of osteogenic differentiation-related markers (ALP and OCN), p53 phosphorylation, ATP and GSH as well as RECQL4 and apoptosis-related factors (Cytochrome C and Cleaved caspase-3) upregulating MMP loss and MDA content were reversed following RECQL4 over expression (p < 0.01). Sirtuin 1 (SIRT1) over expression promoted the viability and the levels of ALP and OCN, while silencing RECQL4 did the opposite (p < 0.05) and caused a reversion in HG-treated osteoblasts (p < 0.01). Additionally, silencing SIRT1 inhibited the acetylation of RECQL4 (p < 0.01) and the interaction between SIRT1 and RECQL4. Conclusions: HG repressed the osteogenic differentiation and downregulated MMP via SIRT1/RECQL4 axis in osteoblasts.

Keywords

diabetes mellitus;high glucose;osteogenic differentiation;sirtuin 1;RecQ helicase-like 4;deacetylation

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Medical Genetics, University of Torino Medical School, Italy

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Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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2025-02-01

Notice of Change in Publication Schedule

In addition to the first issue that has already been published by the original publisher, there will be four more issues released this year, with scheduled publication dates in March, June, September, and December respectively.

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Starting from Volume 39 Issue 2 (2025), the ownership of Journal of Biological Regulators and Homeostatic Agents (ISSN: 0393-974X (P); 1724-6083 (O)) will be transferred from Biolife Sas to Asia Pacific Academy of Science Pte. Ltd. As of 21 January 2025, authors should make submissions to the new journal system and follow the author guidelines. Asia Pacific Academy of Science Pte. Ltd. will take over the publication of manuscripts being processed.

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