Scholarlink

Objective <p>This study aimed to elucidate the role of circular RNA SUCLG2 (circSUCLG2) in diabetic osteoporosis (DOP) and to identify the underlying microRNA (miRNA)/messenger RNA (mRNA) regulatory pathways.</p> Methods <p>The osteoblast cell line MC3T3-E1 was cultured with 25.5&#xa0;mM glucose to simulate DOP in vitro. After transfection, levels of reactive oxygen species, malondialdehyde, catalase, superoxide dismutase, and lactate dehydrogenase were quantified. Alizarin Red staining and alkaline phosphatase (ALP) staining were performed to evaluate bone remodeling. The interactions among hsa_circ_0004276, microRNA-181c-5p (miR-181c-5p), and heat shock protein family A member 5 (HSPA5) were examined. A DOP mouse model was also established, with short hairpin RNA adeno-associated virus injections targeting circSUCLG2. After treatment, tibial tissues were analyzed by pathological assessment and computed tomography. Inflammatory cytokines and relevant gene expressions were measured in both MC3T3-E1 cells and tibial tissues.</p> Results <p>CircSUCLG2 was markedly overexpressed in DOP. Silencing circSUCLG2 ameliorated high glucose-induced osteoblast inflammation, oxidative stress, and bone formation impairment. Mechanistic studies revealed that circSUCLG2 competitively sponged miR-181c-5p, thereby regulating HSPA5 expression. Through this pathway, circSUCLG2 promoted osteoblast inflammation, oxidative stress, and bone formation defects. In vivo knockdown of circSUCLG2 further alleviated DOP in mice.</p> Conclusion <p>CircSUCLG2 accelerates high glucose-induced osteoblast inflammation and oxidative stress while diminishing bone formation by competitively binding miR-181c-5p and modulating HSPA5. Targeting circSUCLG2 may thus offer a promising therapeutic strategy for DOP.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

The role of circSUCLG2 in mediating inflammatory response and bone remodeling imbalance in diabetic osteoporosis

  • 期刊论文

  • 发表日期：

    2025年3月14日

查看全文
  • RenZhou Wang,
  • LinNa Ma

摘要

Objective

This study aimed to elucidate the role of circular RNA SUCLG2 (circSUCLG2) in diabetic osteoporosis (DOP) and to identify the underlying microRNA (miRNA)/messenger RNA (mRNA) regulatory pathways.

Methods

The osteoblast cell line MC3T3-E1 was cultured with 25.5 mM glucose to simulate DOP in vitro. After transfection, levels of reactive oxygen species, malondialdehyde, catalase, superoxide dismutase, and lactate dehydrogenase were quantified. Alizarin Red staining and alkaline phosphatase (ALP) staining were performed to evaluate bone remodeling. The interactions among hsa_circ_0004276, microRNA-181c-5p (miR-181c-5p), and heat shock protein family A member 5 (HSPA5) were examined. A DOP mouse model was also established, with short hairpin RNA adeno-associated virus injections targeting circSUCLG2. After treatment, tibial tissues were analyzed by pathological assessment and computed tomography. Inflammatory cytokines and relevant gene expressions were measured in both MC3T3-E1 cells and tibial tissues.

Results

CircSUCLG2 was markedly overexpressed in DOP. Silencing circSUCLG2 ameliorated high glucose-induced osteoblast inflammation, oxidative stress, and bone formation impairment. Mechanistic studies revealed that circSUCLG2 competitively sponged miR-181c-5p, thereby regulating HSPA5 expression. Through this pathway, circSUCLG2 promoted osteoblast inflammation, oxidative stress, and bone formation defects. In vivo knockdown of circSUCLG2 further alleviated DOP in mice.

Conclusion

CircSUCLG2 accelerates high glucose-induced osteoblast inflammation and oxidative stress while diminishing bone formation by competitively binding miR-181c-5p and modulating HSPA5. Targeting circSUCLG2 may thus offer a promising therapeutic strategy for DOP.