Excessive glucocorticoids combined with RANKL promote the differentiation of bone marrow macrophages (BMM) into osteoclasts and accelerate the progression of osteoporosis by activating the SYK/SHP2/NF-κB signaling pathway.

The primary objective of this study was to explore the extensive implications and complex molecular interactions arising from the confluence of excessive glucocorticoids and RANKL on the differentiation process of BMM into osteoclasts, profoundly impacting osteoporosis development. The methodology encompassed X-ray analysis and HE staining for evaluating bone loss in mice, while immunohistochemical staining was utilized to observe phosphorylated SHP2 (p-SHP2) expression. The assessment of several phosphorylated and total protein expression levels, including NF-κB, SHP2, SYK, JAK2, TAK1, NFATC1, c-fos, and Cathepsin K, was conducted via Western blotting.

Association of the Expression Levels of Long-Chain Noncoding RNA TUG1 and Its Gene Polymorphisms with Knee Osteoarthritis.

To study the association of the expression levels of long noncoding RNA Taurine-upregulated gene 1 (lncRNA TUG1) and TUG1 polymorphisms with knee osteoarthritis (KOA). A total of 255 KOA patients and 255 controls from May 2017 to December 2019 were selected for the study. Sanger sequencing was conducted to detect the genotypes of the TUG1 rs5749201, rs7284767, and rs886471 loci in all study subjects.