This study assessed the effectiveness of a combination of platelet-rich plasma (PRP) and β-tricalcium phosphate/polylactic-co-glycolic acid (β-TCP/PLGA) fibers in the treatment of osteoporotic vertebral defects in rats. Seventy-two female Sprague-Dawley rats subjected to ovariectomy to induce osteoporosis were divided into three groups to receive different treatments for critical bone defects created in the lumbar vertebrae. The PRP group received β-TCP/PLGA fibers infused with PRP, the control group received no material, and the other group received the same fibers infused with phosphate-buffered saline (PBS). Over a period of 12 weeks, bone regeneration, macrophage differentiation, and inflammatory responses were evaluated histologically. Compared to the PBS group, the PRP-treated group demonstrated significantly enhanced early stage bone formation, increased expression of osteogenic markers, and a favorable shift in macrophage activity from the M1 inflammatory phenotype to the M2 healing phenotype. These outcomes suggest that the combination of PRP and β-TCP/PLGA fibers not only effectively promotes bone repair under osteoporotic conditions but also modulates the immune response to facilitate better healing, indicating its potential as a beneficial surgical intervention for osteoporotic vertebral fractures.

The long non-coding RNA PVT1 reportedly forms a circular RNA variant (circPVT1). As circPVT1 is expressed in various cancers and has been implicated in promoting cancer cell proliferation and tumor progression, it is considered a potential biomarker and therapeutic target. We previously confirmed that circPVT1 expression varies according to the Gleason pattern, a morphological indicator of malignancy in prostate cancer. In this study, we assessed the expression of circPVT1 using BaseScope^TM assay with prostate cancer tissues and evaluated the correlation with the Grade Group (based on Gleason pattern), an indicator used to morphologically evaluate the degree of malignancy of prostate cancer. The relationship between circPVT1 expression and tumor proliferation was evaluated using cells in which circPVT1 expression was suppressed using the clustered regularly interspaced short palindromic repeats (CRISPR)/RfxCas13d system. BaseScope^TM assay confirmed that circPVT1 expression was significantly higher in Grade Group 2–5 (intermediate- and high-grade groups) than Grade Group 1 (low-grade group). In vitro experiments using the CRISPR/RfxCas13d system showed that specific suppression of circPVT1 expression resulted in a significant reduction in the number of prostate cancer cells. The results of this study suggest that circPVT1 is involved in tumor growth in prostate cancer and may serve as a therapeutic target for moderately and highly malignant prostate cancers that express circPVT1.

α-Synuclein is the causative gene for PARK1 and PARK4 (heterozygous triplication of SNCA) and is associated with Parkinson’s disease, where it localizes to presynaptic terminals in mature neurons. Beyond Parkinson’s disease, α-synuclein has also been implicated in various other neuronal disorders. In vitro studies using purified α-synuclein protein have suggested it is involved in synaptic vesicle assembly. However, its physiological function and the ultrastructure of its localization sites in presynaptic terminals remain unclear. To address this, we generated transgenic mice overexpressing human α-synuclein tagged with mKate2 (hSNCA-mKate2 mice) to investigate its in vivo role in synaptic vesicle pool formation at presynaptic terminals. These mice showed normal growth and fertility, and even at 1-yr. old, they showed no motor dysfunction compared to their wild-type littermates. Additionally, no abnormal protein aggregates indicative of neurodegeneration were observed. In this review, we summarize recent findings on the in vivo role of α-synuclein within presynaptic terminals, utilizing hSNCA-mKate2 mice in combination with in-resin correlative light and electron microscopy, electron microscopy, and immunohistochemistry.

O-linked N-acetylglucosamine (O-GlcNAc) modification, known as O-GlcNAcylation, is a dynamic post-translational modification involving the addition of N-acetylglucosamine to ser‍ine or threonine residues. It has emerged as a critical regulator in diabetic pathophysiology. This review summarizes current research on the role of O-GlcNAcylation in hyperglycemia-induced cellular dysfunction, and focuses on vascular smooth muscle cells, renal cytoskeletal proteins, and diabetic complications in animal and human models. Studies reveal that hyperglycemia upregulates O-GlcNAc transferase activity, disrupting the interplay between glycosylation and phosphorylation, thereby impairing signaling pathways and exacerbating vascular proliferation and renal cytoskeletal disorganization. Notable findings include the imbalance of β-actin modifications in diabetic nephropathy, correlated with podocyte damage and glomerular abnormalities. By elucidating these mechanistic pathways, this review underscores the potential of O-GlcNAcylation as a biomarker and a therapeutic target. Future research should focus on tissue-specific effects and pharmacological strategies that mitigate diabetes-induced complications while preserving normal cellular functions.