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Peripheral nerve injury triggers sequential phenotype alterations in Schwann cells, which are critical for axonal regeneration. Long noncoding RNAs (lncRNAs) are long transcripts without obvious coding potential. It has been reported that lncRNAs participate in diverse biological processes and diseases. However, the role of lncRNA in Schwann cells and peripheral nerve regeneration is unclear. Here, we identified an lncRNA, loc680254, which is upregulated in rat sciatic nerve after peripheral nerve injury. The loc680254 knockdown inhibits Schwann cell proliferation, enhances apoptosis, and hinders cell cycle, while loc680254 overexpression has the opposite effect. Mechanically, we found that loc680254 might act as a microRNA sponge to regulate the expression of mitosis-related gene, spindle and kinetochore associated complex subunit 1 (Ska1) and proline/serine-rich coiled-coil 1 (Psrc1). Silencing of Psrc1 or Ska1 attenuates the effect of loc680254 overexpression on Schwann cell proliferation. Finally, we repaired the rat sciatic nerve gap with chitosan scaffolds loaded with loc680254-overexpressing Schwann cells and evaluated axon regeneration and functional recovery. Our results indicated that loc680254 is a new potential modulator for Schwann cell proliferation, which could be targeted to develop novel therapeutic strategies for peripheral nerve repair.
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http://dx.doi.org/10.1002/glia.24045 | DOI Listing |
Adv Sci (Weinh)
September 2025
State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200240, P. R. China.
Perineural invasion (PNI) is a common pathological characteristic of pancreatic ductal adenocarcinoma (PDAC), closely linked to postoperative recurrence, metastasis, and unfavorable prognosis. Nevertheless, the precise mechanisms that govern PNI in PDAC remain poorly elucidated. Here, group-specific component protein (GC) is identified as one of the most significantly upregulated genes related to PNI, primarily derived from malignant ductal cells compared to other cell types.
View Article and Find Full Text PDFExp Clin Endocrinol Diabetes
August 2025
Department of Endocrinology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, China.
Painful diabetic neuropathy (PDN), a severe microvascular complication of diabetes, is closely associated with neuroinflammation. This study aimed to investigate the mechanism of circ_0002590 in neuroinflammation associated with PDN.The Schwann cells (HEI193) were treated with high glucose (HG, 150 mM) to simulate the diabetic microenvironment.
View Article and Find Full Text PDFFront Cell Neurosci
August 2025
Department of Ophthalmology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Background: Imeglimin (Ime), the first in a novel class of antidiabetic agents, has potential therapeutic effects on diabetic peripheral neuropathy (DPN). This study aimed to evaluate and compare the effects on cellular metabolic function and reactive oxygen species (ROS) levels in high glucose-treated mouse Schwann cells (SCs), an DPN model, with those of metformin (Met), a conventional antidiabetic agent known for its beneficial effects on DPN. The roles of PPARα and fatty acid-binding proteins 5 and 7 (FABP5 and FABP7), both of which have been implicated in the pathogenesis of DPN, were also investigated.
View Article and Find Full Text PDFBiomaterials
August 2025
Department of Oral and Cranio-maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laborator
Bone healing requires Schwann cells (SCs) paracrine factors for mesenchymal stem cell function. Diabetes mellitus (DM) patients are susceptible to developing SCs dysfunction and impairing bone healing. Rare research considered reconstructing mesenchymal stem cell-schwann cell circuitry in diabetic bone regeneration.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
Department of Radiation Oncology, Stanford University, Stanford, CA 94305.
Reduced mitochondrial quality and quantity in tumors is associated with dedifferentiation and increased malignancy. However, it remains unclear how to restore mitochondrial quantity and quality in tumors and whether mitochondrial restoration can drive tumor differentiation. Our study shows that restoring mitochondrial function using retinoic acid (RA) to boost mitochondrial biogenesis and a mitochondrial uncoupler to enhance respiration synergistically drives neuroblastoma differentiation and inhibits proliferation.
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