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MiR-7 has been recognized as an osteoarthritis (OA-)-promoting factor, but the specific downstream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA. In this study, we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7 and presented a negative regulatory relation with SEMA6D and . SEMA6D could improve OA in rat OA models, as indicated by H&E and Safranin O-Fast green staining, and also CT analysis. Further evaluation of SEMA6D suggested that SEMA6D promotes the anabolism and reduces the catabolism of C28/I2 chondrocytes via inhibiting the activation of the p38 pathway. The present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of catabolism and anabolism in C28/I2 chondrocytes. SEMA6D exerts its function via inhibiting the activation of the p38 pathway.
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http://dx.doi.org/10.1155/2022/9674221 | DOI Listing |
ACS Omega
August 2025
Department of Spine Orthopedics, General Hospital of Ningxia Medical University, Yinchuan, Ningxia 750001, China.
Spinal cord injury (SCI) represents one of the recognized difficulties, and its pathological mechanisms remain unclear. Aberrant regulation of the RNA-binding protein (RBP) and selective splicing are associated with SCI. Nonetheless, the mechanisms of RBP regulation and abnormal selective splicing events associated with SCI are unexplored.
View Article and Find Full Text PDFAfr Health Sci
September 2024
Department of Traumatic Orthopedics, Second Affiliated Hospital of Dalian Medical University, Dalian, China.
Background: To analyse how Semaphorin 6D (SEMA6D) expression and extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signal pathways are activated and how they influence gastric cancer proliferation, migration, and invasion.
Methodology: SEMA6D expression was knocked down in human gastric cancer cells using RNA interference technology. In vitro assays were used to analyse how SEMA6D knockdown affects clone formation, migration, and invasion.
Sci Transl Med
July 2025
Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Cellular cross-talk, mediated by membrane receptors and their ligands, is crucial for brain homeostasis and can contribute to neurodegenerative diseases such as Alzheimer's disease (AD). To find cross-talk dysregulations involved in AD, we reconstructed cross-talk networks from single-nucleus transcriptional profiles of 67 clinically and neuropathologically well-characterized controls and AD brain donors from the Knight Alzheimer Disease Research Center and the Dominantly Inherited Alzheimer Network cohorts. We predicted a role for TREM2 and additional AD risk genes mediating neuron-microglia cross-talk in AD.
View Article and Find Full Text PDFGenes (Basel)
May 2025
L. K. Ernst Federal Research Center for Animal Husbandry, Dubrovitsy, Podolsk 142132, Moscow Oblast, Russia.
: Finding single nucleotide polymorphisms (SNPs) and candidate genes that influence the expression of key traits is essential for genomic selection and helps improve the efficiency of poultry production. Here, we aimed to conduct a genome-wide association study (GWAS) for egg production traits in an F resource population of chickens (). : The examined F population was produced by crossing two divergently selected breeds with contrasting phenotypes for egg performance traits, namely Russian White (of higher egg production) and Cornish White (of lower egg production).
View Article and Find Full Text PDFFASEB J
April 2025
Department of Orthopedics, The Second People's Hospital of Changzhou, The Third Affiliated Hospital of Nanjing Medical University, Changzhou Medical Center, Changzhou, China.
The tissue-localized renin-angiotensin system (tRAS) plays a pivotal role in the crosstalk between cardiovascular factors and osteoarthritis (OA). Semaphorin 6D (SEMA6D), a cardiovascular neuroeffector, may contribute to chondrocyte homeostasis; however, its cartilage-specific functions remain unclear. Chondrocytes with altered SEMA6D expression were established via gene transfection.
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