Objective The occurrence of osteoarthritis is related to genetic and environmental factors. Among them, the change of chondrocyte gene expression pattern regulated by epigenetic modification is an important participant. This study analyzed the effect of CAMP gene methylation on the level of oxidative stress and inflammation of chondrocytes. Methods We analyzed the changes of the transcriptome in the articular cartilage tissue of osteoarthritis (OA) patients from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. Cell Counting Kit-8 (CCK-8) and flow cytometry analysis of short hairpin RNA (shRNA) silencing CAMP gene and 5-μM 5-Aza-2’-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human chondrocytes osteoarthritis (HC-OA) cells. The Dichloro-dihydro-fluorescein diacetate (DCFH-DA) assay was used to detect the level of reactive oxygen species (ROS), and the expression level of inflammatory factors was analyzed by Western Blot. Results The expression of CAMP in cartilage tissue of OA patients was upregulated, and the level of methylation was downregulated. CAMP was highly expressed in osteoarthritis articular cartilage cells. Silencing CAMP inhibited the proliferation of HC-OA cells and promoted their apoptosis. CAMP gene methylation inhibited ROS levels and tumor necrosis factor-α (TNF-α) expression levels in HC-OA cells, and promoted transforming growth factor beta (TGF-β) expression. CAMP gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis. Conclusion CAMP gene promoter methylation inhibits ROS levels and inflammation and induces chondrocyte apoptosis.
Objective: The occurrence of osteoarthritis is related to genetic and environmental factors. Among them, the change of chondrocyte gene expression pattern regulated by epigenetic modification is an important participant. This study analyzed the effect of CAMP gene methylation on the level of oxidative stress and inflammation of chondrocytes. Methods: We analyzed the changes of the transcriptome in the articular cartilage tissue of osteoarthritis patients (OA) from the GSE117999 dataset. The GSE48422 dataset was used to analyze the changes in the methylation level of osteoarthritis cells. MTT assay and flow cytometry analysis of short hairpin RNA (shRNA) silencing CAMP gene and 5μM 5-Aza-2’-Deoxycytidine (AZA) treatment on the proliferation and apoptosis of Human Chondrocytes Osteoarthritis (HC-OA) cells. The DCFH-DA assay was used to detect the level of reactive oxygen species (ROS), and the expression level of inflammatory factors was analyzed by Western Blot. Results: The expression of CAMP in cartilage tissue of OA patients was up-regulated, and the level of methylation was down-regulated. CAMP was highly expressed in osteoarthritis articular cartilage cells. Silencing CAMP inhibited the proliferation of HC-OA cells and promoted their apoptosis. CAMP gene methylation inhibited ROS levels and TNF-α expression levels in HC-OA cells, and promoted TGF-β expression. CAMP gene methylation inhibited the proliferation of HC-OA cells and promoted their apoptosis. Conclusion: CAMP gene promoter methylation induces chondrocyte apoptosis by inhibiting ROS levels and inflammation.
This study aimed to investigate the evaluation of biomechanical changes in articular cartilage in patients after anterior cruciate ligament (ACL) reconstruction by magnetic resonance imaging (MRI) based on a three-dimensional (3D) finite element model. The data of 90 patients undergoing arthroscopic ACL reconstruction in the hospital were collected and divided into the stable group (54 cases) and the unstable group (36 cases). A load of up to 134N was applied to the 3D finite element model, and the kinematics of knee flexion at 0°, 30°, 60°, and 90° were examined. The tibial anteversion, tibial rotation, and ACL/graft tension were recorded in the 3D finite element model, which was randomly divided into the normal group (intact group, n = 30), the ACL rupture group (deficient group, n = 30), and the anatomical reconstruction group (anatomical group, n = 30). When the graft was fixed at 0°, the anterior tibial translation at 30°, 60°, and 90° in the anatomic group was 8–19% higher than the normal value under 134 N anterior load. The tibial internal rotation in the anatomic group was 18% and 28% higher than the normal value at 30° and 90°. When the graft was fixed at 30°, the anterior tibial translation at 60° and 90° of the anatomic group was 15% higher than the normal value. The tibial internal rotation at 90° of the anatomic group was 16% higher than the normal value, and the above differences had statistical significance P < 0.05 . MRI images were used to assess the bone tunnel angle, and the statistical analysis by the independent-samples t-test showed that there were significant differences in the bone tunnel angle between the stable group and the unstable group P < 0.05 . Currently, based on the 3D finite element model, MRI can accurately evaluate the postoperative effect of anatomical ACL reconstruction in the position, diameter, and angle of tibial and femoral bone tunnels, which can be applied to clinical promotion.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.