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CYR61 作为合并症性骨关节炎潜在的凋亡生物标志物。

CYR61 as a Potential Apoptosis Biomarker in Osteoarthritis with Comorbidities.

机构信息

Cukurova University Faculty of Medicine, Department of Biophysics Adana, Turkiye.

University of Health Sciences, Adana Faculty of Medicine, Department of Orthopedics and Traumatology, Turkiye.

出版信息

J Musculoskelet Neuronal Interact. 2024 Dec 1;24(4):385-393.

Abstract

OBJECTIVE

Obesity and diabetes mellitus (DM) are major risk factors for osteoarthritis (OA), but it remains unclear how comorbidity affects apoptosis signaling in OA. This study investigated the effect of metabolic diseases on apoptosis and apoptosis-related intracellular and extracellular signaling in OA.

METHODS

Excision materials of human articular cartilage from total knee arthroplasties were collected. The samples were divided into four groups as, control OA, OA+DM, OA+Obese, and OA+DM+obesity. Protein activities were determined using Western blot and ELISA.

RESULTS

Caspase-3 levels were significantly increased in chondrocytes in which OA was associated with DM or obesity. However, an increase in Bcl-2 activity was also observed in these comorbidities. The increased levels of CaMKII in the same groups also indicate an increase in cellular activity in comorbidities. While IL-6 and TNF-α did not show significant changes, matrix regulatory protein CYR61 levels reflected the intracellular apoptotic activity.

CONCLUSION

Metabolic diseases have a stimulatory effect on the etiopathology of osteoarthritis by enhancing cellular signaling towards apoptosis and that matrix signaling proteins may play a key role in regulating these effects. Examining OA with its accompanying diseases will lead to a better understanding of the cellular mechanisms that differ in OA.

摘要

目的

肥胖和糖尿病(DM)是骨关节炎(OA)的主要危险因素,但合并症如何影响 OA 中的细胞凋亡信号仍不清楚。本研究探讨了代谢性疾病对 OA 中细胞凋亡及凋亡相关细胞内和细胞外信号的影响。

方法

从全膝关节置换术中采集人关节软骨的切除物。将样本分为四组,即对照性 OA、OA+DM、OA+肥胖和 OA+DM+肥胖。使用 Western blot 和 ELISA 测定蛋白活性。

结果

与 DM 或肥胖相关的 OA 患者的软骨细胞中 caspase-3 水平显著升高,但在这些合并症中也观察到 Bcl-2 活性增加。同一组中 CaMKII 的增加水平也表明合并症中细胞活性增加。虽然 IL-6 和 TNF-α没有显示出显著变化,但基质调节蛋白 CYR61 水平反映了细胞内凋亡活性。

结论

代谢性疾病通过增强细胞凋亡信号对骨关节炎的病因学具有刺激作用,而基质信号蛋白可能在调节这些作用中发挥关键作用。检查伴有疾病的 OA 将有助于更好地理解 OA 中不同的细胞机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa40/11609561/15b0b481db40/JMNI-24-385-g001.jpg

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