CYR61 as a Potential Apoptosis Biomarker in Osteoarthritis with Comorbidities.

Murat Tokus, Hakan Cicek, Hüseyin Ates, Cagil Coskun, Yusuf Dogus, Figen Cicek

Abstract read

In one paragraph

Article in Journal of musculoskeletal & neuronal interactions, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

6 authors.

Murat TokusCukurova University Faculty of Medicine, Department of Biophysics Adana, Turkiye.

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

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

Cagil CoskunCukurova University Faculty of Medicine, Department of Biophysics Adana, Turkiye.

Yusuf DogusCukurova University Faculty of Medicine, Department of Biochemistry Adana, Turkiye.

Figen CicekCukurova University Faculty of Medicine, Department of Biophysics Adana, Turkiye.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveObesity 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.

methodsExcision 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.

resultsCaspase-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.

conclusionMetabolic 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.

Indexed as

ApoptosisBiomarkersCysteine-Rich Protein 61AgedCartilage, ArticularChondrocytesComorbidityDiabetes MellitusFemaleHumansMaleMiddle AgedObesityOsteoarthritisOsteoarthritis, KneeBiomarkersCCN1 protein, humanCysteine-Rich Protein 61ApoptosisCYR61Diabetes MellitusObesityOsteoarthritis

Identifiers

PMID39616508

PMCPMC11609561

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.