Biomarkers of Chondrocyte Apoptosis and Autophagy  in Osteoarthritis

Musumeci, Giuseppe; Castrogiovanni, Paola; Trovato, Francesca M.; Weinberg, Annelie; Alwasiyah, Mohammad Khalid; Al-Qahtani, Mohammed Hussein; Mobasheri, Ali

doi:10.3390/ijms160920560

Cited by 249 publications

(233 citation statements)

References 80 publications

(138 reference statements)

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“…The chondro-protective effect of ART might be associated with its role in the prevention of chondrocyte apoptosis. Accumulating evidence suggests that chondrocyte apoptosis plays an important role in the development and progression of OA [38, 39]. During the repair process, the apoptotic cells represented by an increased survival of chondrocytes might be a protection mechanism.…”

Section: Discussionmentioning

confidence: 99%

Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

Zhong

Liang

Yao

et al. 2018

Cell Physiol Biochem

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Background/Aims: Current drug therapies for osteoarthritis (OA) are not practical because of the cytotoxicity and severe side-effects associated with most of them. Artemisinin (ART), an antimalarial agent, is well known for its safety and selectivity to kill injured cells. Based on its anti-inflammatory activity and role in the inhibition of OA-associated Wnt/β-catenin signaling pathway, which is crucial in the pathogenesis of OA, we hypothesized that ART might have an effect on OA. Methods: The chondro-protective and antiarthritic effects of ART on interleukin-1-beta (IL-1β)-induced and OA patient-derived chondrocytes were investigated in vitro using cell viability assay, glycosaminoglycan secretion, immunofluorescence, quantitative reverse transcription-polymerase chain reaction, and western blotting. We also used OA model rats constructed by anterior cruciate ligament transection and medial meniscus resection (ACLT+MMx) in the joints to investigate the effects of ART on OA by gross observation, morphological staining, immunohistochemistry, and enzyme-linked immunosorbent assay. Results: ART exhibited potent anti-inflammatory effects by inhibiting the expression of proinflammatory chemokines and cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor alpha, and matrix metallopeptidase-13. It also showed favorable chondro-protective effect as evidenced by enhanced cell proliferation and viability, increased glycosaminoglycan deposition, prevention of chondrocyte apoptosis, and degeneration of cartilage. Further, ART inhibited OA progression and cartilage degradation via the Wnt/β-catenin signaling pathway, suggesting that it might serve as a Wnt/β-catenin antagonist to reduce inflammation and prevent cartilage degradation. Conclusion: In conclusion, ART alleviates IL-1β-mediated inflammatory response and OA progression by regulating the Wnt/β-catenin signaling pathway. Thereby, it might be developed as a potential therapeutic agent for OA.

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Section: Discussionmentioning

confidence: 99%

Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

Zhong

Liang

Yao

et al. 2018

Cell Physiol Biochem

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“…4 Furthermore, in degenerative cartilage, there is evidence of cell death in chondrocytes, which will enhance the degenerative course. 5 Due to the limited regenerative ability of articular cartilage, OA is one of the most challenging joint diseases. Current pharmacologic treatments include analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs).…”

Section: Introductionmentioning

confidence: 99%

Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Hu¹,

Li²,

Xin³

et al. 2018

Adv Clin Exp Med

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“…Apoptosis has been shown to be involved in the pathogenesis of many pathological conditions [67–71]. For instance, apoptosis of chondrocytes has been shown to cause degenerative processes in articular cartilage osteoarthritis [67,68].…”

Section: Discussionmentioning

confidence: 99%

Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study

Erekat

Al-Jarrah

2018

Med Sci Monit Basic Res

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BackgroundApoptosis plays a key role in the pathogenesis of Parkinson disease (PD). Active caspase-3, which is a proapoptotic factor, has been shown to reduce cardiac contractility, causing cardiac dysfunction in many pathological diseases. Reduced cardiac contractility and cardiac autonomic dysfunction have been reported in PD patients and PD mice treated with MPTP. The aim of this study was to show the impact of PD induction on the expression of the apoptotic mediators p53 and active caspase-3 in the heart.Material/MethodsEqual control and PD groups were formed by 20 randomly selected normal albino mice. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) and probenecid (250 mg/kg) (MPTP/p) to induce chronic Parkinsonism in the PD group. Immunohistochemistry was performed to investigate the expression of p53, active caspase-3, and β-adrenergic receptor in hearts from the 2 animal groups.ResultsP53 and active caspase-3 expression was significantly higher in PD hearts than in the control hearts (p value <0.01). β-adrenergic receptor expression was significantly lower in PD hearts than in control hearts (p value <0.01).ConclusionsOur results show an association of PD with p53 and active caspase-3 overexpression and β-adrenergic receptor underexpression in the heart, potentially promoting the cardiac autonomic dysfunction frequently observed in PD.

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Biomarkers of Chondrocyte Apoptosis and Autophagy in Osteoarthritis

Cited by 249 publications

References 80 publications

Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

Artemisinin Ameliorates Osteoarthritis by Inhibiting the Wnt/β-Catenin Signaling Pathway

Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study

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