Assessment of subclinical carotid atherosclerosis in patients with primary osteoarthritis: Correlation with disease severity and insulin resistance

Fouda, Neven; Abdelaziz, H; Fouda, Eman

doi:10.1016/j.ejr.2013.12.001

Cited by 11 publications

(11 citation statements)

References 36 publications

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“…1,2 As a degenerative disease, the degeneration of articular cartilage is the main reason for osteoarthritis occurrence. 1,2 As a degenerative disease, the degeneration of articular cartilage is the main reason for osteoarthritis occurrence.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Lin

Liu

Zhao

et al. 2018

J of Cellular Biochemistry

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Osteoarthritis is the most frequent chronic bone-joint disease in middle-aged and older people worldwide. This study investigated the effects of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on lipopolysaccharide (LPS)-induced murine chondrogenic ATDC5 cell inflammatory injury. Cell viability and apoptosis were assessed using cell counting kit-8 assay and annexin V-phycoerythrin (PE) staining, respectively. The expression levels of interleukin-1β (IL)-1β, IL-6, IL-8, tumor necrosis factor α (TNF-α), MALAT1, and microRNA-19b (miR)-19b were measured using quantitative reverse-transcription polymerase chain reaction. Enzyme-linked immunosorbent assay was conducted to detect the concentrations of IL-1β, IL-6, IL-8, and TNF-α in culture supernatant of ATDC5 cells. Expressions of key factors involved in cell apoptosis, proinflammatory response, Wnt/β-catenin, and nuclear factor κB (NF-κB) pathways were analyzed using Western blot analysis. We found that LPS treatment remarkably induced ATDC5 cell apoptosis and inflammatory injury. MALAT1 was upregulated in LPS-stimulated ATDC5 cells. Overexpression of MALAT1 significantly reversed the LPS-induced ATDC5 cell inflammatory injury, while suppression of MALAT1 had opposite effects. Further results showed that MALAT1 positively regulated the expression of miR-19b in ATDC5 cells. Knockdown of miR-19b reversed the protective effect of MALAT1 on LPS-induced ATDC5 cells. In addition, MALAT1 reduced LPS-induced Wnt/β-catenin and NF-κB pathways activation in ATDC5 cells by upregulating miR-19. To conclude, our research verified that MALAT1 alleviated LPS-induced ATDC5 cell inflammatory injury by upregulating miR-19b and inactivating Wnt/β-catenin and NF-κB pathways. This finding will be helpful for further understanding the critical roles of MALAT1 and miR-19b in osteoarthritis and may provide possible targets for osteoarthritis diagnosis and treatment.

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Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Lin

Liu

Zhao

et al. 2018

J of Cellular Biochemistry

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“…The role of duplex scanning in the investigation of carotid artery disease is well established, and there is evidence to suggest that it has a predictive role in identifying those patients with a greater than normal risk of stroke [5]. The study of the IMT in other rheumatic diseases on Egyptian patients showed subclinical atherosclerosis in rheumatoid arthritis [9], systemic lupus erythematosus [10], Behc¸ets disease [11] and primary osteoarthritis [12].…”

Section: Introductionmentioning

confidence: 98%

Subclinical atherosclerosis and peripheral vascular disease in systemic sclerosis patients: Relation to potential risk factors

Farag

Serougy

Metawee

et al. 2015

The Egyptian Rheumatologist

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Aim of the work: To measure the extent of subclinical atherosclerosis in patients with systemic sclerosis, and to evaluate any potential vascular risk factors in these patients.Patients and methods: This study included 30 patients with systemic sclerosis diagnosed according to the American college of rheumatology criteria and 20 healthy individuals were also included as a control group. Non-invasive vascular tests including; carotid duplex scanning measuring common carotid arteries (CCA) intima-media thickness (IMT), and ankle brachial pressure index (ABPI) were performed. Traditional vascular risk factors such as blood pressure, blood sugar, lipid profiles, steroid usage and other immunosuppressive medications were assessed.Results: The mean IMT of CCA was higher in systemic sclerosis patients (right 0.67 ± 0.11 mm, left 0.67 ± 0.12 mm) when compared with the control group (right 0.48 ± 0.2 mm, left 0.54 ± 0.13 mm) (p < 0.001). Carotid plaques were found in 4 SSc patients. Mean IMT was correlated with patients' age (p < 0.001), disease duration (p < 0.001), systolic blood pressure (p < 0.05), and dyslipidemia (p < 0.01). Ankle brachial pressure index (ABPI) was significantly lower in SSc patients (0.94 ± 0.13) when compared with controls (1.16 ± 0.12) (p < 0.001). No difference was found between limited (n = 25) and diffuse (n = 5) disease subtypes in mean IMT, nor in mean ABPI. There was no significant correlation between mean IMT and steroid dose or other immunosuppressive intake.Conclusion: There is an increased risk of subclinical atherosclerosis and peripheral arterial disease in SSc patients. Increased systolic blood pressure, dyslipidemia, long disease duration and older age were possible risk factors.

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“…The IMT has been found to be increased in many rheumatic diseases such as rheumatoid arthritis [10], SLE [11,12], Behcets disease [13] and osteoarthritis [14]. Together with classical conventional risk factors, other mechanisms (disease-specific factors) promote accelerated atherosclerosis in SLE.…”

Section: Introductionmentioning

confidence: 98%

Intima-media thickness in secondary anti-phospholipid syndrome patients: Impact of disease activity

Raafat

Fawzy

Fishawy

2015

The Egyptian Rheumatologist

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Aim of the work: To assess the carotid intima-media thickness (IMT) and plaque formation in systemic lupus erythematosus (SLE) patients with and without antiphospholipid syndrome (APS) by doppler ultrasonography and to correlate it with the clinical features, disease activity and damage.Patients and methods: Thirty-six female SLE patients with secondary APS and another 36 without were included. Thirty-six matching healthy volunteers were included as control. In patients, the disease activity and damage were assessed using the SLE Disease Activity Index (SLEDAI) and Systemic Lupus International Collaborating Clinics (SLICC) index, respectively. Doppler ultrasound was carried out for patients and control and the IMT was measured.Results: The demographic and clinical characteristics of patients are presented. The disease activity was significantly higher in SLE patients with APS (19.7 ± 7.9) compared to SLE only patients (15.1 ± 9.2) (p = 0.03). The low density lipoprotein (LDL) was significantly increased in APS patients (p = 0.04). The IMT was comparable between both groups (0.83 ± 0.15 mm) vs (0.86 ± 0.2 mm) (p = 0.55) and both were significantly increased compared to the control (0.61 ± 0.11 mm) (p < 0.0001). The dyslipidemia present in the patients showed a significant difference in the measured lipid profile parameters (p < 0.0001). The IMT significantly correlated with the SLEDAI in both groups (p < 0.002 and <0.001 respectively).Conclusion: The increased IMT as a marker of atherosclerosis is confirmed in SLE patients with no obvious difference in those with secondary APS. The link between the increased IMT and disease activity favors the role of disease-specific potential risk factors, in addition to the traditional conventional ones, in the development of atherosclerosis.

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Assessment of subclinical carotid atherosclerosis in patients with primary osteoarthritis: Correlation with disease severity and insulin resistance

Cited by 11 publications

References 36 publications

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Retracted: Long noncoding RNA MALAT1 alleviates lipopolysaccharide‐induced inflammatory injury by upregulating microRNA‐19b in murine chondrogenic ATDC5 cells

Subclinical atherosclerosis and peripheral vascular disease in systemic sclerosis patients: Relation to potential risk factors

Intima-media thickness in secondary anti-phospholipid syndrome patients: Impact of disease activity

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