Systemic treatment and narrowband ultraviolet B differentially affect cardiovascular risk markers in psoriasis

Sigurdardottir, Gunnthorunn; Ekman, Anna-Karin; Ståhle, Mona; Bivik, Cecilia; Enerbäck, Charlotta

doi:10.1016/j.jaad.2013.12.044

Cited by 32 publications

(32 citation statements)

References 46 publications

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“…For example, in a recent study, increases in known cardiovascular biomarkers, including soluble ICAM-1 (sICAM-1), soluble E (sE)-selectin, matrix metalloproteinase (MMP)-9, myeloperoxidase (MPO), and total PAI-1 (tPAI-1), did not correlate significantly with Psoriasis Area and Severity Index (PASI), and it was suggested that this represented increased systemic inflammation rather than increases resulting from local cutaneous inflammation. 103 Because the pathomechanisms leading to increased cardiovascular risk in patients with psoriasis may differ from mechanisms in the nonpsoriatic population, it is not known whether conventional inflammatory biomarkers of atherosclerotic disease are reliable predictors of risk in patients with psoriasis. Studies have shown that conventional biomarkers of inflammation and cardiovascular disease, such as CRP, human soluble CD40 ligand (sCD40L), human matrix gla-protein, and fetuin-A, are significantly altered in patients with psoriasis after controlling for age and BMI.…”

Section: Biomarkersmentioning

confidence: 99%

“…108 In several studies patients with psoriasis have shown significant increases in serum MPO, which is a known biomarker of cardiovascular inflammation that mediates its effects through lipid oxidation and endothelial dysfunction. 103,109 MPO is also highly expressed in psoriasis plaques. In one of these studies, serum levels of MPO correlated with coronary artery calcification, carotid plaque burden, carotid intima media thickness, and flow-mediated dilatation in patients with psoriasis but showed no association with psoriasis severity.…”

Section: Biomarkersmentioning

confidence: 99%

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Psoriasis Is a Systemic Disease with Multiple Cardiovascular and Metabolic Comorbidities

Ryan

Kirby

2015

Dermatologic Clinics

146

132

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Section: Biomarkersmentioning

confidence: 99%

Section: Biomarkersmentioning

confidence: 99%

Psoriasis Is a Systemic Disease with Multiple Cardiovascular and Metabolic Comorbidities

Ryan

Kirby

2015

Dermatologic Clinics

146

132

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“…Psoriasis may progressively worsen with age, or wax and wane in its severity, and thus causes considerable psychosocial disability and has a major impact on patients' quality of life [2]. Moreover, psoriasis is also regarded to have a connection with cardiovascular disease, depressive illness, obesity, dyslipidemia, hypertension, and psoriatic arthritis [3,4]. Despite conventional systemic therapy (e.g., methotrexate, cyclosporine, acitretin, and photochemotherapy) and biological agents (e.g., efalizumab, etanercept, infliximab, and adalimumab) being advanced [5], the treatment effect was temporary and there were side effects and a potential cumulative toxicity of these drugs [6].…”

Section: Introductionmentioning

confidence: 99%

PGRN Suppresses Inflammation and Promotes Autophagy in Keratinocytes Through the Wnt/β-Catenin Signaling Pathway

Tian

Yao

2016

Inflammation

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Psoriasis is a chronic, immune-mediated inflammatory skin disease that has a major impact on patients' quality of life. Progranulin (PGRN) is highly expressed in skin diseases and plays an important role in inflammation response and autophagy. However, the function of PGRN in the immune system and autophagy in psoriasis has not been clearly identified and elaborated on. Thus, this study aimed to investigate the role of PGRN on the inflammatory and autophagy process underlying inflammation in HaCaT cells. We showed that PGRN was markedly highly expressed in psoriasis lesions and inflammatory HaCaT cells. Specific silencing of PGRN promoted the production of the inflammatory cytokines IL-1β, IL-6, COX-2, iNOs, and MCP-1. Furthermore, PGRN siRNA promoted autophagy-related gene p62 and suppressed LC3II and Atg7 in HaCaT cells, while overexpression of PGRN showed a contrary effect. Moreover, knockdown of PGRN upregulated the expression levels of β-catenin, cyclin D1, and c-myc proteins. Finally, we demonstrated that IWP-2, an inhibitor of the Wnt/β-catenin signaling pathway, stemmed the pro-inflammatory and anti-autophagy effect of PGRN siRNA in TNF-α-treated HaCaT cells. Collectively, our findings suggest that PGRN is upregulated in psoriasis lesions and that the overexpression of PGRN inhibits the inflammation in keratinocytes induced by TNF-α by negatively regulating the production of inflammatory factors and positively mediating autophagy through the Wnt/β-catenin signaling pathway; this indicated that overexpression of PGRN may be a potential therapeutic option in psoriasis.

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“…Interestingly, we have previously found elevated levels of soluble ICAM-1 in this psoriasis population [13]. It may be speculated that the reduced endocan-1 levels may be the result of a feedback loop stemming from the increased levels of ICAM-1, and that the low levels of endocan-1 may result in a lack of inhibition of leukocyte transmigratory responses.…”

Section: Discussionmentioning

confidence: 61%

“…We have identified several circulating cytokines, chemokines, and factors associated with cardiovascular disease that were elevated systemically in psoriasis but were unresponsive to narrowband (NB)-ultraviolet (UV) B treatment [12,13].…”

Section: Introductionmentioning

confidence: 99%

Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment

et al. 2018

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Background: In psoriasis, a common immune-mediated disease affecting 2–3% of the population worldwide, there is an increased prevalence of extracutaneous diseases including obesity, the metabolic syndrome, and cardiovascular disease. This is believed to be linked to systemic inflammation. In previous studies, we have explored various markers in plasma and serum to characterize the ongoing systemic inflammation in psoriasis patients compared to controls. We have identified several markers that were altered in psoriasis patients, but which all were unresponsive to narrowband UVB (NB-UVB) treatment. Objective: The objective of the study was to evaluate the effect of NB-UVB treatment on markers of cardiovascular risk and systemic inflammation in psoriasis. Methods: The levels of 17 potential biomarkers with an association with cardiovascular risk were quantitated in plasma from 37 age- and gender-matched psoriasis patients and controls at baseline and in 21 psoriasis patients after 12 weeks of NB-UVB treatment to identify a systemic treatment response. Results: We identified the mediators endocan-1, CXCL16, and sVEGFR1, which were systemically decreased in psoriasis at baseline, as well as FABP3, FABP4, and sIL-1R1, which showed normal baseline levels. After 10–12 weeks of NB-UVB treatment, endocan-1 and CXCL16 were restored to normal levels, while sVEGFR1, FABP3, FABP4, and sIL-1R1 showed a significant reduction. Conclusion: The current study expands the number of potential biomarkers in psoriasis by including a greater number and variety of mediators, approaching the systemic inflammation from additional vantage points, including soluble immune receptors and adipocyte contribution, to provide a more complete picture of the systemic inflammatory state in psoriasis.

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Systemic treatment and narrowband ultraviolet B differentially affect cardiovascular risk markers in psoriasis

Abstract: Background: Psoriasis is associated with a systemic inflammation and an increased frequency of

Cited by 32 publications

References 46 publications

Psoriasis Is a Systemic Disease with Multiple Cardiovascular and Metabolic Comorbidities

Psoriasis Is a Systemic Disease with Multiple Cardiovascular and Metabolic Comorbidities

PGRN Suppresses Inflammation and Promotes Autophagy in Keratinocytes Through the Wnt/β-Catenin Signaling Pathway

Decreased Systemic Levels of Endocan-1 and CXCL16 in Psoriasis Are Restored following Narrowband UVB Treatment

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