Assessment of selected angiogenesis markers in the serum of middle‐aged male patients with plaque psoriasis

Socha, Mateusz; Kiciński, Paweł; Feldo, Marcin; Zubilewicz, Tomasz; Pietrzak, Aldona

doi:10.1111/dth.14727

Cited by 8 publications

(6 citation statements)

References 30 publications

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“… 19 , 20 Studies showed VEGF is up‐regulated in the psoriatic lesions and serum and VEGF expression is positively related to the severity of psoriasis. 21 , 22 , 23 , 24 In our study, we confirmed the level of VEGF is elevated in mice psoriatic skin tissues. We found that C10orf99 knockdown could reduce IMQ‐induced VEGF expression in mice.…”

Section: Discussionsupporting

confidence: 83%

“…VEGF is the most important proangiogenic factor and it's role in angiogenesis has been well known 19,20 . Studies showed VEGF is up‐regulated in the psoriatic lesions and serum and VEGF expression is positively related to the severity of psoriasis 21–24 . In our study, we confirmed the level of VEGF is elevated in mice psoriatic skin tissues.…”

Section: Discussionsupporting

confidence: 79%

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C10orf99 regulates angiogenesis by regulating VEGF and MMP2 in psoriasis

Chen,

2024

Skin Research and Technology

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BackgroundPsoriasis is a common chronic inflammatory skin disease characterized by epidermal hyperplasia, inflammatory cell infiltration and excessive neovascularization. It was previously found that C10orf99 regulates keratinocyte proliferation and inflammation in psoriasis. However, the role of C10orf99 on angiogenesis associated with psoriasis is unknown.MethodsWe used imiquimod (IMQ)‐induced psoriasis mice and M5‐induced cellular model of psoriasis to research the effects of C10orf99 knockdown on angiogenesis in psoriasis in vivo and in vitro.ResultsIn this study, our data showed that C10orf99 knockdown ameliorated imiquimod (IMQ)‐induced red plaques in mice and reduced the number of microvessels. Furthermore, we found such an effect was achieved by down‐regulating the expression of vascular endothelial growth factor (VEGF) and metallomatrix proteinase 2 (MMP2). Consistently, C10orf99 knockdown significantly downgraded the expression of MMP2 and VEGF in cellular model of psoriasis.ConclusionThese results suggested that C10orf99 could regulate angiogenesis in psoriasis and it might be a promising potential target of psoriasis.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionsupporting

confidence: 79%

C10orf99 regulates angiogenesis by regulating VEGF and MMP2 in psoriasis

Chen,

2024

Skin Research and Technology

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“…[16][17][18][19] Patients with psoriasis also have increased plasma levels of VEGF-A, which correlate with disease severity. 16,[20][21][22] The emergence of biologic therapy over the last two decades 23 has shifted psoriasis management from treatment with conventional systemic treatments (methotrexate, oral retinoids and ciclosporin) to those which target key cytokines in the inflammatory pathways involved in psoriasis [e.g. tumour necrosis factor (TNF)-a, interleukin (IL)-23 or IL-17A].…”

Section: Discussionmentioning

confidence: 99%

“…Expression of VEGF‐A, which binds to VEGF‐A receptor‐1 (VEGFR‐1) and VEGFR‐2, 15 is increased within plaques of psoriasis compared with nonlesional skin (Figure 1). 16–19 Patients with psoriasis also have increased plasma levels of VEGF‐A, which correlate with disease severity 16,20–22 …”

Section: Figurementioning

confidence: 99%

A novel personalized treatment approach for psoriasis: anti‐vascular endothelial growth factor‐A (VEGF‐A) therapy

2022

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Summary Chronic plaque psoriasis is an inflammatory skin disease in which genetic predisposition along with environmental factors lead to the development of the disease, which affects 2% of the UK’s population and is associated with extracutaneous morbidities and a reduced quality of life. A complex crosstalk between innate and adaptive immunity, the epithelia and the vasculature maintain the inflammatory milieu in psoriasis. Despite the development of promising treatment strategies, mostly targeting the immune system, treatments fail to fulfil every patient’s goals. Vascular endothelial growth factor‐A (VEGF‐A) mediates angiogenesis and is upregulated in the plaques and plasma of patients with psoriasis. Transgenic expression of VEGF‐A in experimental models led to the development of skin lesions that share many psoriasis features. Targeting VEGF‐A in in vivo models of psoriasis‐like inflammation resulted in disease clearance. Anti‐angiogenesis treatments are widely used for cancer and eye disease and there are clinical reports of patients treated with VEGF‐A inhibitors who have experienced Psoriasis Area and Severity Index improvement. Existing psoriasis treatments downregulate VEGF‐A and angiogenesis as part of their therapeutic effect. Pharmacogenetics studies suggest the existence of different genetic signatures within patients with psoriasis that correspond with different treatment responsiveness and disease severity. There is a subset of patients with psoriasis with an increased predisposition to produce high levels of VEGF‐A, who may be most likely to benefit from anti‐VEGF‐A therapy, offering an opportunity to personalize treatment in psoriasis. Anti‐VEGF‐A therapies may offer an alternative to existing anticytokine strategies or be complementary to standard treatments for the management of psoriasis.

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“…Plasma levels of VEGF-A are higher in patients with psoriasis than in healthy individuals, and they correlate with disease severity [ 31 , 32 ]. VEGF-A is produced principally by activated keratinocytes in the skin of patients with psoriasis [ 29 , 33 , 43 ]. Other VEGFs (not produced by keratinocytes) are synthesized by fibroblasts [ 29 ] and immune cells such as mast cells [ 34 , 35 ].…”

Section: Psoriasismentioning

confidence: 99%

Angiogenesis in Chronic Inflammatory Skin Disorders

Lee

Hong

Kim

2021

IJMS

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Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.

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Assessment of selected angiogenesis markers in the serum of middle‐aged male patients with plaque psoriasis

Cited by 8 publications

References 30 publications

C10orf99 regulates angiogenesis by regulating VEGF and MMP2 in psoriasis

C10orf99 regulates angiogenesis by regulating VEGF and MMP2 in psoriasis

A novel personalized treatment approach for psoriasis: anti‐vascular endothelial growth factor‐A (VEGF‐A) therapy

Angiogenesis in Chronic Inflammatory Skin Disorders

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