Angiogenesis in Dermatology – Insights of Molecular Mechanisms and Latest Developments

Richarz, Nina A.; Boada, Aram; Carrascosa, J.M.

doi:10.1016/j.ad.2016.12.001

Cited by 25 publications

(22 citation statements)

References 66 publications

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“…The most well-known conditions where this switch is seen are malignant and inflammatory skin disorders as well as other pathological events, e.g., age-related macular degeneration, rheumatoid arthritis, tumor growth, proliferative retinopathies, and skin diseases (psoriasis, atopic dermatitis (AD), systemic sclerosis (SSc), cutaneous carcinoma, etc.) [5–8]. Either physiological or pathological angiogenesis is in need of initial mediation by various proangiogenic factors, consisting of endothelial growth factor (VEGF), fibroblast growth factors (FGF), interleukin-8 (IL-8), platelet-derived growth factor (PDGF), placental growth factor (PGF), angiopoietin-1 (Ang-1), and transforming growth factor- β (TGF- β ) [9].…”

Section: Introductionmentioning

confidence: 99%

Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Xian

Song

Yang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

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Section: Introductionmentioning

confidence: 99%

Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Xian

Song

Yang

et al. 2019

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

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“…Angiogenesis consists of the development of new vessels from pre-existing vascular structures, naturally occurring during embryonic growth and in pathological situations, in response to different stimuli including hypoxia, inflammation or tissue injuries [1]. Angiogenesis involves a finely regulated sequence of morphogenetic changes that mainly affect endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Angiogenic response in an in vitro model of dog microvascular endothelial cells stimulated with antigenic extracts from Dirofilaria immitis adult worms

Zueva

Morchón

Carretón³

et al. 2019

Parasites Vectors

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Background Angiogenesis can occur under pathological conditions when stimuli such as inflammation, vascular obstruction or hypoxia exist. These stimuli are present in cardiopulmonary dirofilariosis ( Dirofilaria immitis ). The aim of this study was to analyze the capacity of D. immitis antigens to modify the expression of angiogenic factors and trigger the formation of pseudocapillaries (tube-like structures) in an in vitro model of endothelial cells. Methods The expression of VEGF-A, sFlt, mEndoglin and sEndoglin in cultures of canine microvascular endothelial cells stimulated with extract of adult worms of D. immitis obtained from an untreated dog (DiSA) and from a dog treated for 15 days with doxycycline (tDiSA), was determined by using commercial kits. The capacity of pseudocapillary formation was evaluated analyzing cell connections and cell groups in Matrigel cell cultures stimulated with DiSA and tDiSA. In both cases non-stimulated cultures were used as controls. Results First, we demonstrated that worms obtained from the dog treated with doxycycline showed a significantly lower amount of Wolbachia (less than 60%) than worms removed from the untreated dog. Only DiSA was able to significantly increase the expression of the proangiogenic factor VEGF-A in the endotelial cells cultures. None of the D. immitis extracts modified the expression of sFlt. tDiSA extract was able to modify the expression of the endoglins, significantly decreasing the expression of the pro-angiogenic mEndoglin and increasing the anti-angiogenic sEndoglin. The formation of pseudocapillaries was negatively influenced by tDiSA, which reduced the organization and number of cellular connections. Conclusions The ability of antigens from adult D. immitis worms to modify the expression of pro and anti-angiogenic factors in endotelial cell cultures was demonstrated, as well as the trend to form pseudocapillaries in vitro . The capacity of stimulation may be linked to the amount of Wolbachia present in the antigenic extracts.

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“…This results in a cascade of inflammatory cytokines and growth factors, such as IFN-γ, IL-2, TNF-α, and TNF-β, produced by Th11; IL-17, IL-22, IL-23, and TNF-α, by Th17; and antimicrobial peptide (AMP), TNF-α, IL-6, IL-8, polymorphonuclears (PMN), and VGEF, by activated keratinocytes [12,15]. These inflammatory mediators further activate T cells and mast cells to give rise to a self-amplifying loop that results in keratinocyte overproliferation, neutrophil recruitment, hypervascular hyperplasia, and sustained skin inflammation [15,16]. Angiogenesisa marker of psoriasis pathogenesiscould also be promoted by angiogenic mediators like VEGF, TNF-α, IL-8, and IL-17 [16,17].…”

Section: Ros Mainly Include Superoxide Anion (O 2 −mentioning

confidence: 99%

“…These inflammatory mediators further activate T cells and mast cells to give rise to a self-amplifying loop that results in keratinocyte overproliferation, neutrophil recruitment, hypervascular hyperplasia, and sustained skin inflammation [15,16]. Angiogenesisa marker of psoriasis pathogenesiscould also be promoted by angiogenic mediators like VEGF, TNF-α, IL-8, and IL-17 [16,17]. As reported, oxidative stress and a high level of TNF-α induce endothelial dysfunction, which can consequently contribute to autoimmune and cardiovascular diseases [18,19].…”

Section: Ros Mainly Include Superoxide Anion (O 2 −mentioning

confidence: 99%

Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation

et al. 2019

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Objectives: To unveil the role of SIRT1 in limiting oxidative stress in psoriasis and to further discuss the therapeutic prospects of salidroside in psoriasis. Methods: Literature from 2002 to 2019 was searched with "psoriasis", "oxidative stress", "SIRT1", "salidroside" as the key words. Then, Oxidative stress in psoriasis and the role of SIRT1 were summarized and the potential role of salidroside in the disease was speculated. Results: Oxidative stress might contribute to the pathogenesis of psoriasis. High levels of ROS produced during oxidative stress lead to the release of inflammatory mediators, that, in turn, induce angiogenesis and excessive proliferation of keratinocytes. SIRT1 is a member of the sirtuin family, of which the activation lead to the inhibition of such oxidative stress signaling pathways MAPK, NF-κB, and STAT3, down-regulation of inflammatory factors, suppression of inflammation and keratinocyte hyperproliferation, and inhibition of angiogenesis. Salidroside, the main ingredient of Rhodiola, is known to exert antioxidant roles, which has been attributed to SIRT1 activation. Conclusion: Salidroside might inhibit oxidative stress singling pathways via SIRT1 activation, and could be as an ideal candidate for management of psoriasis.

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Angiogenesis in Dermatology – Insights of Molecular Mechanisms and Latest Developments

Cited by 25 publications

References 66 publications

Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Angiogenic response in an in vitro model of dog microvascular endothelial cells stimulated with antigenic extracts from Dirofilaria immitis adult worms

Salidroside inhibits MAPK, NF-κB, and STAT3 pathways in psoriasis-associated oxidative stress via SIRT1 activation

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