TWEAK Enhances E-selectin and ICAM-1 Expression, and May Contribute to the Development of Cutaneous Vasculitis

Chen, Tao; Guo, Zhanfang; Li, Li; Li, Mengmeng; Wang, Tingting; Jia, Ruizhen; Cao, Na; Li, Jingyi

doi:10.1371/journal.pone.0056830

Cited by 14 publications

(23 citation statements)

References 44 publications

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“…We showed that the pro‐inflammatory effects of TWEAK in vessels are associated with the induction of adhesion molecule and chemokine production. In addition, we also found that TWEAK blockade substantially reduced vascular damage and perivascular leukocyte infiltrates in lipopolysaccharide‐induced cutaneous vasculitis . In this study, both TWEAK and Fn14 expression were elevated in the dermal vessel wall of skin lesions in patients with UV, and the results suggest that TWEAK and Fn14 may contribute to the pro‐inflammatory effects on vascular EC; moreover, TWEAK‐dependent Fn14 signaling may be dominant.…”

Section: Discussionsupporting

confidence: 61%

Tumor necrosis factor‐like weak inducer of apoptosis and its receptor fibroblast growth factor‐inducible 14 are expressed in urticarial vasculitis

Chen

Guo

et al. 2013

The Journal of Dermatology

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Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), a member of the TNF family, has been implicated as a pro-inflammatory cytokine in many types of autoimmune and infectious diseases. However, information about TWEAK in dermatological diseases is limited. To date, no studies have investigated the roles of TWEAK in patients with urticarial vasculitis (UV). This study aimed to assess serum TWEAK levels, together with TWEAK and fibroblast growth factor-inducible 14 (Fn14) expressions of skin lesions in patients with UV. Serum TWEAK levels in patients with UV, together with patients with cutaneous leukocytoclastic angiitis (CLA) and healthy controls were detected by enzyme-linked immunosorbent assay; TWEAK and Fn14 expressions of skin lesions were analyzed by immunohistochemistry. Results showed that TWEAK and Fn14 were abundantly expressed in the dermal vessel wall of lesional skin in patients with UV but not healthy controls. Serum TWEAK levels in the acute stage in patients with UV were significantly higher than those in the convalescent stage and healthy controls. Serum TWEAK levels were elevated significantly in patients with CLA compared with those in healthy controls. Our previous study indicated that TWEAK may be an important mediator for the development of vascular inflammation in skin. In addition, we also found that TWEAK blockade substantially reduced vascular damage and perivascular leukocyte infiltrates in lipopolysaccharide-induced cutaneous vasculitis. Our study shows that TWEAK may be associated with the pathogenesis of UV; it is therefore suggested that TWEAK may be a potential therapeutic target for UV and other types of cutaneous vasculitis.

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Section: Discussionsupporting

confidence: 61%

Tumor necrosis factor‐like weak inducer of apoptosis and its receptor fibroblast growth factor‐inducible 14 are expressed in urticarial vasculitis

Chen

Guo

et al. 2013

The Journal of Dermatology

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“…TWEAK induces CCL5 (RANTES) and CXCL8 (IL-8) expression in a human dermal endothelial cell line (209). TWEAK also upregulates E-selectin and ICAM-1 as shown in vitro and in an in vivo model of cutaneous vasculits (210). …”

Section: Endothelial Response To Gcs In Vasculitismentioning

confidence: 92%

Endothelial Response to Glucocorticoids in Inflammatory Diseases

et al. 2016

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The endothelium plays a crucial role in inflammation. A balanced control of inflammation requires the action of glucocorticoids (GCs), steroidal hormones with potent cell-specific anti-inflammatory properties. Besides the classic anti-inflammatory effects of GCs on leukocytes, recent studies confirm that endothelial cells also represent an important target for GCs. GCs regulate different aspects of endothelial physiology including expression of adhesion molecules, production of pro-inflammatory cytokines and chemokines, and maintenance of endothelial barrier integrity. However, the regulation of endothelial GC sensitivity remains incompletely understood. In this review, we specifically examine the endothelial response to GCs in various inflammatory diseases ranging from multiple sclerosis, stroke, sepsis, and vasculitis to atherosclerosis. Shedding more light on the cross talk between GCs and endothelium will help to improve existing therapeutic strategies and develop new therapies better tailored to the needs of patients.

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“…Moreover, the TWEAK/Fn14 signals participate in the development of various dermatoses, such as psoriasis [7], atopic dermatitis [8], cutaneous vasculitis [18], human papillomavirus (HPV) infection [9], and bullous pemphigoid [10]. TWEAK/Fn14 activation also contributes to the biological processes of tumors [19].…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling

Wang¹,

Xiao²,

Xia³

2017

Cell Physiol Biochem

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Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor–inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators. An Fn14-TRAF2-TNFR axis has been suggested in the function of TWEAK/Fn14 signaling, which may serve as a target in the development of novel therapeutic strategies for many diseases that have Fn14-overexpressing cells in affected tissues. The aims of this review are: 1) to present the main results on TWEAK/Fn14 regulation of cell fates, 2) to analyze the mechanism of the Fn14-TRAF2-TNFR axis, and 3) to summarize the potential strategies in the pharmacologic targeting of this axis.

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TWEAK Enhances E-selectin and ICAM-1 Expression, and May Contribute to the Development of Cutaneous Vasculitis

Cited by 14 publications

References 44 publications

Tumor necrosis factor‐like weak inducer of apoptosis and its receptor fibroblast growth factor‐inducible 14 are expressed in urticarial vasculitis

Tumor necrosis factor‐like weak inducer of apoptosis and its receptor fibroblast growth factor‐inducible 14 are expressed in urticarial vasculitis

Endothelial Response to Glucocorticoids in Inflammatory Diseases

Tumor Necrosis Factor Receptor Mediates Fibroblast Growth Factor-Inducible 14 Signaling

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