Oxidative stress and high-mobility group box 1 (HMGB1) protein release in vitiligo

Becatti, Matteo

doi:10.1111/bjd.15538

Cited by 11 publications

(14 citation statements)

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“…As a classic damage-associated molecular pattern molecule, HMGB1 is involved in the development of many autoimmune skin diseases, including psoriasis (Zhang et al, 2017), atopic dermatitis (Karuppagounder et al, 2015;Wang et al, 2018), and lichen planus (de Carvalho et al, 2018). Recently, some studies have reported that HMGB1 may directly induce the apoptosis of melanocytes in vitiligo (Becatti, 2017;Mou et al, 2018). We found that HMGB1 secreted by melanocytes under oxidative stress was able to promote the secretion of chemokines from keratinocytes, which could induce the cutaneous infiltration of CD8 þ T cells and the maturation of DCs.…”

Section: Discussionmentioning

confidence: 99%

“…Vitiligo is a chronic inflammatory disease characterized by skin depigmentation caused by the loss of epidermal melanocytes. The destruction of melanocytes in vitiligo has been attributed to several etiologic theories, including the occurrence of oxidative stress that can directly cause the apoptosis of melanocytes and the generation of CD8 þ cytotoxic T cells that specifically destroy melanocytes (Becatti, 2017;Jian et al, 2014;. Notably, recent studies have demonstrated that oxidative stress facilitates the exposure of self-antigens derived from melanocytes, which are essential for the activation of autoreactive T cells (Xie et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Cui

Zhang

et al. 2019

Journal of Investigative Dermatology

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Vitiligo is a cutaneous depigmentation disorder caused by the destruction of epidermal melanocytes. The generation and the skin infiltration of autoreactive CD8 þ cytotoxic T cells triggered by oxidative stress play a critical role in vitiligo. High-mobility group protein B1 (HMGB1) is a classic damage-associated molecular pattern molecule with strong proinflammatory effects in inflammatory reactions. A previous study reported an enhanced expression of HMGB1 in vitiligo lesions, but the role of HMGB1 in cutaneous inflammation of vitiligo is still unknown. In the present study, we initially found that HMGB1 was released from the nucleus of melanocytes in vitiligo perilesional skin. Furthermore, cultured normal human melanocytes could release HMGB1 under treatment with hydrogen peroxide. Moreover, HMGB1 facilitated the secretion of CXCL16 and IL-8 from keratinocytes by binding to the receptor for advanced glycation end products and activating NF-kB and extracellular signaleregulated kinase signaling pathways. Subsequently, HMGB1 led to the formation of chemotaxis for the migration of CD8 þ T cells from patients with vitiligo by increasing the release of CXCL16 from keratinocytes. Additionally, HMGB1 promoted the maturation of dendritic cells from patients with vitiligo. Altogether, our study demonstrates that HMGB1 released from melanocytes contributes to the formation of oxidative stresseinduced autoimmunity in vitiligo.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Cui

Zhang

et al. 2019

Journal of Investigative Dermatology

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“…Notably, HMGB1 has been well recognized as an important signaling molecule involved in both acute and chronic inflammation process . Its expression was significantly increased in a variety of skin diseases, such as psoriasis, alopecia areata, vitiligo, atopic dermatitis, Henoch‐Schönlein purpura (HSP), pemphigus, and drug‐induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms (DRESS) . Due to the similar pharmacological efficacy to corticosteroids but with milder side effects, Glycyrrhizin has been widely utilized in several dermatologic disorders for many years, such as active‐stage generalized vitiligo, psoriasis, alopecia areata, and is also reported to be effective in alleviating the symptoms of atopic dermatitis and systemic sclerosis in animal model .…”

Section: Discussionmentioning

confidence: 99%

A pilot study of oral tranexamic acid and Glycyrrhizin compound in the treatment of recalcitrant Riehl’s melanosis

Xing

Zhang

et al. 2018

J of Cosmetic Dermatology

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Summary Background Up till now, there is no standardized and satisfactory treatment strategy for Riehl’s melanosis. Objective In this pilot study, we evaluated the efficacy and safety of a novel combination therapy with oral administration of tranexamic acid (TA) and Glycyrrhizin compound for recalcitrant Riehl’s melanosis. Methods Ten patients with Riehl’s melanosis were recruited in this study. After elimination of potential contraindication, all patients were treated with 500 mg TA together with 150 mg Glycyrrhizin compound per day orally for 3 months, followed by 500 mg TA per day orally alone for another 3 months. Lesions were imaged by reflectance confocal microscopy (RCM), dermatoscopy, and VISIA® Complexion Analysis System monthly. Mexameter was adopted to evaluate Melanin Index (MI) and Erythema Index (EI). Clinical outcome scores were given by both physicians and patients. Results Seven out of ten patients received “marked improvement”, while two received “moderate improvement” and one “minimal improvement” at the final visit. Both mean MI and EI were significantly decreased compared with baselines. Furthermore, RCM and dermatoscopy analyses confirmed the improvement of pigmentation and erythema with decreased pigment granules and telangiectatic vessels. Conclusion Oral administration of TA in combination with Glycyrrhizin compound may be an effective therapy for Asian patients with recalcitrant Riehl’s melanosis.

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“…All the primary antibodies employed for Western blots were at a 1:1000 dilution. The chemical inhibitors used in this study, U73122 (cat# HY-13419), Gefitinib [28] (cat# HY-50895), and LY294002 [28] (cat# HY-10108), were provided by MedChemExpress (Monmouth Junction, NJ, USA). U73122 is an inhibitor that can specifically inhibit PLC-γ1 phosphorylation at Ser1248 [19,29].…”

Section: Antibodies and Reagentsmentioning

confidence: 99%

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

Qiu

Chang

et al. 2020

Viruses

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Accumulating studies have shown that the epidermal growth factor receptor (EGFR) signaling pathway plays an essential role in mediating cellular entry of numerous viruses. In this study, we report that bovine herpesvirus 1 (BoHV-1) productive infection in both the human lung carcinoma cell line A549 and bovine kidney (MDBK) cells leads to activation of EGFR, as demonstrated by the increased phosphorylation of EGFR at Tyr1068 (Y1068), which in turn plays important roles in virus infection. A time-of-addition assay supported that virus replication at post-entry stages was affected by the EGFR specific inhibitor Gefitinib. Interestingly, both phospholipase C-γ1 (PLC-γ1) and Akt, canonical downstream effectors of EGFR, were activated following virus infection in A549 cells, while Gefitinib could inhibit the activation of PLC-γ1 but not Akt. In addition, virus titers in A549 cells was inhibited by chemical inhibition of PLC-γ1, but not by the inhibition of Akt. However, the Akt specific inhibitor Ly294002 could significantly reduce the virus titer in MDBK cells. Taken together, our data suggest that PLC-γ1 is stimulated in part through EGFR for efficient replication in A549 cells, whereas Akt can be stimulated by virus infection independent of EGFR, and is not essential for virus productive infection, indicating that Akt modulates BoHV-1 replication in a cell type-dependent manner. This study provides novel insights on how BoHV-1 infection activates EGFR signaling transduction to facilitate virus replication.

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Oxidative stress and high-mobility group box 1 (HMGB1) protein release in vitiligo

Abstract: Linked Article: Kim et al. Br J Dermatol 2017; 176:1558–1568.

Cited by 11 publications

References 9 publications

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

A pilot study of oral tranexamic acid and Glycyrrhizin compound in the treatment of recalcitrant Riehl’s melanosis

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

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