Repigmentation by combined narrow‑band ultraviolet B/adipose‑derived stem cell transplantation in the mouse model: Role of Nrf2/HO‑1‑mediated Ca<sup>2+</sup> homeostasis

Bian, Yuanyuan; Yu, Hao; Jin, Mingzhu; Gao, Xing‐Hua

doi:10.3892/mmr.2021.12522

Cited by 9 publications

(8 citation statements)

References 33 publications

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“…By comparing the existing vitiligo models, it was found that MBEH-induced depigmentation models were most similar in terms of phenotype and pathological mechanism. Due to the influence of the hair follicle cycle, the model of MBEH reported in the literature was modified, and 40% MBEH was applied [ 48 ]. On this basis, CUMS was also administered to construct the vitiligo model induced by chronic mental stress ( Figure 2 A).…”

Section: Discussionmentioning

confidence: 99%

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Dong

Lai

Zhang

et al. 2023

IJMS

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Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.

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Section: Discussionmentioning

confidence: 99%

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Dong

Lai

Zhang

et al. 2023

IJMS

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“…There was only one trial to use the combination of ADSCs injection and NB-UVB conducted on mice that had induced vitiligo by monobenzone and concluded that clinically, there was significant reduction in vitiligo patches confirmed by presence of cellular infiltration and acanthosis by histopathological examination [14].…”

Section: Discussionmentioning

confidence: 99%

Adipose Derived Stem Cells in the Treatment of Vitiligo

Fahmy¹,

Elfar²,

Shaker³

et al. 2022

JAMMR

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Background: Vitiligo is an acquired skin disorder with challenging treatment options. Adipose-derived stem cells can stimulate the differentiation of the adjacent cells into specialized cells owing to the effect of several growth factors. They may be able to differentiate into melanocyte precursors. Objective: To detect the safety and effectiveness of ADSCs in the vitiligo treatment. Methods: We recruited 15 patients in this study with stable vitiligo which is resistant to the ordinary methods of treatment. The injection of ADSCs was done in single session then followed by narrow band-UVB sessions twice weekly and the patients were assessed clinically after three months. Results: The median percentage of re-pigmentation was 60%, while regarding the degree of improvement, 26-6% of patients showed excellent and 33.3% of patients had good responses. 53.3% of patients did not have any side effects while other patients experienced minimal side effects. Conclusion: ADSCs could be a promising and safe alternative treatment for resistant vitiligo cases.

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“…Rapid Ca2+ release through a well-connected network of ER tubules, 32 which links the function of ER to its structure. Disruption of ER homeostasis disturbs Ca 2+ signaling, which in turn activates accumulation of unfolded or incompletely folded proteins in the ER lumen 33 (details shown in 1.3 and 1.4). These structural and functional alterations of the ER could be seen as stages in the initiation and progression of cell damages in vitiligo.…”

Section: Ermentioning

confidence: 99%

“…The possible mechanism is related to the inhibition of ERS and regulation of ER Ca2+ homeostasis through Nrf2/HO-1 signaling. 99 These studies and action mechanisms are summarized in Table 1 . It indicated that some classical therapy might combine with other emerging approaches, which could achieve therapeutic effects far beyond themselves by targeting ER.…”

Section: Clinical Treatmentsmentioning

confidence: 99%

Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis

Xie,

Wu,

Tang

et al. 2024

CCID

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The endoplasmic reticulum (ER) is the main site of protein synthesis, transport, and modification. Its abnormal status has now emerged as an established cause of many pathological processes, such as tumors and autoimmune diseases. Recent studies also demonstrated that the defective functions of ER may lead to pigmentary diseases. Vitiligo is a depigmenting ailment skin disorder whose pathogenesis is now found to be associated with ER. However, the detailed mechanism is still unclear. In this review, we try to link the association between ER with its inter- and intra-organellar interactions in vitiligo pathogenesis and focus on the function, mechanism, and clinical potential of ER with vitiligo. Expand ER is found in melanocytes of vitiligo and ER stress (ERS) might be a bridge between oxidative stress and innate and adaptive immunity. Meanwhile, the tight association between ER and mitochondria or melanosomes in organelles levels, as well as genes and cytokines, is the new paradigm in the pathogenesis of vitiligo. This undoubtedly adds a new aspect to the understanding of vitiligo, facilitating the design of targeted therapies for vitiligo.

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Repigmentation by combined narrow‑band ultraviolet B/adipose‑derived stem cell transplantation in the mouse model: Role of Nrf2/HO‑1‑mediated Ca²⁺ homeostasis

Cited by 9 publications

References 33 publications

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Adipose Derived Stem Cells in the Treatment of Vitiligo

Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis

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Repigmentation by combined narrow‑band ultraviolet B/adipose‑derived stem cell transplantation in the mouse model: Role of Nrf2/HO‑1‑mediated Ca2+ homeostasis

Cited by 9 publications

References 33 publications

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Adipose Derived Stem Cells in the Treatment of Vitiligo

Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis

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Product

Resources

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Repigmentation by combined narrow‑band ultraviolet B/adipose‑derived stem cell transplantation in the mouse model: Role of Nrf2/HO‑1‑mediated Ca²⁺ homeostasis