Dermatology and Venereology Department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt.
Pathology Department, Faculty of Medicine, Menoufia University, Shebin El Kom, Egypt.
Clin Exp Dermatol. 2021 Jul;46(5):851-860. doi: 10.1111/ced.14554. Epub 2021 Feb 5.
Abnormal autophagy is known to be associated with the pathogenesis of some skin disorders. The protein Beclin1 plays a central role in the machinery of autophagy.
To assess the expression of Beclin1 in psoriasis, using immunohistochemical study in lesional and perilesional skin in patients with psoriasis, and to compare the results with those of an apparently healthy control (HC) group.
This case-control study enrolled a total of 40 participants: 20 patients with chronic plaque psoriasis and 20 age- and sex-matched, apparently HCs. Skin biopsies were taken from (i) lesional and (ii) perilesional skin of patients with psoriasis and from (iii) normal skin of HCs for immunohistochemical evaluation of Beclin1 expression.
Epidermal Beclin1 expression was positive in all three studied groups. There was a significant difference between the three studied groups regarding Beclin1 epidermal topographic distribution, epidermal staining intensity, H score and H-score category (P < 0.01 for all). Significant differences were found between the three studied groups regarding Beclin1 H score and H-score category for skin adnexal structures (P < 0.01 for both). For dermal inflammatory infiltrate, significant differences were found between lesional and perilesional skin regarding Beclin1 expression status, staining intensity, H score and H-score category (P < 0.01, P = 0.01, P < 0.01 and P < 0.03, respectively).
The increased expression of Beclin1 in psoriatic skin, both lesional and perilesional, reflects increased autophagy, which could be a consequence of the rapid keratinocyte proliferation in psoriasis, which would also ramp up all the cellular processes including autophagy. The cellular localization of Beclin1 was nucleocytoplasmic in psoriasis skin but cytoplasmic only in normal HC skin, which needs further study to allow its interpretation.
异常自噬与一些皮肤疾病的发病机制有关。Beclin1 蛋白在自噬机制中起核心作用。
通过免疫组织化学研究，评估银屑病皮损和皮损旁皮肤中 Beclin1 的表达，并将结果与明显健康对照（HC）组进行比较。
这项病例对照研究共纳入 40 名参与者：20 名慢性斑块状银屑病患者和 20 名年龄和性别匹配的明显健康对照者。对银屑病患者的（i）皮损和（ii）皮损旁皮肤以及（iii）HC 的正常皮肤进行皮肤活检，用于 Beclin1 表达的免疫组织化学评估。
所有三组的表皮 Beclin1 表达均为阳性。三组间 Beclin1 表皮拓扑分布、表皮染色强度、H 评分和 H 评分类别均存在显著差异（所有 P 值均<0.01）。三组间皮肤附属结构的 Beclin1 H 评分和 H 评分类别也存在显著差异（均 P 值<0.01）。对于真皮炎症浸润，在 Beclin1 表达状态、染色强度、H 评分和 H 评分类别方面，皮损与皮损旁皮肤之间存在显著差异（均 P 值<0.01、P 值=0.01、P 值<0.01 和 P 值<0.03）。
银屑病皮损和皮损旁皮肤中 Beclin1 的表达增加，反映了自噬增加，这可能是银屑病中角质形成细胞快速增殖的结果，也会加速包括自噬在内的所有细胞过程。银屑病皮肤中 Beclin1 的细胞定位为核质，而正常 HC 皮肤中仅为细胞质，这需要进一步研究以允许对其进行解释。
