Abdou Asmaa Gaber, Farag Azza G A, Hammam Moustafa, Taie Doha Maher, Abdelaziz Reem Ahmed
a Pathology Departments, Faculty of Medicine , Menoufia University , Shebein Elkom , Egypt.
b Dermatology Departments, Faculty of Medicine , Menoufia University , Shebein Elkom , Egypt.
J Immunoassay Immunochem. 2018;39(3):249-262. doi: 10.1080/15321819.2018.1472605. Epub 2018 May 17.
Psoriasis is characterized by excessive cell proliferation, angiogenesis, and regions of hypoxia. Hypoxia stimulates production of hypoxia inducible factors (HIFs) such as HIF1α. The aim of the present study is to investigate the possible role of HIF1α in pathogenesis of psoriasis and to correlate its expression with angiogenesis and proliferation in involved and uninvolved skin in patients with plaque psoriasis using CD34 and Ki-67. The current study was performed on 40 skin specimens of patients presented with chronic plaque psoriasis both involved and uninvolved together with 40 specimens from age- and sex-matched healthy volunteers as a control group. The specimens were submitted for HIF1α, CD34, and Ki-67 immunostaining. HIF1α was expressed in 37.5% of normal skin with mild intensity and cytoplasmic localization instead of its expression in 72.5% and 100% of uninvolved and involved psoriatic skin, respectively. Nucleocytoplasmic pattern of HIF1α was seen in 34.5% and 37.5% of uninvolved and involved psoriatic skin, respectively. Positive and intense expression of HIF1α as well as its nucleocytoplasmic localization were significantly in favor of psoriatic skin either involved or uninvolved in comparison to normal skin (P < 0.05). Intense HIF1α was significantly associated with microvessel density in both involved and uninvolved skin (P < 0.05). Nucleocytoplasmic pattern was significantly associated with epidermal acanthosis (P < 0.05) and tended to be associated with percentage of Ki-67 of psoriatic skin (P = 0.06). The present study demonstrated that HIF1α is upregulated in the skin of psoriatic cases (involved and uninvolved) compared to normal skin indicating its role in pathogenesis of psoriasis especially its active nuclear form that showed an association with angiogenesis and proliferation.
银屑病的特征是细胞过度增殖、血管生成以及缺氧区域。缺氧会刺激缺氧诱导因子（HIFs）如HIF1α的产生。本研究的目的是探讨HIF1α在银屑病发病机制中的可能作用，并使用CD34和Ki-67将其在斑块状银屑病患者受累和未受累皮肤中的表达与血管生成和增殖相关联。本研究对40例慢性斑块状银屑病患者的皮肤标本（包括受累和未受累的）以及40例年龄和性别匹配的健康志愿者的标本作为对照组进行。将标本进行HIF1α、CD34和Ki-67免疫染色。HIF1α在37.5%的正常皮肤中呈轻度表达且定位于细胞质，而在未受累和受累银屑病皮肤中的表达分别为72.5%和100%。HIF1α的核质模式分别在34.5%和37.5%的未受累和受累银屑病皮肤中可见。与正常皮肤相比，HIF1α的阳性和强表达及其核质定位在受累或未受累的银屑病皮肤中均显著占优势（P<0.05）。在受累和未受累皮肤中，强HIF1α均与微血管密度显著相关（P<0.05）。核质模式与表皮棘皮症显著相关（P<0.05），并且倾向于与银屑病皮肤的Ki-67百分比相关（P=0.06）。本研究表明，与正常皮肤相比，银屑病患者（受累和未受累）皮肤中的HIF1α上调，表明其在银屑病发病机制中的作用，尤其是其活性核形式与血管生成和增殖相关。
