钙激活氯离子通道相关蛋白 rCLCA2 在大鼠表皮中广泛表达,促进细胞凋亡,并被 UVB 下调。
The calcium-activated chloride channel-associated protein rCLCA2 is expressed throughout rat epidermis, facilitates apoptosis and is downmodulated by UVB.
机构信息
Institute of Biomedicine/Anatomy, University of Eastern Finland, P.O. Box 1627, N70211, Kuopio, Finland.
Department of Environmental and Biological Sciences, University of Eastern Finland, P.O. Box 1627, N70211, Kuopio, Finland.
出版信息
Histochem Cell Biol. 2021 May;155(5):605-615. doi: 10.1007/s00418-021-01962-5. Epub 2021 Jan 23.
The rodent chloride channel regulatory proteins mCLCA2 and its porcine and human homologues pCLCA2 and hCLCA2 are expressed in keratinocytes but their localization and significance in the epidermis have remained elusive. hCLCA2 regulates cancer cell migration, invasion and apoptosis, and its loss predicts poor prognosis in many tumors. Here, we studied the influences of epidermal maturation and UV-irradiation (UVR) on rCLCA2 (previous rCLCA5) expression in cultured rat epidermal keratinocytes (REK) and correlated the results with mCLCA2 expression in mouse skin in vivo. Furthermore, we explored the influence of rCLCA2 silencing on UVR-induced apoptosis. rClca2 mRNA was strongly expressed in REK cells, and its level in organotypic cultures remained unchanged during the epidermal maturation process from a single cell layer to fully differentiated, stratified cultures. Immunostaining confirmed its uniform localization throughout the epidermal layers in REK cultures and in rat skin. A single dose of UVR modestly downregulated rClca2 expression in organotypic REK cultures. The immunohistochemical staining showed that CLCA2 localized in basal and spinous layers also in mouse skin, and repeated UVR induced its partial loss. Interestingly, silencing of rCLCA2 reduced the number of apoptotic cells induced by UVR, suggesting that by facilitating apoptosis, CLCA2 may protect keratinocytes against the risk of malignancy posed by UVB-induced corrupt DNA.
啮齿动物氯离子通道调节蛋白 mCLCA2 及其猪和人同源物 pCLCA2 和 hCLCA2 表达在角质形成细胞中,但它们在表皮中的定位和意义仍不清楚。hCLCA2 调节癌细胞的迁移、侵袭和凋亡,其缺失预示着许多肿瘤的预后不良。在这里,我们研究了表皮成熟和紫外线照射 (UVR) 对培养的大鼠表皮角质形成细胞 (REK) 中 rCLCA2(以前的 rCLCA5)表达的影响,并将结果与体内小鼠皮肤中 mCLCA2 的表达相关联。此外,我们还探讨了 rCLCA2 沉默对 UVR 诱导的细胞凋亡的影响。rClca2 mRNA 在 REK 细胞中强烈表达,并且其在从单层细胞到完全分化的层状培养的表皮成熟过程中的水平保持不变。免疫染色证实其在 REK 培养物和大鼠皮肤中的表皮层中均匀定位。单次 UVR 照射适度下调了器官型 REK 培养物中的 rClca2 表达。免疫组织化学染色显示 CLCA2 定位于基底和棘层,也存在于小鼠皮肤中,并且重复 UVR 诱导其部分丢失。有趣的是,rCLCA2 的沉默减少了 UVR 诱导的凋亡细胞数量,表明通过促进凋亡,CLCA2 可能保护角质形成细胞免受 UVB 诱导的腐败 DNA 引起的癌变风险。