دورية أكاديمية

Downregulation of β-catenin blocks fibrosis via Wnt2 signaling in human keloid fibroblasts

التفاصيل البيبلوغرافية
العنوان: Downregulation of β-catenin blocks fibrosis via Wnt2 signaling in human keloid fibroblasts
المؤلفون: Yumei Cai, Shize Zhu, Weiqun Yang, Mingmeng Pan, Chaoyang Wang, Wenyi Wu
المصدر: Tumor Biology, Vol 39 (2017)
بيانات النشر: IOS Press, 2017.
سنة النشر: 2017
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
مصطلحات موضوعية: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
الوصف: Keloid is a disorder of fibroproliferative diseases that occurs in wounds, characterized by an exaggerated response to injury. The key factor responsible for the disease process has not been identified. This study sought to elucidate the role of β-catenin in the regulation of keloid phenotypes and signaling. Expression of β-catenin in keloid and normal non-keloid samples was measured by real-time polymerase chain reaction. Knockdown of β-catenin was achieved by delivering small interfering RNA to target β-catenin. Cell proliferation, cell cycle progression, and apoptosis of keloid cells were measured by functional assays in vitro. The proteins related to keloid fibrosis were measured by Western blotting. β-catenin expression was significantly upregulated in keloid tissue samples compared with the normal non-keloid age-adjusted skin sample counterparts. Functionally, targeting β-catenin with lipofection-delivered small interfering RNA oligonucleotide inhibited the proliferation and cell cycle arrest in G0/G1 phase and increased apoptosis of fibroblast cells, accompanied by downregulation of Wnt2 and cyclin D1 as well as the phosphorylation level of glycogen synthase kinase 3 beta in the keloid fibrosis. Our study supports a crucial role of β-catenin in the regulation of fibroproliferation and extracellular matrix deposition. Targeting β-catenin using small interfering RNA oligonucleotide may be a promising approach for preventing excessive fibroproliferative development after wound healing and may lead to the development of novel strategies for restoring keloid diseases.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1423-0380
10104283
Relation: https://doaj.org/toc/1423-0380
DOI: 10.1177/1010428317707423
URL الوصول: https://doaj.org/article/090299243058433a92ae4890c6e9363f
رقم الأكسشن: edsdoj.090299243058433a92ae4890c6e9363f
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14230380
10104283
DOI:10.1177/1010428317707423