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HYAL1 Is Downregulated in Idiopathic Pulmonary Fibrosis and Inhibits HFL-1 Fibroblast Proliferation When Upregulated
المؤلفون المشاركون
Leng, Dong
Huang, Xiaoxi
Yi, Jiawen
Zhao, Hongying
Zhang, Yuhui
المصدر
العدد
المجلد 2020، العدد 2020 (31 ديسمبر/كانون الأول 2020)، ص ص. 1-15، 15ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2020-03-11
دولة النشر
مصر
عدد الصفحات
15
التخصصات الرئيسية
الملخص EN
Background.
Idiopathic pulmonary fibrosis (IPF), the most common interstitial lung disease, arises from transforming growth factor beta 1- (TGFβ1-) induced aberrant fibroproliferation in response to epithelial injury.
The TGFβ1 antagonists—hyaluronidases (HYALs)—have been used to clinically treat pulmonary fibrosis.
This study focused on characterizing the effect of HYAL1, the main enzyme in hyaluronan degradation, on human lung fibroblast proliferation and apoptosis, and elucidating its potential underlying mechanism of action.
Methods.
We first performed microarray data mining of previously published gene expression datasets to identify key gene signatures in IPF lung tissues.
HYAL1 expression levels in IPF and normal lung tissues were then characterized using immunohistochemistry followed by real-time quantitative reverse transcription-PCR (qRT-PCR) and western blot analysis on isolated fibroblasts from fresh lung tissues of IPF and healthy donors.
A human fetal lung fibroblast HFL-1 cell line, which was used in place of primary lung fibroblasts, was used to assess the proliferative or apoptotic effects associated with lentiviral-induced HYAL1 overexpression using CCK-8 cell proliferation assay and Annexin V-APC staining.
The identification of potentially associated molecular pathways was performed using microarray analysis followed by qRT-PCR and western blot analysis.
Results.
Lung tissue microarray data mining and immunohistochemistry revealed significantly downregulation of HYAL1 in IPF lung tissue.
However, HYAL1 expression level in IPF fibroblasts was significantly upregulated at the mRNA level, but not altered at the protein level.
HYAL1 overexpression in HFL-1 fibroblasts reduced fibroproliferation modestly but did not promote apoptosis.
In addition, HYAL1 overexpression led to concomitant transcription factor downregulation, bone morphogenetic protein receptor 2 (BMPR2) signaling activation, but had no effect on TGFβ receptor 2 (TGFβR2) signaling.
Conclusions.
We showed that HYAL1 overexpression could prevent HFL-1 fibroproliferation.
Furthermore, our findings suggest that transcriptional regulators and BMP receptor signaling may be involved in HYAL1 modulation in IPF therapy.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Leng, Dong& Huang, Xiaoxi& Yi, Jiawen& Zhao, Hongying& Zhang, Yuhui. 2020. HYAL1 Is Downregulated in Idiopathic Pulmonary Fibrosis and Inhibits HFL-1 Fibroblast Proliferation When Upregulated. BioMed Research International،Vol. 2020, no. 2020, pp.1-15.
https://search.emarefa.net/detail/BIM-1133376
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Leng, Dong…[et al.]. HYAL1 Is Downregulated in Idiopathic Pulmonary Fibrosis and Inhibits HFL-1 Fibroblast Proliferation When Upregulated. BioMed Research International No. 2020 (2020), pp.1-15.
https://search.emarefa.net/detail/BIM-1133376
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Leng, Dong& Huang, Xiaoxi& Yi, Jiawen& Zhao, Hongying& Zhang, Yuhui. HYAL1 Is Downregulated in Idiopathic Pulmonary Fibrosis and Inhibits HFL-1 Fibroblast Proliferation When Upregulated. BioMed Research International. 2020. Vol. 2020, no. 2020, pp.1-15.
https://search.emarefa.net/detail/BIM-1133376
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1133376
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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