The expression levels of Notch-related signaling molecules in pulmonary microvascular endothelial cells in bleomycin-induced rat pulmonary fibrosis

Title:

The expression levels of Notch-related signaling molecules in pulmonary microvascular endothelial cells in bleomycin-induced rat pulmonary fibrosis

Creator:

Yin, Q., Wang, W., Cui, G., Nan, H., Yan, L., Zhang, W., Zhang, S., and Wei, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:aa9a55f1-7b86-42e1-a0b5-e71c34bc238f
uuid:aa9a55f1-7b86-42e1-a0b5-e71c34bc238f
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, plicní fibróza, pulmonary fibrosis, Notch1, Jagged1, Dll4, beomycin, pulmonary microvascular endothelial cells, 14, and 612

Type:

article, články, journal articles, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Previous studies have suggested that the Notch signaling pathway plays a very important role in the proliferation and differentiation of pulmonary microvascular endothelial cells (PMVECs). Therefore, we aimed to investigate the expression level of Notch-related signaling molecules in PMVECs in bleomycin (BLM)-induced rat pulmonary fibrosis. Immunohistochemistry, immunofluorescence, Western blotting, and real-time PCR were used to analyze the differences in protein and mRNA expression levels of Notch-related signaling molecules, i.e. Notch1, Jagged1, Delta-like ligand 4 (Dll4), and hairy and enhancer of split homolog 1 (Hes1), between a control group treated with intratracheal instillation of saline and a study group treated with intratracheal instillation of BLM solution. Expression levels of the receptor Notch1 and one of its ligands, Jagged1, were upregulated, while the expression levels of the ligand Dll4 and the target molecule of the Notch signaling pathway, Hes1, were downregulated. The differences in protein and mRNA expression levels between the control and study groups were significant (p<0.001). The Jagged1/Notch1 signaling pathway is activated in the pathogenesis of BLM-induced rat pulmonary fibrosis, while the Dll4/Notch1 signaling pathway is inhibited, which inhibits the suppressive effect of Dll4/Notch1 signaling on PMVEC overproliferation, further causing PMVEC dysfunction in cell sprouting and maturation as well as abnormal differentiation of the cell phenotype. Conversely, the downexpression of Hes1 indicates that the Jagged1/Notch1 signaling pathway could be a non-canonical Notch signaling pathway independent of Hes1 activation, which differs from the canonical Dll4/Notch1 signaling pathway., Q. Yin, W. Wang, G. Cui, H. Nan, L. Yan, W. Zhang, S. Zhang, J. Wei., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:2

Harvested from:

CDK

Metadata only:

false