Corticotropin-releasing hormone attenuates vascular endothelial growth factor release from human HaCaT keratinocytes

Corticotropin-releasing hormone (CRH) is a central component of the local hypothalamic-pituitary-adrenal (HPA) axis, which has a functional equivalent in the skin. To determine whether CRH and its receptor, CRH-R1, modulate the expression of vascular endothelial growth factor (VEGF), which is overex...

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Bibliographic Details
Published in:Regulatory peptides 2010-02, Vol.160 (1), p.115-120
Main Authors: Zhou, Chun-Lei, Yu, Xiao-Jing, Chen, La-Mei, Jiang, Hong, Li, Chun-Yang
Format: Article
Language:English
Subjects:
Biological and medical sciences
Blotting, Western
Cell Line
Corticotropin-releasing hormone
Corticotropin-Releasing Hormone - pharmacology
Fundamental and applied biological sciences. Psychology
HaCaT keratinocyte
Humans
Keratinocytes - drug effects
Mitogen-activated protein kinase
Mitogen-Activated Protein Kinase Kinases - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Signal Transduction
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A - genetics
Vascular Endothelial Growth Factor A - metabolism
Vertebrates: endocrinology
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Summary:Corticotropin-releasing hormone (CRH) is a central component of the local hypothalamic-pituitary-adrenal (HPA) axis, which has a functional equivalent in the skin. To determine whether CRH and its receptor, CRH-R1, modulate the expression of vascular endothelial growth factor (VEGF), which is overexpressed in psoriatic epidermis and plays a causal role in the pathogenesis of psoriasis, we investigated the effect of CRH on the expression of VEGF in a human keratinocyte cell line (HaCaT) and whether this effect is via the mitogen-activated protein kinase (MAPK) signal transduction pathways. Real-time RT-PCR, ELISA assay and western blot were used in the present study to investigate the expression of VEGF in CRH-treated HaCaT cells. The mRNA and protein levels of VEGF in CRH-treated HaCaT cells were significantly attenuated. However, this downregulation was abrogated by pretreatment with antalarmin, SB203580 and SP600125; pretreatment with PD98059 did not attenuate the effects of CRH on the expression of VEGF. In addition, CRH treatment induced rapid phosphorylation of p38 MAPK and JNK1/2, and antalarmin, SB203580 and SP600125 inhibited CRH-induced phosphorylation of p38 MAPK and JNK1/2. CRH might downregulate the expression of VEGF through the CRH-R1 and MAPK (p38 MAPK and JNK1/2) signaling pathways in human HaCaT cells.
ISSN:0167-0115
1873-1686
DOI:10.1016/j.regpep.2009.10.001