17beta-estradiol enhances vascular endothelial growth factor production and dihydrotestosterone antagonizes the enhancement via the regulation of adenylate cyclase in differentiated THP-1 cells

J Invest Dermatol. 2002 Mar;118(3):519-29. doi: 10.1046/j.0022-202x.2002.01672.x.

Abstract

We studied the in vitro effects of sex hormones on vascular endothelial growth factor (VEGF) production in differentiated THP-1 monocytic cells. Phorbol-12-myristate-13-acetate differentiated THP-1 into macrophage-like cells. 17beta-estradiol (10 (-9) M) increased VEGF secretion of controls 3.1-fold in differentiated THP-1 and this effect of 17beta-estradiol was antagonized by dihydrotestosterone, although dihydrotestosterone alone did not alter VEGF secretion. 17beta-estradiol increased steady-state mRNA level of VEGF and the increase was counteracted by dihydrotestosterone in differentiated THP-1, although dihydrotestosterone alone did not alter the VEGF mRNA level. Progesterone did not affect the constitutive and 17beta-estradiol-induced VEGF secretion and mRNA level. Transient transfection revealed that 17beta-estradiol enhanced chloramphenicol acetyl transferase expression driven by VEGF promoter and the enhancement was antagonized by dihydrotestosterone. Adenylate cyclase inhibitor suppressed 17beta-estradiol-induced enhancement of VEGF secretion, mRNA level, and promoter activity, whereas dihydrotestosterone-induced suppression on the effects of 17beta-estradiol was counteracted by 3',5'-adenosine cyclic monophosphate (cAMP) analog. 17beta-estradiol increased intracellular cAMP level by activating adenylate cyclase, while dihydrotestosterone reduced the basal and 17beta-estradiol-increased cAMP level by inhibiting adenylate cyclase. Transfection with 5'-deleted VEGF promoters demonstrated that the region between -88 and -66 bp may be involved in the transcriptional regulation by each hormone. The mutation within activator protein-2 element in this region abrogated the transcriptional stimulation and repression by the respective hormones. 17beta-estradiol activated transcription from activator protein-2-responsive reporter plasmid while dihydrotestosterone antagonized the effect of 17beta-estradiol. These results suggest that 17beta-estradiol enhances VEGF production while dihydrotestosterone antagonizes the effect of 17beta-estradiol via up- or downregulation of adenylate cyclase in differentiated THP-1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenylyl Cyclases / metabolism*
  • Cell Differentiation / physiology
  • Cell Division / physiology
  • Cell Line
  • Culture Media, Conditioned / pharmacology
  • Cyclic AMP / physiology
  • DNA-Binding Proteins / physiology
  • Dihydrotestosterone / pharmacology*
  • Endothelial Growth Factors / antagonists & inhibitors*
  • Endothelial Growth Factors / biosynthesis*
  • Endothelial Growth Factors / genetics
  • Endothelial Growth Factors / physiology
  • Endothelium, Vascular / cytology
  • Estradiol / pharmacology*
  • Humans
  • Intracellular Membranes / metabolism
  • Lymphokines / antagonists & inhibitors*
  • Lymphokines / biosynthesis*
  • Lymphokines / genetics
  • Lymphokines / physiology
  • Monocytes / cytology*
  • Monocytes / drug effects
  • Monocytes / metabolism*
  • Phosphoric Diester Hydrolases / metabolism
  • Progesterone / pharmacology
  • Promoter Regions, Genetic / drug effects
  • Promoter Regions, Genetic / physiology
  • RNA, Messenger / metabolism
  • Transcription Factor AP-2
  • Transcription Factors / physiology
  • Transcription, Genetic / drug effects
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Substances

  • Culture Media, Conditioned
  • DNA-Binding Proteins
  • Endothelial Growth Factors
  • Lymphokines
  • RNA, Messenger
  • Transcription Factor AP-2
  • Transcription Factors
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Dihydrotestosterone
  • Progesterone
  • Estradiol
  • Cyclic AMP
  • Phosphoric Diester Hydrolases
  • Adenylyl Cyclases