Skip to main content
. Author manuscript; available in PMC: 2016 Nov 17.
Published in final edited form as: J Mol Endocrinol. 2015 Aug 4;55(2):133–146. doi: 10.1530/JME-15-0124

Table 1.

Summary of major findings on GR expression regulation in HUVECs



Figure 1: GR mRNA isoform levels Resistant cells have higher expression of GR isoforms 1C and 1D, and lower expression of
isoform 1F than sensitive cells in basal conditions.
Dexamethasone-treatment downregulated 5′UTR mRNA isoform 1C and 3′UTR mRNA
isoform α in resistant cells only.
Figure 2: Effect of GR-1Cα
Overexpression
GR-1Cα overexpression in resistant cells did not improve in vitro response to dexamethasone
as determined by NOS3 downregulation, SERPINE1 upregulation, and decreases in aPTT.
GR-1Cα overexpression further downregulated the expression of 5′UTR mRNA isoforms 1B
(in resistant cells only) and 1H in both sensitivity groups.
Figure 3: GR promoter activity There were no significant differences in basal GR promoter (unmethylated) activity between
sensitive and resistant cells.
Dexamethasone treatment decreased promoter 1F activity in both sensitivity groups,
decreased promoter 1B activity in resistant cells only and increased promoter 1D activity in
sensitive cells only.
Promoter activity differences between sensitive and resistant cells did not correlate with
differences in GR 5′UTR mRNA levels.
Figure 4: GR promoter methylation
and AZA treatment
Sensitive cells have higher promoter 1D methylation levels and lower promoter 1F and 1H
methylation levels compared to resistant cells.
Promoter methylation levels correlated with GR 5′UTR mRNA levels.
AZA treatment upregulated the expression of all GR mRNA isoforms except isoform 1D in
resistant cells.
AZA treatment improved in vitro dexamethasone response in resistant cells as determined
by NOS3 downregulation and SERPINE1 upregulation.