Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P10145 (
IL-8
)
23,849
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The extracellular sulfatases (Sulfs),
sulfatase 1
(Sulf1) and sulfatase 2 (Sulf2), have an important role in cell signaling by modulating the 6-O-sulfation of heparan sulfate proteoglycans (HSPGs) on the cell surface. Gene expression and enzyme activity of Sulfs are elevated in hypertensive vascular smooth muscle cells (VSMCs) compared to those in normotensive VSMCs. CXC-chemokine ligand (CXCL) 8 has a pathogenic role in the development and progression of hypertension. In this study, we investigated the effect of Sulfs on the expression of
CXCL8
-induced endothelin (ET)-1, a hypertensive mediator, in VSMCs from spontaneously hypertensive rats (SHR). Expression of ET-1 and elevation of angiotensin (Ang) II-induced ET-1 expression by
CXCL8
were reduced in Sulf2 small interfering RNA (siRNA)-transfected SHR VSMCs. But, downregulation of Sulf1 did not affect the expression of
CXCL8
-induced ET-1 and additive effect of
CXCL8
on Ang II-induced ET-1 expression in SHR VSMCs.
CXCL8
-induced ET-1 expression and the additive effect of
CXCL8
on Ang II-induced ET-1 expression were dependent on the Ang II type 1 receptor (AT
1
R) pathway, not the Ang II type 2 receptor (AT
2
R) pathway. In addition, downregulation of Sulf2 reduced the expression of
CXCL8
-induced AT
1
R and abrogated the additive effect of
CXCL8
on Ang II-induced AT
1
R expression in SHR VSMCs. Sulf2 mediated, partially, the expression of ET-1 and the additive expression of Ang II-induced ET-1 mRNA by
CXCL8
via the AT
1
R pathway in SHR VSMCs. These findings suggest that Sulf2 is an up-regulatory factor in the additive action of
CXCL8
via the AT
1
R pathway on Ang II-induced ET-1 expression in VSMCs under hypertension environment.
...
PMID:Sulfatase 2 mediates, partially, the expression of endothelin-1 and the additive effect of Ang II-induced endothelin-1 expression by CXCL8 in vascular smooth muscle cells from spontaneously hypertensive rats. 3047 Jun 61
