Sulfatase 1 mediates the inhibitory effect of angiotensin II type 2 receptor inhibitor on angiotensin II-induced hypertensive mediator expression and proliferation in vascular smooth muscle cells from spontaneously hypertensive rats
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Background: Extracellular sulfatases (Sulfs), sulfatase 1 (Sulf1) and sulfatase 2 (Sulf2), play a pivotal role in cell signaling by remodeling the 6-O-sulfation of heparan sulfate proteoglycans on the cell surface. The present study examined the effects of Sulfs on angiotensin II (Ang II)-induced hypertensive mediator expression and vascular smooth muscle cells (VSMCs) proliferation in spontaneously hypertensive rats (SHR). Methods: Ang II receptors, 12-lipoxygenase (12-LO), and endothelin-1 (ET-1) messenger RNA (mRNA) expressions in SHR VSMCs were analyzed by real-time polymerase chain reaction and Western blotting. VSMCs proliferation was determined by [3H]-thymidine incorporation. Results: Basal Sulfs mRNAs expression and enzyme activity were elevated in SHR VSMCs. However, Sulfs had no effect on the basal or Ang II-induced 12-LO and ET-1 mRNA expression in SHR VSMCs. The inhibition of Ang II-induced 12-LO and ET-1 expression by blockade of the Ang II type 2 receptor (AT2 R) pathway was not observed in Sulf1 siRNA-transfected SHR VSMCs. However, Sulf2 did not affect the action of AT2 R inhibitor on Ang II-induced 12-LO and ET-1 expression in SHR VSMCs. The down-regulation of Sulf1 induced a reduction of AT2 R mRNA expression in SHR VSMCs. In addition, the inhibition of Ang II-induced VSMCs proliferation by blockade of the AT2 R pathway was mediated by Sulf1 in SHR VSMCs. Conclusion: These findings suggest that extracellular sulfatase Sulf1 plays a modulatory role in the AT2 R pathway that leads to an Ang II-induced hypertensive effects in SHR VSMCs.
Abstract
Background: Extracellular sulfatases (Sulfs), sulfatase 1 (Sulf1) and sulfatase 2 (Sulf2), play a pivotal role in cell signaling by remodeling the 6-O-sulfation of heparan sulfate proteoglycans on the cell surface. The present study examined the effects of Sulfs on angiotensin II (Ang II)-induced hypertensive mediator expression and vascular smooth muscle cells (VSMCs) proliferation in spontaneously hypertensive rats (SHR). Methods: Ang II receptors, 12-lipoxygenase (12-LO), and endothelin-1 (ET-1) messenger RNA (mRNA) expressions in SHR VSMCs were analyzed by real-time polymerase chain reaction and Western blotting. VSMCs proliferation was determined by [3H]-thymidine incorporation. Results: Basal Sulfs mRNAs expression and enzyme activity were elevated in SHR VSMCs. However, Sulfs had no effect on the basal or Ang II-induced 12-LO and ET-1 mRNA expression in SHR VSMCs. The inhibition of Ang II-induced 12-LO and ET-1 expression by blockade of the Ang II type 2 receptor (AT2 R) pathway was not observed in Sulf1 siRNA-transfected SHR VSMCs. However, Sulf2 did not affect the action of AT2 R inhibitor on Ang II-induced 12-LO and ET-1 expression in SHR VSMCs. The down-regulation of Sulf1 induced a reduction of AT2 R mRNA expression in SHR VSMCs. In addition, the inhibition of Ang II-induced VSMCs proliferation by blockade of the AT2 R pathway was mediated by Sulf1 in SHR VSMCs. Conclusion: These findings suggest that extracellular sulfatase Sulf1 plays a modulatory role in the AT2 R pathway that leads to an Ang II-induced hypertensive effects in SHR VSMCs.
참고문헌 (32)
- Buono M, "Sulfatase activities towards the regulation of cell metabolism and signaling in mammals", Cell Mol Life Sci, 67, pp.769~780 (2010)
- Sardiello M, "Sulfatases and sulfatase modifying factors: an exclusive and promiscuous relationship", Hum Mol Genet, 14, pp.3203~3217 (2005)
- Nagamine S, "Expression of a heparan sulfate remodeling enzyme, heparan sulfate 6-Oendosulfatase sulfatase FP2, in the rat nervous system", Brain Res Dev Brain Res, 159, pp.135~143 (2005)
- Morimoto-Tomita M, "Cloning and characterization of two extracellular heparin-degrading endosulfatases in mice and humans", J Biol Chem, 277(51), pp.49175~49185 (2002)
- Honke K, "Sulfotransferases and sulfated oligosaccharides", Med Res Rev, 22, pp.637~654 (2002)
- Langsdorf A, "Sulfs are regulators of growth factor signaling for satellite cell differentiation and muscle regeneration", Dev Biol, 311, pp.464~477 (2007)
- Dai Y, "HSulf-1 and HSulf-2 are potent inhibitors of myeloma tumor growth in vivo", J Biol Chem, 280(48), pp.40066~40073 (2005)
- Holst CR, "Secreted sulfatases Sulf1 and Sulf2 have overlapping yet essential roles in mouse neonatal survival", PLoS One, 2, pp.e575~ (2007)
- Ratzka A, "Redundant function of the heparan sulfate 6-O-endosulfatases Sulf1 and Sulf2 during skeletal development", Dev Dyn, 237, pp.339~353 (2008)
- Narita K, "HSulf-1 inhibits angiogenesis and tumorigenesis in vivo", Cancer Res, 66, pp.6025~6032 (2006)
- Zhang H, "HSULF-1 inhibits ERK and AKT signaling and decreases cell viability in vitro in human lung epithelial cells", Respir Res, 13, pp.69~ (2012)
- Morimoto-Tomita M, "Sulf-2, a proangiogenic heparan sulfate endosulfatase, is upregulated in breast cancer", Neoplasia, 7, pp.1001~1010 (2005)
- Uchimura K, "HSulf-2, an extracellular endoglucosamine-6-sulfatase, selectively mobilizes heparin-bound growth factors and chemokines: effects on VEGF, FGF-1, and SDF-1", BMC Biochem, 7, pp.2~ (2006)
- Heintz B, "Decreased glomerular basement membrane heparan sulfate proteoglycan in essential hypertension", Hypertension, 25, pp.399~407 (1995)
- Sala-Newby GB, "Regulation of vascular smooth muscle cell proliferation, migration and death by heparan sulfate 6-O-endosulfatase1", FEBS Lett, 579, pp.6493~6498 (2005)
- Kim HY, "Upregulation of interleukin-8", CXCL8 in vascular smooth muscle cells from spontaneously hypertensive rats, 2008, pp.31, 515~523
- 김정해, "Downregulation of Angiotensin II-Induced 12-Lipoxygenase Expression and Cell Proliferation in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats by CCL5", The Korean Journal of Physiology & Pharmacology, 13(5), pp.385~392 (2009), 대한약리학회
- Kim HY, "Reparixin, an inhibitor of CXCR1 and CXCR2 receptor activation, attenuates blood pressure and hypertension-related mediators expression in spontaneously hypertensive rats", Biol Pharm Bull, 34, pp.120~127 (2011)
- Otsuki S, "Expression of novel extracellular sulfatases Sulf-1and Sulf-2 in normal and osteoarthritic articular cartilage", Arthritis Res Ther, 10, pp.R61~ (2008)
- Tsai TT, "Increased sulfatase 1 gene expression in degenerative intervertebral disc cells", J Orthop Res, 33, pp.312~317 (2015)
- Sasaki M, "Elevated 12-lipoxygenase activity in the spontaneously hypertensive rat", Am J Hypertens, 10, pp.371~378 (1997)
- Wu R, "Enhanced superoxide anion formation in vascular tissues from spontaneously hypertensive and desoxycorticosterone acetate-salt hypertensive rats", J Hypertens, 19, pp.741~748 (2001)
- Kim HY, "Comparison of 12-lipoxygenase expression in vascular smooth muscle cells from old normotensive Wistar-Kyoto rats with spontaneously hypertensive rats", Hypertens Res, 36, pp.65~73 (2013)
- Horiuchi M, "Signaling mechanism of the AT2 angiotensin II receptor: crosstalk between AT1 and AT2 receptors in cell growth", Trends Endocrinol Metab, 10, pp.391~396 (1999)
- Guo F, "Role of angiotensin II type 1 receptor in angiotensin II-induced cytokine production in macrophages", J Interferon Cytokine Res, 31, pp.351~361 (2011)
- Kim HY, "CCL5 upregulates activation of AMP-activated protein kinases in vascular smooth muscle cells of spontaneously hypertensive rats", Cytokine, 67, pp.77~84 (2014)
- Kim HY, "Dimethylarginine dimethylaminohydrolase-1 mediates inhibitory effect of interleukin-10 on angiotensin II-induced hypertensive effects in vascular smooth muscle cells of spontaneously hypertensive rats", Cytokine, 77, pp.203~210 (2016)
- Kim HY, "Effect of CCL5 on dimethylarginine dimethylaminohydrolase-1 production in vascular smooth muscle cells from spontaneously hypertensive rats", Cytokine, 64, pp.227~233 (2013)
- Li J, "HSulf-1inhibits cell proliferation and invasion in human gastric cancer", Cancer Sci, 102, pp.1815~1821 (2011)
- Liu CT, "SULF1inhibits proliferation and invasion of esophageal squamous cell carcinoma cells by decreasing heparin-binding growth factor signaling", Dig Dis Sci, 58, pp.1256~1263 (2013)
- Yang JD, "Sulfatase 1 and sulfatase 2 in hepatocellular carcinoma: associated signaling pathways, tumor phenotypes, and survival", Genes Chromosomes Cancer, 50, pp.122~135 (2011)
- Lai JP, "Sulfatase 2 up-regulates glypican 3, promotes fibroblast growth factor signaling, and decreases survival in hepatocellular carcinoma", Hepatology, 47, pp.1211~1222 (2008)