Upregulation of Interleukin-8/CXCL8 in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats

Kim, Hyo Young; Kang, Young Jin; Song, In‐Hwan; Choi, Hyung Chul; Kim, Hee Sun

doi:10.1291/hypres.31.515

Cited by 47 publications

(39 citation statements)

References 36 publications

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“…VSMCs were obtained from the thoracic aortas of 12-16 week-old-male SHR and WKY using the explant method as described by Kim et al 8 VSMCs were cultured in Dulbecco's modified Eagle's medium, which was supplemented with 10% fetal bovine serum and 1% penicillin-streptomycin. Cells were detached with 0.25% trypsin/EDTA and seeded onto 75-cm 2 tissue culture flasks at a density of 10 5 cells ml À1 .…”

Section: Vsmcs Preparationmentioning

confidence: 99%

“…22 Some chemokines upregulate Ang II-induced hypertension and a high expression of chemokines has been detected in VSMCs isolated from spontaneously hypertensive rats (SHR). [8][9][10][11] The increase of chemokine CCL2 or CXCL8 expression by Ang II has been shown in SHR VSMCs and rat glomerular endothelial cells. 6,8,9,23,24 The increase of CCL5 expression by Ang II has been also demonstrated in rat glomerular endothelial cells and the renal cortex.…”

Section: Introductionmentioning

confidence: 97%

“…[8][9][10][11] The increase of chemokine CCL2 or CXCL8 expression by Ang II has been shown in SHR VSMCs and rat glomerular endothelial cells. 6,8,9,23,24 The increase of CCL5 expression by Ang II has been also demonstrated in rat glomerular endothelial cells and the renal cortex. 2,3 However, CCL5 has been shown to inhibit the expression of Ang II-induced 12-lipoxygenase (LO), a hypertensive modulator in SHR VSMCs.…”

Section: Introductionmentioning

confidence: 97%

“…In addition, Ang II has been shown to function as a potential mediator of inflammation and was reported to exert some of its effects on the vasculature by stimulating chemokines. [1][2][3][4][5][6][7] Chemokines have an important role in Ang II-induced vascular hypertension, [8][9][10][11] and controlling chemokine production is important for regulating inflammatory reactions in hypertensive vascular walls. In fact, the suppression of chemokine-induced inflammatory cell infiltration has been shown to ameliorate hypertension in experimental animal models.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 However, CCL5 has been shown to inhibit the expression of Ang II-induced 12-lipoxygenase (LO), a hypertensive modulator in SHR VSMCs. 25 Although the relationships between Ang II and some chemokines or chemokine receptors, including CCL2 and CXCL8, in renal disease and vascular hypertension have been studied, 4,8,9,23,24 the relationship between Ang II and CCL5 has not yet been characterized and little is known in SHR VSMCs. Therefore, as a first step to understand the relationship between Ang II and CCL5 in Ang II-induced vascular hypertension, the effect of Ang II on CCL5 expression was evaluated in SHR VSMCs.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

et al. 2011

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Angiotensin II (Ang II) exerts some of its effects on the vasculature by stimulating chemokines and 12-lipoxygenase (12-LO). In addition, a high expression of chemokines by Ang II has been observed in vascular smooth muscle cells (VSMCs) in spontaneously hypertensive rats (SHR). In this study, the action mechanism of Ang II on CCL5 expression in SHR VSMCs was examined. Expression of CCL5 in SHR thoracic aorta tissues and VSMCs was lower than that in normotensive Wistar-Kyoto rats (WKY) thoracic aorta tissues and VSMCs. Moreover, Ang II inhibited CCL5 expression in SHR VSMCs, but not in WKY VSMCs. Inhibition of CCL5 by Ang II was mediated by both Ang II subtype 1 receptor (AT 1 R) and subtype 2 receptor (AT 2 R) activation in SHR VSMCs. However, Ang II did not inhibit CCL5 expression in SHR VSMCs that were transfected with 12-LO small interfering RNA. In addition, 12-LO metabolite, 12(S)-hydroxyeicosatetraenoic acid (HETE) inhibited CCL5 mRNA expression in SHR VSMCs. The expression of Ang II-induced 12-LO was also blocked by both AT 1 R and AT 2 R inhibitors. Mitogen-activated protein (MAP) kinase, extracellular signal-regulated kinase (ERK)1/2, p38 and Jun N-terminal kinase pathways all mediated the inhibitory action of Ang II on CCL5 expression in SHR VSMCs. Taken together, the inhibitory action of Ang II on CCL5 expression was shown to be mediated by the 12-LO pathway through the activation of both of AT 1 R and AT 2 R and this process was associated with MAP kinase pathways in SHR VSMCs. This result suggests that upregulation of 12-LO by Ang II leads to the downregulation of CCL5 expression in SHR VSMCs.

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Section: Vsmcs Preparationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

et al. 2011

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Heteromerization between α_1B‐adrenoceptor and chemokine (C‐C motif) receptor 2 biases α_1B‐adrenoceptor signaling: Implications for vascular function

et al. 2022

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Previously, we reported that chemokine (C‐C motif) receptor 2 (CCR2) heteromerizes with α1B‐adrenoceptor (α1B‐AR) in leukocytes, through which α1B‐AR controls CCR2. Whether such heteromers are expressed in human vascular smooth muscle cells (hVSMCs) is unknown. Bioluminescence resonance energy transfer confirmed formation of recombinant CCR2:α1b‐AR heteromers. Proximity ligation assays detected CCR2:α1B‐AR heteromers in hVSMCs and human mesenteric arteries. CCR2:α1B‐AR heteromerization per se enhanced α1B‐AR‐mediated Gαq‐coupling. Chemokine (C‐C motif) ligand 2 (CCL2) binding to CCR2 inhibited Gαq activation via α1B‐AR, cross‐recruited β‐arrestin to and induced internalization of α1B‐AR in recombinant systems and in hVSMCs. Our findings suggest that CCR2 within CCR2:α1B‐AR heteromers biases α1B‐AR signaling and provide a mechanism for previous observations suggesting a role for CCL2/CCR2 in the regulation of cardiovascular function.

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Differential effects of substrate modulus on human vascular endothelial, smooth muscle, and fibroblastic cells

Robinson

Nie

Baldwin

et al. 2012

J Biomedical Materials Res

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Regenerative medicine approaches offer attractive alternatives to standard vascular reconstruction; however, the biomaterials to be used must have optimal biochemical and mechanical properties. To evaluate the effects of biomaterial properties on vascular cells, heparinized poly(ethylene glycol) (PEG)-based hydrogels of three different moduli, 13.7 kPa, 5.2 kPa, and 0.3 kPa, containing fibronectin and growth factor were utilized to support the growth of three human vascular cell types. The cell types exhibited differences in attachment, proliferation, and gene expression profiles associated with the hydrogel modulus. Human vascular smooth muscle cells demonstrated preferential attachment on the highest modulus hydrogel, adventitial fibroblasts demonstrated preferential growth on the highest modulus hydrogel, and human umbilical vein endothelial cells demonstrated preferential growth on the lowest modulus hydrogel investigated. Our studies suggest that the growth of multiple vascular cell types can be supported by PEG hydrogels and that different populations can be controlled by altering the mechanical properties of biomaterials.

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Upregulation of Interleukin-8/CXCL8 in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats

Cited by 47 publications

References 36 publications

Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

Heteromerization between α_1B‐adrenoceptor and chemokine (C‐C motif) receptor 2 biases α_1B‐adrenoceptor signaling: Implications for vascular function

Differential effects of substrate modulus on human vascular endothelial, smooth muscle, and fibroblastic cells

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Upregulation of Interleukin-8/CXCL8 in Vascular Smooth Muscle Cells from Spontaneously Hypertensive Rats

Cited by 47 publications

References 36 publications

Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

Angiotensin II inhibits chemokine CCL5 expression in vascular smooth muscle cells from spontaneously hypertensive rats

Heteromerization between α1B‐adrenoceptor and chemokine (C‐C motif) receptor 2 biases α1B‐adrenoceptor signaling: Implications for vascular function

Differential effects of substrate modulus on human vascular endothelial, smooth muscle, and fibroblastic cells

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Product

Resources

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Heteromerization between α_1B‐adrenoceptor and chemokine (C‐C motif) receptor 2 biases α_1B‐adrenoceptor signaling: Implications for vascular function