Angiotensin IV Activates the Nuclear Transcription Factor-κB and Related Proinflammatory Genes in Vascular Smooth Muscle Cells

Esteban, Vanesa; Rupérez, Mónica; Sánchez-López, Elsa; Rodríguez-Vita, Juan; Lorenzo, Óscar; Demaegdt, Heidi; Vanderheyden, Patrick; Egido, Jesús; Ruíz-Ortega, Marta

doi:10.1161/01.res.0000166326.91395.74

Cited by 97 publications

(65 citation statements)

References 48 publications

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“…[36][37][38][39]. In VSMCs (vascular smooth muscle cells) Ang II stimulates the production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, osteopontin, and MCP-1, which is an important mediator for the direct migration of monocytes into the intima.…”

Section: Part II -Role Of the Renin-angiotensin-aldosterone System Onmentioning

confidence: 99%

“…In VSMC from AT1a receptor knockout mice, Ang IV, an angiotensin related peptide, also activated NF-B pathway via AT4 receptors and increased the expression of proinflammatory factors under NF-B control, such as MCP-1, IL-6, TNF-, intercellular adhesion molecule-1 (ICAM-1), and tissue plasminogen activator inhibitor-1 (PAI-1) [38]. Moreover, NF-B also plays a key role in other phases of inflammation cascade, such as Ang II-induced migration and proliferation of VSMCs, both of them under normal physiological conditions and following vascular injury [39].…”

Section: Introductionmentioning

confidence: 99%

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Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

108

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Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.

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Section: Part II -Role Of the Renin-angiotensin-aldosterone System Onmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

108

View full text Add to dashboard Cite

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“…Moreover, the expression of the CCL2 gene has also been reported to require the activation of NF-B (23,24). We previously reported via EMSA and Western blot analysis that the stimulation of human monocytes with SAA elicits the activation of NF-B (25).…”

Section: Saa Stimulates Ccl2 Production Via Nf-b Activity In Human Momentioning

confidence: 99%

Serum Amyloid A Induces CCL2 Production via Formyl Peptide Receptor-Like 1-Mediated Signaling in Human Monocytes

Lee

Kim

Shim

et al. 2008

The Journal of Immunology

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Although the presence of an elevated level of serum amyloid A (SAA) has been regarded as a cardiovascular risk factor, the role of SAA on the progress of atherosclerosis has not been fully elucidated. In the present study, we investigated the effect of SAA on the production of CCL2, an important mediator of monocyte recruitment, and the mechanism underlying the action of SAA in human monocytes. The stimulation of human monocytes with SAA elicited CCL2 production in a concentration-dependent manner. The production of CCL2 by SAA was found to be mediated by the activation of NF-κB. Moreover, the signaling events induced by SAA included the activation of ERK and the induction of cyclooxygenase-2, which were required for the production of CCL2. Moreover, SAA-induced CCL2 induction was inhibited by a formyl peptide receptor-like 1 (FPRL1) antagonist. We also found that the stimulation of FPRL1-expressing RBL-2H3 cells induced CCL2 mRNA accumulation, but the vector-expressing RBL-2H3 cells combined with SAA did not. Taken together, our findings suggest that SAA stimulates CCL2 production and, thus, contributes to atherosclerosis. Moreover, FPRL1 was found to be engaged in SAA-induced CCL2 induction, and cyclooxygenase-2 induction was found to be essential for SAA-induced CCL2 expression. These results suggest that SAA and FPRL1 offer a developmental starting point for the treatment of atherosclerosis.

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“…After a 24-h serum starvation step, we stimulated cells for 24 h and then evaluated the luciferase/renilla activity with Promega kits. 61 …”

Section: Immunofluorescence Staining Of Nf-b Subunitsmentioning

confidence: 99%

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

Sánchez-López¹,

Rayego²,

Rodrigues‐Díez³

et al. 2009

Journal of the American Society of Nephrology

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118

100

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Connective tissue growth factor (CTGF) is an important profibrotic factor in kidney diseases. Blockade of endogenous CTGF ameliorates experimental renal damage and inhibits synthesis of extracellular matrix in cultured renal cells. CTGF regulates several cellular responses, including adhesion, migration, proliferation, and synthesis of proinflammatory factors. Here, we investigated whether CTGF participates in the inflammatory process in the kidney by evaluating the nuclear factor-kappa B (NF-B) pathway, a key signaling system that controls inflammation and immune responses. Systemic administration of CTGF to mice for 24 h induced marked infiltration of inflammatory cells in the renal interstitium (T lymphocytes and monocytes/macrophages) and led to elevated renal NF-B activity. Administration of CTGF increased renal expression of chemokines (MCP-1 and RANTES) and cytokines (INF-␥, IL-6, and IL-4) that recruit immune cells and promote inflammation. Treatment with a NF-B inhibitor, parthenolide, inhibited CTGF-induced renal inflammatory responses, including the up-regulation of chemokines and cytokines. In cultured murine tubuloepithelial cells, CTGF rapidly activated the NF-B pathway and the cascade of mitogen-activated protein kinases, demonstrating crosstalk between these signaling pathways. CTGF, via mitogen-activated protein kinase and NF-B activation, increased proinflammatory gene expression. These data show that in addition to its profibrotic properties, CTGF contributes to the recruitment of inflammatory cells in the kidney by activating the NF-B pathway.

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Angiotensin IV Activates the Nuclear Transcription Factor-κB and Related Proinflammatory Genes in Vascular Smooth Muscle Cells

Cited by 97 publications

References 48 publications

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Serum Amyloid A Induces CCL2 Production via Formyl Peptide Receptor-Like 1-Mediated Signaling in Human Monocytes

CTGF Promotes Inflammatory Cell Infiltration of the Renal Interstitium by Activating NF-κB

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