Angiotensin II stimulates MCP-1 production in rat glomerular endothelial cells via NAD(P)H oxidase-dependent nuclear factor-kappa B signaling

Abstract

Angiotensin II (Ang II) plays a crucial role in the pathogenesis of renal diseases. The objective of the present study was to investigate the possible inflammatory effect of Ang II on glomerular endothelial cells and the underlying mechanism. We isolated and characterized primary cultures of rat glomerular endothelial cells (GECs) and observed that Ang II induced the synthesis of monocyte chemoattractant protein-1 (MCP-1) in GECs as demonstrated by Western blot. Ang II stimulation, at concentrations ranging from 0.1 to 10 μm, of rat GECs induced a rapid increase in the generation of reactive oxygen species as indicated by laser fluoroscopy. The level of p47 phox protein, an NAD(P)H oxidase subunit, was also increased by Ang II treatment. These effects of Ang II on GECs were all reduced by diphenyleneiodonium (1.0 μm), an NAD(P)H oxidase inhibitor. Ang II stimulation also promoted the activation of nuclear factor-kappa B (NF-κB). Telmisartan (1.0 μm), an AT 1 receptor blocker, blocked all the effects of Ang II on rat GECs. These data suggest that the inhibition of NAD(P)H oxidase-dependent NF-κB signaling reduces the increase in MCP-1 production by GECs induced by Ang II. This may provide a mechanistic basis for the benefits of selective AT 1 blockade in dealing with chronic renal disease.

Correlation of Different NADPH Oxidase Homologues with Late Endothelial Progenitor Cell Senescence Induced by Angiotensin II: Effect of Telmisartan

“…According to recent research, Tel may attenuate endothelial inflammation and oxidative cell damage induced by Ang II-dependent stimuli (17)(18)(19). But whether telmisartan is able to alter expression of NOX and consequently antagonize Ang IIinduced late EPC senescence remains unclear.…”

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

“…[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.…”

“…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.…”

Catalpol attenuates oxidative stress and promotes autophagy in TNF-α-exposed HAECs by up-regulating AMPK

“…16,23 To examine the inuence of catalpol on NF-kB signal pathway, IkBa degradation, NF-kB/p65 nuclear translocation and phosphorylation were measured by western blotting. As shown in Fig.…”

“…Thus, augmentation of AMPK activity is posited to be a potential target for therapeutic interventions in AS. 15,16 Catalpol, whose structure is shown in Fig. S1, † is an iridoid glucoside and has been found to be present in large quantities in the root of Romania glutinosa L. 12 As a traditional medicine, catalpol demonstrates a variety of biological activities including anticancer, neuro-protective, anti-inammatory, diuretic, hypoglycemic and anti-hepatitis virus effects.…”