Angiotensin II Angiogenic Effect In Vivo Involves Vascular Endothelial Growth Factor- and Inflammation-Related Pathways

Tamarat, Radia; Silvestre, Jean‐Sébastien; Durie, Micheline; Lévy, Bernard

doi:10.1097/01.lab.0000017372.76297.eb

Cited by 206 publications

(172 citation statements)

References 32 publications

(51 reference statements)

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“…11,49 -51 In terms of angiogenesis, studies using blockade of the RAS in cancer and experimental models of angiogenesis have highlighted this interaction. 9,52 Similar findings have been reported in ocular tissues including bovine retinal endothelial cells (BREC) 11 and streptozotocin diabetes. 25 Of interest is our finding in ROP 7 where we reported that ACE inhibition but not AT1-RB attenuated the rise in VEGF and VEGF-R2 gene expression.…”

Section: Discussionsupporting

confidence: 70%

“…20,21 Recent studies indicate that vascular endothelial growth factor (VEGF) may be the major mediator of the angiogenic effects of ANG II. 9,11 VEGF is a ligand for the receptor tyrosine kinase (RTK) receptors, Flt-1 (VEGF-R1) and Flk-1 (VEGF-R2), and is a potent permeability and angiogenic factor. [22][23][24] With respect to the retina, recent studies show that blockade of the RAS attenuates angiogenesis and the rise in VEGF and VEGF-R2 expression in vitro, 11 in ROP, 7 and in streptozotocin diabetic rats.…”

mentioning

confidence: 99%

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Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Sarlos

Rizkalla

Moravski

et al. 2003

The American Journal of Pathology

131

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There is evidence that angiotensin II, vascular endothelial growth factor (VEGF), angiopoietins, and their cognate receptors participate in retinal angiogenesis. We investigated whether angiotensin type 2-receptor blockade (AT2-RB) reduces retinal angiogenesis and alters the expression of VEGF/VEGF-R2 and angiopoietin-Tie2. Retinopathy of prematurity (ROP) was induced in Sprague Dawley (SD) rats by exposure to 80% oxygen from postnatal (P) days 0 to 11, followed by 7 days in room air. ROP shams were in room air from P0 -18. A group of ROP rats received the AT2-RB, PD123319, by mini-osmotic pump (5 mg/kg/day) from P11-18 (angiogenesis period). Evaluation of the retinal status of the AT2 receptor indicated that this receptor, as assessed by real-time PCR, immunohistochemistry, and in vitro autoradiography, was present in the retina, was more abundant than the AT1 receptor in the neonatal retina, and was increased in the ROP model. AT2-RB reduced retinal angiogenesis. VEGF and VEGF-R2 mRNA were increased in ROP and localized to blood vessels, ganglion cells, and the inner nuclear layer, and were decreased by PD123319. Angiopoietin2 and Tie2, but not angiopoietin1 mRNA were increased with ROP, and angiopoietin2 was reduced with PD123319. This study has identified a potential retinoprotective role for AT2-RB possibly mediated via interactions with VEGF-and angiopoietin-dependent pathways.

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Section: Discussionsupporting

confidence: 70%

mentioning

confidence: 99%

Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Sarlos

Rizkalla

Moravski

et al. 2003

The American Journal of Pathology

131

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“…After the injection, the Matrigel formed rapidly a subcutaneous plug that was left 14 days before removal. On day 14, the mice were euthanized and the skins were pulled back to expose the Matrigel, as previously described [17]. Plugs were then removed and fixed with 3.7% formaldehyde at 4 C for 12 hours, embedded in paraffin, sectioned, and stained with Masson Trichrome.…”

Section: Effect On Vessel Growthmentioning

confidence: 99%

Plasminogen Activator Inhibitor-1 Controls Bone Marrow-Derived Cells Therapeutic Effect Through MMP9 Signaling: Role in Physiological and Pathological Wound Healing

et al. 2012

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We assessed the role of plasminogen activator inhibitor-1 (PAI-1) and matrix metalloproteinase 9 (MMP9) in wound healing process and in the bone marrow mononuclear cells (BMMNC)-related effects on physiological and pathological wound healing. A full thickness excision wound was created by removal of the skin on the midback of irradiated and nonirradiated animals. Angiogenesis and re-epithelialization were markedly increased in PAI-12/2 mice compared to wild-type (WT) animals. We revealed high MMP activity in tissue of PAI-12/2 animals. Of interest, the wound healing process was reduced in PAI-12/2:MMP92/2 animals compared to PAI-12/2 mice, suggesting a key role of MMP9 in beneficial effect of PAI-1 deficiency on wound closure. To unravel the role of PAI-1 in BMMNC relative effects, mice were treated with or without local injection of BMMNC isolated from WT, PAI-12/2, and PAI-12/2: MMP92/2 animals for 14 days (10 6 cells, n 5 6 per group). In WT nonirradiated mice, transplantation of BMMNC isolated from PAI-12/2 animals enhanced wound formation when compared with WT BMMNC. BMMNC differentiation into cells with endothelial phenotype was enhanced by PAI-1 deficiency. These effects were abrogated in PAI-12/2:MMP92/2 and MMP92/2 BMMNC. In addition, using chimeric mice, we demonstrated that PAI-1 deficiency environment increased the BMMNC-GFP recruitment to the wound site, whereas this effect was abrogated when using PAI-12/2:MMP92/2 BMMNC. PAI-1 deficiency, at least through MMP9 upregulation, enhanced wound healing and BMMNC therapeutic potential in irradiated and nonirradiated animals.

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“…Moreover, the ACEI cilazapril was shown to decrease microalbuminuria and MMP-9 plasma concentrations in eight patients with non-insulin-dependent diabetes (13). It is interesting that angiotensin II treatment of C57B1/6 female mice did not affect MMP-2 and MMP-9 activity (14). Conclusive data on the effect of ARB on MMP and TIMP are still missing.…”

mentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibition but not Angiotensin II Receptor Blockade Regulates Matrix Metalloproteinase Activity in Patients with Glomerulonephritis

Lods

Ferrari

Frey

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Equivalent long-term effects on the kidney are attributed to angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II type 1 receptor blockers (ARB). Nevertheless, it is unknown to which degree effects of these compounds on individual inflammatory mediators, including matrix metalloproteinases (MMP), are comparable. On the basis of structural and functional differences, it was hypothesized that ACEI and ARB differentially regulate MMP activity. In a randomized, prospective crossover trial, the effect of an ACEI (fosinopril; 20 mg/d) and of an ARB (irbesartan; 150 mg/d) on MMP activity was evaluated. Ten hypertensive patients with glomerulonephritis and normal or mildly reduced creatinine clearance were studied. MMP activity and tissue inhibitors of metalloproteinase (TIMP) levels were analyzed in serum and urine: without therapy, with ACEI, with ARB, and with both agents combined. Treatment periods continued for 6 wk separated by periods of 4 wk each without therapy. Untreated patients with glomerulonephritis displayed distinctively higher serum levels of MMP-2 but much lower MMP-1/-8/-9 concentrations compared with healthy control subjects. Immunohistology of MMP-2 and MMP-9 in kidney biopsy specimen was accordingly. However, these patients excreted higher amounts of MMP-2 and MMP-9 in urine than healthy control subjects, possibly reflecting ongoing glomerular inflammation. In patients with glomerulonephritis, ACEI significantly reduced overall MMP serum activity to 25%, whereas ARB did not show any effect. Activities of MMP-1/-2/-8/-9 were also significantly inhibited by fosinopril but not by irbesartan. Levels of TIMP-1/-2 remained unaffected. In conclusion, ACEI and ARB differentially regulate MMP activity, which may ultimately have consequences in certain types of MMP-dependent glomerulonephritis.Glomerular inflammatory diseases represent frequent and often difficult-to-treat causes of end-stage kidney failure. Hypertension and proteinuria are important independent determinants and risk factors for progression of these diseases (1). Therefore, these two conditions are prime targets for the therapy of all types of glomerulonephritis.Pharmacologic inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II type 1 receptor blockers (ARB) has been particularly well demonstrated to treat high BP and proteinuria successfully (1). Moreover, the decline of kidney function occurring in diabetic as well as in nondiabetic glomerulopathies was greatly reduced by these agents in many investigations (2,3). Although ARB have only recently been introduced to common clinical use, several studies reported equivalent renoprotection for both classes of agents, ACEI and ARB (1). However, the issue of long-term effects with regard to the kidney is not yet fully resolved, and the identification of patient groups in which one of these agents demonstrates potential advances over the other one remains of pivotal clinical interest.Angiotensin II plays a key role...

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Angiotensin II Angiogenic Effect In Vivo Involves Vascular Endothelial Growth Factor- and Inflammation-Related Pathways

Cited by 206 publications

References 32 publications

Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Retinal Angiogenesis Is Mediated by an Interaction between the Angiotensin Type 2 Receptor, VEGF, and Angiopoietin

Plasminogen Activator Inhibitor-1 Controls Bone Marrow-Derived Cells Therapeutic Effect Through MMP9 Signaling: Role in Physiological and Pathological Wound Healing

Angiotensin-Converting Enzyme Inhibition but not Angiotensin II Receptor Blockade Regulates Matrix Metalloproteinase Activity in Patients with Glomerulonephritis

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