Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

Hillmeister, Philipp; Gatzke, Nora; Dülsner, André; Bäder, Michael; Schadock, Ines; Hoefer, Imo E.; Hamann, Isabell; Infante-Duarte, Carmen; Jung, G.; Troidl, Kerstin; Stawowy, Philipp; Frentsch, Marco; Li, Meijing; Nagorka, Stephanie; Wang, Haitao; Shi, Yu; Noble, Ferdinand le; Buschmann, Ivo

doi:10.1161/circresaha.111.240986

Cited by 38 publications

(45 citation statements)

References 38 publications

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“…Inflammatory cells have been shown to accumulate in the ischemic area and positively modulate neovascularization and arteriogenesis through various mechanisms, including production of angiogenic factors, secretion of proinflammatory cytokines, and matrix degradation (Arras et al, 1998;Tamarat et al, 2002;Silvestre et al, 2003;Stabile et al, 2003Stabile et al, , 2006Hong et al, 2005;Waeckel et al, 2005Waeckel et al, , 2006Hillmeister et al, 2011). In diabetes, monocyte dysfunction and reduced VEGF production have been observed (Waltenberger et al, 2000;Tchaikovski et al, 2009;Waltenberger, 2009;Carr et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Kinin Receptor Agonism Restores Hindlimb Postischemic Neovascularization Capacity in Diabetic Mice

Desposito

Potier

Chollet

et al. 2014

J Pharmacol Exp Ther

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Limb ischemia is a major complication of thromboembolic diseases. Diabetes worsens prognosis by impairing neovascularization. Genetic or pharmacological inactivation of the kallikreinkinin system aggravates limb ischemia in nondiabetic animals, whereas angiotensin I-converting enzyme/kininase II inhibition improves outcome. The role of kinins in limb ischemia in the setting of diabetes is not documented. We assessed whether selective activation of kinin receptors by pharmacological agonists can influence neovascularization in diabetic mice with limb ischemia and have a therapeutic effect. Selective pseudopeptide kinin B1 or B2 receptor agonists resistant to peptidase action were administered by osmotic minipumps at a nonhypotensive dosage for 14 days after unilateral femoral artery ligation in mice previously rendered diabetic by streptozotocin. Comparison was made with ligatured, nonagonist-treated nondiabetic and diabetic mice. Diabetes reduced neovascularization, assessed by microangiography and histologic capillary density analysis, by roughly 40%. B1 receptor agonist or B2 receptor agonist similarly restored neovascularization in diabetic mice. Neovascularization in agonist-treated diabetic mice was indistinguishable from nondiabetic mice. Both treatments restored blood flow in the ischemic hindfoot, measured by laser-Doppler perfusion imaging. Macrophage infiltration increased 3-fold in the ischemic gastrocnemius muscle during B1 receptor agonist or B2 receptor agonist treatment, and vascular endothelial growth factor (VEGF) level increased 2-fold. Both treatments increased, by 50-100%, circulating CD45/CD11b-positive monocytes and CD34 1 /VEGFR21 progenitor cells. Thus, selective pharmacological activation of B1 or B2 kinin receptor overcomes the effect of diabetes on postischemic neovascularization and restores tissue perfusion through monocyte/macrophage mobilization. Kinin receptors are potential therapeutic targets in limb ischemia in diabetes.

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Section: Discussionmentioning

confidence: 99%

Kinin Receptor Agonism Restores Hindlimb Postischemic Neovascularization Capacity in Diabetic Mice

Desposito

Potier

Chollet

et al. 2014

J Pharmacol Exp Ther

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“…1a). Improvement of collateral growth-dependent hemodynamic reserve capacity was assessed by post-mortem latex angiography for morphological changes and the acetazolamide (ACZ) test for functional changes as described previously [5,18] (for all online supplementary material, see www.karger.com?doi=10.1159/000335869). …”

Section: Methodsmentioning

confidence: 99%

Granulocyte Colony-Stimulating Factor Improves Cerebrovascular Reserve Capacity by Enhancing Collateral Growth in the Circle of Willis

Duelsner¹,

Gatzke²,

Gläser³

et al. 2012

Cerebrovasc Dis

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Background and Purpose: Restoration of cerebrovascular reserve capacity (CVRC) depends on the recruitment and positive outward remodeling of preexistent collaterals (arteriogenesis). With this study, we provide functional evidence that granulocyte colony-stimulating factor (G-CSF) augments therapeutic arteriogenesis in two animal models of cerebral hypoperfusion. We identified an effective dosing regimen that improved CVRC and stimulated collateral growth, thereby improving the outcome after experimentally induced stroke. Methods: We used two established animal models of (a) cerebral hypoperfusion (mouse, common carotid artery ligation) and (b) cerebral arteriogenesis (rat, 3-vessel occlusion). Following therapeutic dose determination, both models received either G-CSF, 40 µg/kg every other day, or vehicle for 1 week. Collateral vessel diameters were measured following latex angiography. Cerebrovascular reserve capacities were assessed after acetazolamide stimulation. Mice with left common carotid artery occlusion (CCAO) were additionally subjected to middle cerebral artery occlusion, and stroke volumes were assessed after triphenyltetrazolium chloride staining. Given the vital role of monocytes in arteriogenesis, we assessed (a) the influence of G-CSF on monocyte migration in vitro and (b) monocyte counts in the adventitial tissues of the growing collaterals in vivo. Results: CVRC was impaired in both animal models 1 week after induction of hypoperfusion. While G-CSF, 40 µg/kg every other day, significantly augmented cerebral arteriogenesis in the rat model, 50 or 150 µg/kg every day did not show any noticeable therapeutic impact. G-CSF restored CVRC in mice (5 ± 2 to 12 ± 6%) and rats (3 ± 4 to 19 ± 12%). Vessel diameters changed accordingly: in rats, the diameters of posterior cerebral arteries (ipsilateral: 209 ± 7–271 ± 57 µm; contralateral: 208 ± 11–252 ± 28 µm) and in mice the diameter of anterior cerebral arteries (185 ± 15–222 ± 12 µm) significantly increased in the G-CSF groups compared to controls. Stroke volume in mice (10 ± 2%) was diminished following CCAO (7 ± 4%) and G-CSF treatment (4 ± 2%). G-CSF significantly increased monocyte migration in vitro and perivascular monocyte numbers in vivo. Conclusion: G-CSF augments cerebral collateral artery growth, increases CVRC and protects from experimentally induced ischemic stroke. When comparing three different dosing regimens, a relatively low dosage of G-CSF was most effective, indicating that the common side effects of this cytokine might be significantly reduced or possibly even avoided in this indication.

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“…Usually carry explicit names in human, eg: superior ulnar collateral arte ry, genicular artery and other anastomotic arteries around elbows, knees and other articulations, palmar and plantar arch collaterals, ileolumbar-superior epigastric communicating artery, bronchial-to-pulmonary vein arteries , other collateral arteries in the abdomen and thorax, anterior and posterior communicating arteries/collaterals of the circle of Willis. Compared to microvascular collaterals (defined below), collateral arteries in healthy young adults generally exhibit minimal or no tortuosity, undergo considerably less anatomic lumen enlargement on a percentage basis (“remodeling”) in response to a chronic increase in shear stress in obstructive disease, 5,6 form during embryogenesis by a different process (discussed below). Microvascular collaterals — arteriole-to-arteriole anastomoses that cross-connect a small fraction (generally < 0.05%) of the arterioles in the crowns of adjacent arterial trees. Average less than 100 microns diameter in most healthy species including human (Figure).…”

mentioning

confidence: 99%

A Brief Etymology of the Collateral Circulation

Faber

Chilian

Deindl

et al. 2014

ATVB

139

140

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It is well known that the protective capacity of the collateral circulation falls short in many individuals with ischemic disease of the heart, brain and lower extremities. In the past fifteen years, opportunities created by molecular and genetic tools, together with disappointing outcomes in many “angiogenic” trials, has led to a significant increase in the number of studies that focus on: 1) understanding the basic biology of the collateral circulation; 2) identifying the mechanisms that limit the collateral circulation’s capacity in many individuals; 3) devising methods to measure collateral extent, which has been found to vary widely among individuals; and 4) developing treatments to increase collateral blood flow in obstructive disease. Unfortunately, accompanying this increase in reports has been a proliferation of vague terms used to describe the disposition and behavior of this unique circulation, as well as the increasing miss-use of well-ensconced ones by new (and old) students of the collateral circulation. With this in mind, we provide a brief glossary of readily understandable terms to denote the formation, adaptive growth, and mal-adaptive rarefaction of the collateral circulation. We also propose terminology for several newly discovered processes that occur in the collateral circulation. Finally, we include terms used to describe vessels that are sometimes confused with collaterals, as well as terms describing processes active in the general arterial-venous circulation when ischemic conditions engage the collateral circulation. We hope this brief review will help unify the terminology used in collateral research.

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Arteriogenesis Is Modulated By Bradykinin Receptor Signaling

Cited by 38 publications

References 38 publications

Kinin Receptor Agonism Restores Hindlimb Postischemic Neovascularization Capacity in Diabetic Mice

Kinin Receptor Agonism Restores Hindlimb Postischemic Neovascularization Capacity in Diabetic Mice

Granulocyte Colony-Stimulating Factor Improves Cerebrovascular Reserve Capacity by Enhancing Collateral Growth in the Circle of Willis

A Brief Etymology of the Collateral Circulation

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