Regulation of collateral blood vessel development by the innate and adaptive immune system

Sala, A.; Pontecorvo, Laura; Agresta, Alessia; Rosano, Giuseppe; Stabile, Eugenio

doi:10.1016/j.molmed.2012.06.007

Cited by 65 publications

(64 citation statements)

References 59 publications

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“…35 Previous studies [36][37][38] mainly focused on endothelial NF-κB and found that NF-κB was a key regulator of adult and developmental arteriogenesis and collateral formation. Shear stress 7 and inflammation 8,13 have long been considered key drivers for arteriogenesis in adult tissues. During arterial occlusion, increased shear stress causes NF-κB activation in the endothelium.…”

Section: Discussionmentioning

confidence: 99%

“…Shear stress 7 and inflammation 8,13 have long been considered key drivers for arteriogenesis in adult tissues. During arterial occlusion, increased shear stress causes NF-κB activation in the endothelium.…”

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confidence: 99%

“…4,[8][9][10][11] Previous studies have shown that monocytes accumulated in the surrounding tissues of collateral vessels alter arterial occlusion. 7,[11][12][13] These macrophages are potent sources of cytokines and growth factors, which are required for natural adaptive arteriogenesis. In spite of a mounting number of putative arteriogenic factors, the exact mechanisms that regulate collateral remodeling are poorly characterized.…”

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confidence: 99%

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AMP-Activated Protein Kinase α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice In Vivo

Zhu

Zhang

Liu

et al. 2016

ATVB

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A rteriogenesis is a process of developing collateral circulation through the remodeling and growth of pre-existing collateral arteries after elevated shear stress induced by occlusion.1-3 Arteriogenesis takes place both during embryogenesis and in adult tissues. In the latter case, arteriogenesis, which usually occurs at sites of occlusion or physical disruption of pre-existing arterial conduits such as coronary artery occlusion or femoral artery ligation, plays a vital role in recovery from ischemic insults. 4,5 Understanding the biological factors that affect arteriogenesis will aid in the development of new treatments for patients with arterial stenosis and occlusions.There are 2 commonly considered mechanisms for arteriogenesis: expansion of pre-existing collaterals and de novo arteriogenesis. 2,6,7 Inflammation caused by mechanical hemodynamic forces, such as shear stress and circumferential wall tension, is considered a pivotal trigger and driver for arteriogenesis. 4,[8][9][10][11] Previous studies have shown that monocytes accumulated in the surrounding tissues of collateral vessels alter arterial occlusion. 7,[11][12][13] These macrophages are potent sources of cytokines and growth factors, which are required for natural adaptive arteriogenesis. In spite of a mounting number of putative arteriogenic factors, the exact mechanisms that regulate collateral remodeling are poorly characterized. Furthermore, the processes responsible for arteriogenesis, and its associated molecular signals are poorly understood.AMP-activated protein kinase (AMPK) is a serine/threonine kinase composed of α, β, and γ subunits. 14,15 The α subunit containing the α1 and α2 isoform is the catalytic subunit, whereas the β and γ are regulatory subunits that maintain the stability of the heterotrimer complex. As an energy sensor, AMPK is activated by various cellular stresses, such as hypoxia, nutrient deprivation, and oxidative stress. [16][17][18] Once activated, AMPK phosphorylates and regulates several downstream kinases that reduce energy demand and increase energy supply to maintain whole-body energy homeostasis. 19 In addition, AMPK also regulates many other cellular processes, including cell polarity, cell growth, and proliferation. [20][21][22] Emerging studies have demonstrated that AMPK is activated in response to shear or ischemic stress. 23,24 AMPK signaling is required for angiogenesis in vivo and in vitro. [25][26][27][28] However, there is no information on the consequences of AMPK deletion in arteriogenesis. In this study, we sought to examine the role © 2016 American Heart Association, Inc. Objective-AMP-activated protein kinase (AMPK), an energy and redox sensor, is activated in response to various cellular stresses, including hypoxia, nutrient deprivation, oxidative stress, and fluid shear stress at the site of vessel blockade. The activation of AMPK is involved in angiogenesis. However, it is unknown whether AMPK can influence arteriogenesis. Here, we demonstrate the contribution of macrophage AMPK to arteriogen...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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AMP-Activated Protein Kinase α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice In Vivo

Zhu

Zhang

Liu

et al. 2016

ATVB

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“…15 Angiogenesis results in an overall increment of vessel resistance and is insufficient to improve tissue perfusion 15 ; hence, arteriogenesis is a crucial natural compensatory mechanism for improving tissue perfusion for occlusive arterial disease.…”

Section: Discussionmentioning

confidence: 99%

“…15,18,19 The increased shear stress in the collateral vessels activates the endothelium, where circulating monocytes adhere via upregulated intracellular adhesion molecule-1, transmigrate into the perivascular tissue, and mature into macrophages, producing growth factors and cytokines for collateral artery growth. 20 In this study, we observed a higher number of macrophages on the dorsal surface of the brain in the db/db mice than in the db/+ mice without CCA occlusion, and the number of macrophages in the db/db mice did not change after CCA occlusion, whereas that in the db/+ mice was significantly increased 7 days after CCA occlusion.…”

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Chronic Elevation of Tumor Necrosis Factor-α Mediates the Impairment of Leptomeningeal Arteriogenesis in db/db Mice

Yukami

Yagita

Sugiyama

et al. 2015

Stroke

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C ollateral arterial growth (arteriogenesis) plays a crucial role in ischemic stroke and is a key factor that defines the severity and functional prognosis of this disease. 1 The circle of Willis and leptomeningeal anastomoses are typical intracranial collaterals. 2 In the case of middle cerebral artery occlusion, the Circle of Willis is no longer able to contribute collateral blood supply and leptomeningeal anastomoses become the primary source of collateral blood flow. We previously reported that unilateral common carotid artery (CCA) occlusion induces ipsilateral leptomeningeal collateral growth after 14 days in rodents. 3,4 Using this established model to estimate leptomeningeal arteriogenesis, we showed that hematopoietic factors enhance arteriogenesis in mice. 3,5 We also demonstrated that leptomeningeal collateral growth induced by cerebral hypoperfusion is impaired in spontaneous hypertensive rats 4 and apolipoprotein E-knockout mice. 6 Vascular risk factors induce vascular dysfunction and may be related to impaired arteriogenesis. Diabetes mellitus is also a major vascular risk factor because the prevalence of hypertension, dyslipidemia, and diabetes mellitus is increasing worldwide. Diabetes mellitus is associated with an increased risk of first ischemic stroke, and 60% to 70% patients with ischemic stroke have diabetes mellitus or prediabetes mellitus. 7 It was previously reported that diabetes mellitus impairs arteriogenesis in peripheral 8 and coronary arteries, 9,10 but it is not fully understood whether it impairs arteriogenesis in the cerebral vessels.Background and Purpose-Leptomeningeal collateral growth is a key factor that defines the severity of ischemic stroke.Patients with stroke generally have vascular risk factors, such as diabetes mellitus; however, consensus is lacking on how diabetes mellitus affects leptomeningeal arteriogenesis. We investigate the influence of diabetes mellitus on the leptomeningeal arteriogenesis. Methods-We measured the vessel diameter of the leptomeningeal anastomoses 14 days after the common carotid artery occlusion in db/db, db/+, and streptozotocin-induced hyperglycemic mice. In another set of these mice, we measured the infarct volume attributed to subsequent middle cerebral artery occlusion 14 days after the common carotid artery occlusion. Mac-2-positive cells on the dorsal brain surface and the mRNA expression of several macrophage-related factors in the cerebral cortex were examined. Finally, we tested whether the leptomeningeal arteriogenesis could be restored by pharmaceutical intervention in the db/db mice. Results-Cerebral hypoperfusion led to significant ipsilateral leptomeningeal collateral growth in db/+ mice and streptozotocin-induced hyperglycemic mice. The collateral growth contributed to reduced infarct volume. In contrast, leptomeningeal arteriogenesis was impaired in the db/db mice. The number of Mac-2-positive cells was increased and tumor necrosis factor-α mRNA expression was induced after common carotid artery occlusion in the db/+ mi...

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The dynamics of monocytes in the process of collateralization

Liao

Bai

2019

Aging Medicine

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The present treatment for coronary artery disease mainly includes medication and drug therapy combined with coronary revascularization. However, the rate of restenosis after stent implantation is still as high as 10% to 20%, 1 and approximately 20% of patients with coronary artery diffuse multivessel disease are unable to tolerate percutaneous coronary intervention or coronary artery bypass grafting. 2 Then, does any strategy effectively alleviate myocardial ischemic symptoms for those patients? Collateral circulation might be the answer.Many clinical studies show that well-established collateral circulation can effectively protect cardiac muscle from ischemia and improve patients' prognoses. 3 Collateral vessel refers to the tiny anatomical microvessels that bridge the severe stenosis or occlusion between the proximal and distant parts of the same blood vessel or between different blood vessels, with a diameter of 20-350 μm, which can provide blood supply to the ischemic regions and confine myocardial infarct size. 4 Related studies have shown that good collateral circulation plays a role in protecting myocardium from acute myocardial infarction and chronic myocardial ischemia. 5-8 A metaanalysis enrolling 6529 participants from several studies showed that patients with high collateralization had a 36% reduction in death risk compared with patients with low collateralization. 9 Therefore, the establishment of coronary collateral circulation is of great significance for the prognosis of coronary artery disease.The development of collateral circulation refers to the remodeling and enlargement of pre-existing collateral vessels. 10 It is currently believed that when the coronary artery is stenotic or occluded, AbstractCollateralization is an important way for patients with coronary heart disease to supply blood flow to the ischemic area. At present, research on the mechanism of collateral circulation mainly focuses on the inflammatory response. Monocytes are the kernel of inflammatory response during arteriogenesis. Therefore, we reviewed the recent developments in this field in terms of the dynamic changes of monocytes during collateralization. We searched and scanned PubMed for the following terms until November 2018: collateral, collateralization, monocyte, macrophage, and arteriogenesis.Articles were obtained and examined to figure out the dynamics of monocytes in the progress of collateralization. Substantial research shows that recruitment, infiltration, and phenotypic transformation of monocytes can affect function in various ways, respectively. Mechanical or chemical factors that can produce effects on collateral development may be due partly to impact on dynamics of monocytes. Although mechanisms of dynamics of monocytes during arteriogenesis are not elucidated clearly, there is no doubt that deeper exploration of the underlying mechanisms will contribute to pharmaceutical development aiming for promoting collateral development. K E Y W O R D Sarteriogenesis, collateral, collateralization, macrophage, mono...

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Regulation of collateral blood vessel development by the innate and adaptive immune system

Cited by 65 publications

References 59 publications

AMP-Activated Protein Kinase α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice In Vivo

AMP-Activated Protein Kinase α1 in Macrophages Promotes Collateral Remodeling and Arteriogenesis in Mice In Vivo

Chronic Elevation of Tumor Necrosis Factor-α Mediates the Impairment of Leptomeningeal Arteriogenesis in db/db Mice

The dynamics of monocytes in the process of collateralization

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