Role of plasma kallikrein–kinin system activation in synovial recruitment of endothelial progenitor cells in experimental arthritis

Dai, Jihong; Agelan, Alexis; Yang, Aimei; Zuluaga, Viviana Manrique; Sexton, Daniel J.; Colman, Robert W.; Wu, Yi

doi:10.1002/art.34607

Cited by 19 publications

(20 citation statements)

References 23 publications

(33 reference statements)

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“…25,26 Plasma kallikrein B1 stimulates the recruitment of EPCs in inflamed tissue by bradykinin-mediated up-regulation of chemokine receptor type-4. 27 Hence, the combination of these proangiogenic and EPC-activating factors may have further contributed to the higher numbers of EPCs in endometriotic lesions of estrogen-stimulated mice.…”

Section: Epcs In Endometriosismentioning

confidence: 99%

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Rudzitis‐Auth

Nenicu

Nickels

et al. 2016

The American Journal of Pathology

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The incorporation of endothelial progenitor cells (EPCs) into microvessels contributes to the vascularization of endometriotic lesions. Herein, we analyzed whether this vasculogenic process is regulated by estrogen. Estrogen- and vehicle-treated human EPCs were analyzed for migration and tube formation. Endometriotic lesions were induced in irradiated FVB/N mice, which were reconstituted with bone marrow from FVB/N-TgN (Tie2/green fluorescent protein) 287 Sato mice. The animals were treated with 100 μg/kg β-estradiol 17-valerate or vehicle (control) over 7 and 28 days. Lesion growth, cyst formation, homing of green fluorescent protein(+)/Tie2(+) EPCs, vascularization, cell proliferation, and apoptosis were analyzed by high-resolution ultrasonography, caliper measurements, histology, and immunohistochemistry. Numbers of blood circulating EPCs were assessed by flow cytometry. In vitro, estrogen-treated EPCs exhibited a higher migratory and tube-forming capacity when compared with controls. In vivo, numbers of circulating EPCs were not affected by estrogen. However, estrogen significantly increased the number of EPCs incorporated into the lesions' microvasculature, resulting in an improved early vascularization. Estrogen further stimulated the growth of lesions, which exhibited massively dilated glands with a flattened layer of stroma. This was mainly because of an increased glandular secretory activity, whereas cell proliferation and apoptosis were not markedly affected. These findings indicate that vasculogenesis in endometriotic lesions is dependent on estrogen, which adds a novel hormonally regulated mechanism to the complex pathophysiology of endometriosis.

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Section: Epcs In Endometriosismentioning

confidence: 99%

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Rudzitis‐Auth

Nenicu

Nickels

et al. 2016

The American Journal of Pathology

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“…Although these experimental and clinical observations demonstrate that the KKS plays a critical role in the pathogenesis of arthritis, the molecular and cellular mechanisms by which the activation of the KKS mediates arthritis remains unknown. Recently we report that the inhibition of plasma kallikrein ameliorates arthritis in two Lewis rat models, PG-PS model and collagen-induced arthritis model, the effect of plasma kallikrein is probably through bradykinin [ 51 ]. Bradykinin has two receptors, constitutively expressed B2R and inducible B1R both belong to G protein-coupled receptors.…”

Section: Contact System In Inflammationmentioning

confidence: 99%

“…Recently, we have demonstrated that HKa regulates EPC functions in vitro [ 58 , 59 ], revealing the connection between the KKS activation and EPC biology. In rodent model of arthritis, we found another role of the KKS in the homing function of EPCs in arthritis [ 51 ]. In Lewis rat model of arthritis, EPCs are recruited to inflamed synovium and form new vessels, which was blocked by specific plasma kallikrein inhibitor; Bradykinin stimulates transendothelial migration of EPCs by selectively upregulating expression of homing receptor C-X-C motif receptor 4 (CXCR4) [ 51 ].…”

Section: Contact System In Inflammationmentioning

confidence: 99%

“…In rodent model of arthritis, we found another role of the KKS in the homing function of EPCs in arthritis [ 51 ]. In Lewis rat model of arthritis, EPCs are recruited to inflamed synovium and form new vessels, which was blocked by specific plasma kallikrein inhibitor; Bradykinin stimulates transendothelial migration of EPCs by selectively upregulating expression of homing receptor C-X-C motif receptor 4 (CXCR4) [ 51 ]. Our study provides novel evidence that activation of the KKS is associated with synovial recruitment of EPCs at acute phase of arthritis, EPCs are likely a new target for bradykinin in the setting of acute arthritis.…”

Section: Contact System In Inflammationmentioning

confidence: 99%

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Contact pathway of coagulation and inflammation

2015

Thrombosis J

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171

130

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The contact system, also named as plasma kallikrein-kinin system, consists of three serine proteinases: coagulation factors XII (FXII) and XI (FXI), and plasma prekallikrein (PK), and the nonenzymatic cofactor high molecular weight kininogen (HK). This system has been investigated actively for more than 50 years. The components of this system and their interactions have been elucidated from in vitro experiments, which indicates that this system is prothrombotic by activating intrinsic pathway, and proinflammatory by producing bioactive peptide bradykinin. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. In the last 10 years, our understanding of the contact system, particularly its biology and (patho)physiology has greatly increased through investigations using gene-modified animal models. In this review we will describe a revitalized view of the contact system as a critical (patho)physiologic mediator of coagulation and inflammation.

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“…As previously described, whole blood was collected by cardiac puncture. Immediately after separation of plasma by centrifugation, the levels of BK were measured ( Dai et al, 2012 ).…”

Section: Methodsmentioning

confidence: 99%

An essential role of high-molecular-weight kininogen in endotoxemia

Yang

Xie

Wang

et al. 2017

Journal of Experimental Medicine

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In this study, we show that mice lacking high-molecular-weight kininogen (HK) were resistant to lipopolysaccharide (LPS)-induced mortality and had significantly reduced circulating LPS levels. Replenishment of HK-deficient mice with human HK recovered the LPS levels and rendered the mice susceptible to LPS-induced mortality. Binding of HK to LPS occurred through the O-polysaccharide/core oligosaccharide, consistent with the ability to bind LPS from K. pneumoniae, P. aeruginosa, S. minnesota, and different E. coli strains. Binding of LPS induced plasma HK cleavage to the two-chain form (HKa, containing a heavy chain [HC] and a light chain [LC]) and bradykinin. Both HKa and the LC, but not the HC, could disaggregate LPS. The light chain bound LPS with high affinity (Kd = 1.52 × 10−9 M) through a binding site in domain 5 (DHG15). A monoclonal antibody against D5 significantly reduced LPS-induced mortality and circulating LPS levels in wild-type mice. Thus, HK, as a major LPS carrier in circulation, plays an essential role in endotoxemia.

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Role of plasma kallikrein–kinin system activation in synovial recruitment of endothelial progenitor cells in experimental arthritis

Cited by 19 publications

References 23 publications

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Estrogen Stimulates Homing of Endothelial Progenitor Cells to Endometriotic Lesions

Contact pathway of coagulation and inflammation

An essential role of high-molecular-weight kininogen in endotoxemia

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