Fractalkine and placental growth factor: A duet of inflammation and angiogenesis in cardiovascular disorders

Skoda, Marta; Stangret, Aleksandra; Szukiewicz, Dariusz

doi:10.1016/j.cytogfr.2017.12.001

Cited by 28 publications

(27 citation statements)

References 93 publications

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“…Indeed, C5a, as well as the membrane attack complex, can induce a rapid secretion of preformed inflammatory factors by ECs . Of note, Fractalkine ( CX3XL1 ) was also released in the supernatant in the absence of complement and in the presence of elicited anti‐Neu5Gc Abs.…”

Section: Discussionmentioning

confidence: 99%

Elicited and pre‐existing anti‐Neu5Gc antibodies differentially affect human endothelial cells transcriptome

Berre

Danger

et al. 2019

Xenotransplantation

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Humans cannot synthesize N‐glycolylneuraminic acid (Neu5Gc) but dietary Neu5Gc can be absorbed and deposited on endothelial cells (ECs) and diet‐induced anti‐Neu5Gc antibodies (Abs) develop early in human life. While the interaction of Neu5Gc and diet‐induced anti‐Neu5Gc Abs occurs in all normal individuals, endothelium activation by elicited anti‐Neu5Gc Abs following a challenge with animal‐derived materials, such as following xenotransplantation, had been postulated. Ten primary human EC preparations were cultured with affinity‐purified anti‐Neu5Gc Abs from human sera obtained before or after exposure to Neu5Gc‐glycosylated rabbit IgGs (elicited Abs). RNAs of each EC preparation stimulated in various conditions by purified Abs were exhaustively sequenced. EC transcriptomic patterns induced by elicited anti‐Neu5Gc Abs, compared with pre‐existing ones, were analyzed. qPCR, cytokines/chemokines release, and apoptosis were tested on some EC preparations. The data showed that anti‐Neu5Gc Abs induced 967 differentially expressed (DE) genes. Most DE genes are shared following EC activation by pre‐existing or anti‐human T‐cell globulin (ATG)‐elicited anti‐Neu5Gc Abs. Compared with pre‐existing anti‐Neu5Gc Abs, which are normal component of ECs environment, elicited anti‐Neu5Gc Abs down‐regulated 66 genes, including master genes of EC function. Furthermore, elicited anti‐Neu5Gc Abs combined with complement‐containing serum down‐regulated most transcripts mobilized by serum alone. Both types of anti‐Neu5Gc Abs‐induced a dose‐ and complement‐dependent release of selected cytokines and chemokines. Altogether, these data show that, compared with pre‐existing anti‐Neu5Gc Abs, ATG‐elicited anti‐Neu5Gc Abs specifically modulate genes related to cytokine responses, MAPkinase cascades, chemotaxis, and integrins and do not skew the EC transcriptome toward a pro‐inflammatory profile in vitro.

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Section: Discussionmentioning

confidence: 99%

Elicited and pre‐existing anti‐Neu5Gc antibodies differentially affect human endothelial cells transcriptome

Berre

Danger

et al. 2019

Xenotransplantation

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“…FKN/CX3CL1 is a chemokine with potent proangiogenic properties and has been associated with pathological angiogenesis both in nonocular [77][78][79] and ocular diseases, such as the proliferative form of diabetic retinopathy and retinal vein occlusion. 36,37 It has been shown to mediate angiogenesis in oxygen-induced retinopathy model as well.…”

Section: Discussionmentioning

confidence: 99%

Tear Fluid Angiogenic Factors: Potential Noninvasive Biomarkers for Retinopathy of Prematurity Screening in Preterm Infants

Vinekar

Nair

Sinha

et al. 2021

Invest. Ophthalmol. Vis. Sci.

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“… 79 Numerous reports have documented the involvement of the FKN–CX3CR1 axis in atherosclerosis and cardiovascular events. 80 , 81 The FKN–CX3CR1 axis participates in the atherosclerotic pathological process by mediating the recruitment of leukocytes and their interaction with vascular cells. 82 Interestingly, polymorphisms in the human CX3CR1 gene are genetic risk factors for coronary artery disease and atherosclerosis.…”

Section: Fkn–cx3cr1 Axis Involvement In the Pathogenesis Of Rheumaticmentioning

confidence: 99%

<p>Emerging Role of Fractalkine in the Treatment of Rheumatic Diseases</p>

Tanaka¹,

Hoshino-Negishi²,

Kuboi³

et al. 2020

ITT

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Rheumatoid arthritis (RA) is an autoimmune disorder that affects joints and is characterized by synovial hyperplasia and bone erosion associated with neovascularization and infiltration of proinflammatory cells. The introduction of biological disease-modifying anti-rheumatic drugs has dramatically changed the treatment of RA over the last 20 years. However, fewer than 50% of RA patients enter remission, and 10–15% are treatment refractory. There is currently no cure for RA. Fractalkine (FKN, also known as CX3CL1) is a cell membrane-bound chemokine that can be induced on activated vascular endothelial cells. FKN has dual functions as a cell adhesion molecule and a chemoattractant. FKN binds specifically to the chemokine receptor CX3CR1, which is selectively expressed on subsets of immune cells such as patrolling monocytes and killer lymphocytes. The FKN–CX3CR1 axis is thought to play important roles in the initiation of the inflammatory cascade and can contribute to exacerbation of tissue injury in inflammatory diseases. Accordingly, studies in animal models have shown that inhibition of the FKN–CX3CR1 axis not only improves rheumatic diseases but also reduces associated complications, such as pulmonary fibrosis and cardiovascular disease. Recently, a humanized anti-FKN monoclonal antibody, E6011, showed promising efficacy with a dose-dependent clinical response and favorable safety profile in a Phase 2 clinical trial in patients with RA (NCT02960438). Taken together, the preclinical and clinical results suggest that E6011 may represent a new therapeutic approach for rheumatic diseases by suppressing a major contributor to inflammation and mitigating concomitant cardiovascular and fibrotic diseases. In this review, we describe the role of the FKN–CX3CR1 axis in rheumatic diseases and the therapeutic potential of anti-FKN monoclonal antibodies to fulfill unmet clinical needs.

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Fractalkine and placental growth factor: A duet of inflammation and angiogenesis in cardiovascular disorders

Cited by 28 publications

References 93 publications

Elicited and pre‐existing anti‐Neu5Gc antibodies differentially affect human endothelial cells transcriptome

Elicited and pre‐existing anti‐Neu5Gc antibodies differentially affect human endothelial cells transcriptome

Tear Fluid Angiogenic Factors: Potential Noninvasive Biomarkers for Retinopathy of Prematurity Screening in Preterm Infants

<p>Emerging Role of Fractalkine in the Treatment of Rheumatic Diseases</p>

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