Choline Transporter-Like Protein-2

Bayat, Behnaz; Tjahjono, Yudy; Berghöfer, Heike; Werth, Silke; Deckmyn, Hans; Meyer, Simon F. De; Sachs, Ulrich J.; Santoso, Sentot

doi:10.1161/atvbaha.115.305259

Cited by 35 publications

(10 citation statements)

References 29 publications

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“…As it was previously described that HEK293 cells overexpressing SLC44A2 bind VWF in vitro, we sought to determine whether VWF could be altered in Slc44a2 −/− mice (8). In the FVB line, a non-significant 27% decrease in median plasma levels of VWF was observed in Slc44a2 −/− mice (p=0.1996) (Figure1C).…”

Section: Resultsmentioning

confidence: 99%

“…TRALI, like thrombosis, has a central role in its pathogenesis for endothelial cells and neutrophils, both of which express SLC44A2, in addition to several other tissues (4). Furthermore, a recent TRALI study described SLC44A2 to be a binding partner of VWF, a key molecule in hemostasis (8). Additionally, SLC44A2 has been associated with autoimmune hearing loss, due to its importance in hair cell viability (9).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2

Tilburg

Adili

Nair

et al. 2018

Thrombosis Research

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Introduction Recent genome wide association studies (GWAS) identified a novel susceptibility locus for thrombosis, harbouring the SLC44A2 gene which encodes the Solute Carrier Family 44 Member 2 protein (SLC44A2). Thus far, SLC44A2 has not been studied in the context of thrombosis, and may be a unique contributor to thrombotic disease. Here we utilize mice lacking SLC44A2 (Slc44a2−/−) to evaluate a possible role of SLC44A2 in hemostasis. Methods Slc44a2−/− mice were evaluated in key aspects of normal hemostasis including a challenge of vascular damage by applying laser induced injury to the cremaster muscle arteriole. Results Slc44a2−/− mice had comparable levels of thrombin generation and gene expression of coagulation related genes, as compared to littermate wild type controls. Lower levels of circulating plasma Von Willebrand factor (VWF) were measured in Slc44a2−/− mice, while no difference in VWF multimerization or vascular localization was detected. Upon in vivo laser injury of the cremaster arterioles, we detected an impairment of clot formation for Slc44a2−/− mice. Conclusions Although mice lacking SLC44A2 are normal for several hemostasis parameters, we do observe a reduction of plasma VWF levels and an altered response upon vascular damage, which suggests that SLC44A2 contributes to hemostasis upon injury. These findings are in line with the reported GWAS data and support further research on SLC44A2 in thrombosis.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2

Tilburg

Adili

Nair

et al. 2018

Thrombosis Research

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“…Pulmonary PMN infiltration has been described to occur in multiple animal models of TRALI [11,13,47,48,49,50,51,52,53,54,55,56,57]. Additionally, the abundance of PMNs has been observed in pulmonary tissue of TRALI patients upon autopsy [58,59].…”

Section: Neutrophil Involvement In Tralimentioning

confidence: 99%

“…Also other studies found PMN-mediated endothelial cell damage using an in vitro TRALI model in a setting of both non-antibody mediated TRALI [65] and antibody-mediated TRALI [61,66,67]. Furthermore, PMNs were found to interact with von Willebrand factor via choline transporter-like protein-2 (CTL-2), which allowed anti-HNA-3a antibody to induce signal transduction via CD11b/CD18, leading to PMN activation and agglutination [54]. This mechanism may aggravate endothelial cell damage in anti-HNA 3a antibody-mediated TRALI.…”

Section: Neutrophil Involvement In Tralimentioning

confidence: 99%

The Pathogenic Involvement of Neutrophils in Acute Respiratory Distress Syndrome and Transfusion-Related Acute Lung Injury

Rebetz

Semple

Kapur

2018

Transfus Med Hemother

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The acute respiratory distress syndrome (ARDS) is a serious and common complication of multiple medical and surgical interventions, with sepsis, pneumonia, and aspiration of gastric contents being common risk factors. ARDS develops within 1 week of a known clinical insult or presents with new/worsening respiratory symptoms if the clinical insult is unknown. Approximately 40% of the ARDS cases have a fatal outcome. Transfusion-related acute lung injury (TRALI), on the other hand, is characterized by the occurrence of respiratory distress and acute lung injury, which presents within 6 h after administration of a blood transfusion. In contrast to ARDS, acute lung injury in TRALI is not attributable to another risk factor for acute lung injury. ‘Possible TRALI', however, may have a clear temporal relationship to an alternative risk factor for acute lung injury. Risk factors for TRALI include chronic alcohol abuse and systemic inflammation. TRALI is the leading cause of transfusion-related fatalities. There are no specific therapies available for ARDS or TRALI as both have a complex and incompletely understood pathogenesis. Neutrophils (polymorphonuclear leukocytes; PMNs) have been suggested to be key effector cells in the pathogenesis of both syndromes. In the present paper, we summarize the literature with regard to PMN involvement in the pathogenesis of both ARDS and TRALI based on both human data as well as on animal models. The evidence generally supports a strong role for PMNs in both ARDS and TRALI. More research is required to shed light on the pathogenesis of these respiratory syndromes and to more thoroughly establish the nature of the PMN involvement, especially considering the heterogeneous etiologies of ARDS.

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“…These antibodies bind to and aggregate granulocytes 32,33 . Bayat et al 34 showed that HNA3a antibody induces neutrophil activation through interaction with endothelial cells 34 requiring interaction of SLC44A2, von Willebrand Factor and CD11b/CD18 34 .…”

Section: 0 Discussionmentioning

confidence: 99%

SLC44A2 single nucleotide polymorphisms, isoforms, and expression: Association with severity of Meniere's disease?

et al. 2016

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SLC44A2 was discovered as the target of an antibody that causes hearing loss. Knockout mice develop age related hearing loss, loss of sensory cells and spiral ganglion neurons. SLC44A2 has polymorphic sites implicated in human disease. Transfusion related acute lung injury (TRALI) is linked to rs2288904 and genome wide association studies link rs2288904 and rs9797861 to venous thromboembolism (VTE), coronary artery disease and stroke. Here we report linkage disequilibrium of rs2288904 with rs3087969 and the association of these SLC44A2 SNPs with Meniere’s disease severity. Tissue-specific isoform expression differences suggest that the N-terminal domain is linked to different functions in different cell types. Heterozygosity at rs2288904 CGA/CAA and rs3087969 GAT/GAC showed a trend for association with intractable Meniere’s disease compared to less severe disease and to controls. The association of SLC44A2 SNPs with VTE suggests that thrombi affecting cochlear vessels could be a factor in Meniere’s disease.

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Choline Transporter-Like Protein-2

Cited by 35 publications

References 29 publications

Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2

Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2

The Pathogenic Involvement of Neutrophils in Acute Respiratory Distress Syndrome and Transfusion-Related Acute Lung Injury

SLC44A2 single nucleotide polymorphisms, isoforms, and expression: Association with severity of Meniere's disease?

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