Coagulation factor III (tissue factor) is required for vascularization in zebrafish embryos

Zhou, Ruijiao; Liu, Y; Wang, Y X; Mo, Wen; Ming, Yu

doi:10.4238/2011.october.31.2

Cited by 9 publications

(16 citation statements)

References 23 publications

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“…This region appears stained irrespective of phenotype, and therefore, we did not consider the CCV region for bleeding score. These findings confirm that, similar to f3b [21], f3a plays a role in vascular stability in our zebrafish model.…”

Section: Resultssupporting

confidence: 90%

“…Previously, Zhou and colleagues reported that f3b knockdown in zebrafish exhibits defective vasculogenesis [21]. Because f3a’s role during embryonic development was not known, we therefore examined its role by mRNA knockdown using MO antisense oligonucleotides (Gene Tools, USA) ( Figure 1D ).…”

Section: Resultsmentioning

confidence: 99%

“…For TF, zebrafish has two TF paralogs, designated as f3a and f3b [19], which are homologous to human and mouse TF genes [20] respectively. Knockdown of f3b using a morpholino oligonucleotide (MO) suggests that the f3b gene is important for coagulation and angiogenesis [21]. However, there are no reports on the role of f3a till date.…”

Section: Introductionmentioning

confidence: 99%

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Coagulation Factor IIIa (f3a) Knockdown in Zebrafish Leads to Defective Angiogenesis and Mild Bleeding Phenotype

Subramaniam

Fletcher

et al. 2021

Preprint

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Aim: Tissue factor (TF), an initiator of the extrinsic coagulation pathway, is crucial for embryogenesis, as mice lacking TF are embryonically lethal (E10.5). This lethality may be attributed to defects in vascular development and circulatory failure, suggesting additional roles for TF in embryonic development beyond coagulation. In this study, we characterized the role of one of the TF paralogs (f3a) using a zebrafish model. Methods: To understand the TF evolution across different species, we performed molecular phylogenetic and sequence homology analysis. The expression of f3a during embryonic developmental stages was determined by RT-PCR. Endothelial-specific transgenic lines of zebrafish (flk1:egfp-NLS/kdrl:mCherry-CAAX) was used to image the vascular development. The role of f3a during embryonic development was investigated by mRNA knockdown using Morpholinos (MO), an antisense-based oligonucleotide strategy. The f3a morphants were examined at 52 hpf for defects in morphological appearance, bleeding, and vascular patterning. Results: Spatiotemporal expression of f3a by qPCR revealed expression in all developmental stages, suggesting that f3a transcripts are both maternally and zygotically expressed. High expression of f3a from 28 hpf to 36 hpf confirmed the role of in the development of the yolk sac, circulation, and fins. f3a MO-injected embryos showed morphological abnormalities, including shorter body lengths and crooked tails. O-dianisidine staining showed f3a MO-injected embryos exhibited bleeding in the trunk (5.44%) and head (9.52%) regions. Using endothelial-specific transgenic lines of zebrafish (flk1:egfp-NLS/kdrl:mCherry-CAAX), imaging of caudal vein plexus, which forms immediately following the onset of circulation and sprouting, showed a 3-fold decrease in f3a morphants versus controls at 48 hpf, suggesting a potential role for f3a in flow-induced angiogenesis.

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Section: Resultssupporting

confidence: 90%

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Coagulation Factor IIIa (f3a) Knockdown in Zebrafish Leads to Defective Angiogenesis and Mild Bleeding Phenotype

Subramaniam

Fletcher

et al. 2021

Preprint

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“…Other studies have also shown that the TF +5466 A/G polymorphism modulates thrombin generation initiated by vascular injury. However, other studies show no relationship between the expression of TF and increased risk of thrombus formation (Davis and Erlich, 2008;Steppich et al, 2009;Zhou et al, 2011).…”

Section: Discussionmentioning

confidence: 93%

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

Evangelista¹,

Rios²,

Ribeiro³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Recent studies have shown an association between thrombosis and factor VII (FVII), tissue factor (TF), and angiotensinconverting enzyme (ACE). This suggests that individuals with FVII-402 G/A, FVII-401 G/T, TF+5466 A/G, and ACE-287 insertion/ deletion (I/D) polymorphisms present an increased risk of venous thrombosis, heart disease, and ischemic stroke compared with controls. In this study, we investigated the frequencies of these polymorphisms and their association with arterial and venous thrombosis. For the FVII-402 G/A polymorphism, there were 57.3% heterozygote (HT) genotypes and 8.3% homozygote (HM) genotypes in the patients, and 45.2% HT genotypes and 15.4% HM genotypes in the controls. For the FVII-401 G/T polymorphism, there were 37.5% HT genotypes and 3.1% HM genotypes in the patients, and 32.7% HT genotypes and 4.8% HM genotypes in the controls. The polymorphism TF+5466 A/G was not found in any of the samples analyzed. For the ACE-287 I/D polymorphism, there were 43 (40.6%) HT genotypes and 63 (59.4%) HM genotypes in the controls and 28 (45.2%) HT genotypes and 34 (54.8%) HM genotypes in the patients. No significant difference was observed by comparing patients and controls. In this study, no association was found between the presence of the evaluated polymorphisms and the occurrence of thrombotic events.

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“…An article has indicated that miR-93 directly targets coagulation factor III (F3) to participate in the pathogenesis of leiomyomas (16). Tissue factor (F3) is a cell surface receptor for the coagulation factor VII/VIIa, which is initially found as an initiator of the extrinsic coagulation pathway (17). However, the binding relationship between miR-93 and F3 in SUI needs further confirmation.…”

Section: Introductionmentioning

confidence: 99%

An In Vitro Study on Extracellular Vesicles From Adipose-Derived Mesenchymal Stem Cells in Protecting Stress Urinary Incontinence Through MicroRNA-93/F3 Axis

Wang

Xiang

et al. 2021

Front. Endocrinol.

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Since the potential roles of extracellular vesicles secreted by adipose-derived mesenchymal stem cells (ADSCs) are not well understood in collagen metabolism, the purpose of this research was to evaluate the effects of ADSCs-extracellular vesicles in stress urinary incontinence and the regulatory mechanism of delivered microRNA-93 (miR-93). ADSCs were isolated and cultured, and ADSCs-extracellular vesicles were extracted and identified. Stress urinary incontinence primary fibroblasts or satellite cells were treated with ADSCs-extracellular vesicles to detect the expression of Elastin, Collagen I, and Collagen III in fibroblasts and Pax7 and MyoD in satellite cells. After transfecting ADSCs with miR-93 mimics or inhibitors, extracellular vesicles were isolated and treated with stress urinary incontinence primary fibroblasts or satellite cells to observe cell function changes. The online prediction and luciferase activity assay confirmed the targeting relationship between miR-93 and coagulation factor III (F3). The rescue experiment verified the role of ADSCs-extracellular vesicles carrying miR-93 in stress urinary incontinence primary fibroblasts and satellite cells by targeting F3. ADSCs-extracellular vesicles treatment upregulated expression of Elastin, Collagen I, and Collagen III in stress urinary incontinence primary fibroblasts and expression of Pax7 and MyoD in stress urinary incontinence primary satellite cells. miR-93 expression was increased in stress urinary incontinence primary fibroblasts or satellite cells treated with ADSCs-extracellular vesicles. Extracellular vesicles secreted by ADSCs could deliver miR-93 to fibroblasts and then negatively regulate F3 expression; ADSCs-extracellular vesicles could reverse the effect of F3 on extracellular matrix remodeling in stress urinary incontinence fibroblasts. miR-93 expression was also increased in stress urinary incontinence primary satellite cells treated by ADSCs-extracellular vesicles. Extracellular vesicles secreted by ADSCs were delivered to satellite cells through miR-93, which directly targets F3 expression and upregulates Pax7 and MyoD expression in satellite cells. Our study indicates that miR-93 delivered by ADSCs-extracellular vesicles could regulate extracellular matrix remodeling of stress urinary incontinence fibroblasts and promote activation of stress urinary incontinence satellite cells through targeting F3.

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Coagulation factor III (tissue factor) is required for vascularization in zebrafish embryos

Cited by 9 publications

References 23 publications

Coagulation Factor IIIa (f3a) Knockdown in Zebrafish Leads to Defective Angiogenesis and Mild Bleeding Phenotype

Coagulation Factor IIIa (f3a) Knockdown in Zebrafish Leads to Defective Angiogenesis and Mild Bleeding Phenotype

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

An In Vitro Study on Extracellular Vesicles From Adipose-Derived Mesenchymal Stem Cells in Protecting Stress Urinary Incontinence Through MicroRNA-93/F3 Axis

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