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Nidus or no nidus: Is it a crucial issue for diagnostic assessment of arteriovenous malformations?
Published in Byung-Boong Lee, Peter Gloviczki, Francine Blei, Jovan N. Markovic, Vascular Malformations, 2019
Expression of specific markers in endothelial cells determines their differentiation, either into an artery or into a vein in the early stage of vascular development.4, 5 The Dll4-Hey2-EphrinB2 pathway determines endothelial fate as an artery, and the COUP-TFII pathway signals endothelial cells to become veins.6, 7
Congenital diaphragmatic hernia
Published in Prem Puri, Newborn Surgery, 2017
Experimental studies have suggested that the classical view of embryogenesis of CDH may have to be revised. A toxicological nitrofen model of CDH has shown that abnormalities in the contralateral lung as well as the ipsilateral side are present even before the diaphragm starts to develop.14 Keijzer et al.15 proposed the dual-hit hypothesis to explain the observations on pulmonary hypoplasia in this model. This hypothesis proposes that the early retardation in lung development that occurs before the development of the diaphragmatic defect is caused by nitrofen, whereas the late-gestational increase in lung hypoplasia is caused by mechanical compression from herniated viscera. Kluth et al.16 have shown that pleuroperitoneal canals are not wide enough to allow herniation of gut loops in rats. Several groups have shown aberrant gene/protein expression of different growth factors and transcription factors in experimental models as well as in patients with CDH.17–20 The retinoid signaling pathway and also its downstream target COUP transcription factor 2 (COUP-TFII) have been shown to be disrupted in the nitrofen model of CDH.21–23 Beurskens et al.24 reported significantly lower levels of cord retinol and retinol-binding protein in neonates with CDH. Vitamin A–deficient rats display pulmonary hypoplasia with CDH.25 Furthermore, the lungs in experimental models of CDH exhibit a response to retinoic acid different from normal lungs.23,26 Furthermore, prenatal retinoic acid (RA) treatment has been shown to upregulate pulmonary expression levels of genes involved in lung morphogenesis in the nitrofen-induced hypoplastic lung.27 Although prenatal use of RA has been controversial, these experimental data suggest that prenatal RA treatment may have a therapeutic potential to revert pulmonary hypoplasia associated with CDH.
Label-free quantitative proteomics identifies Smarca4 is involved in vascular calcification
Published in Renal Failure, 2019
Chan Wang, Yun Tang, Yanmei Wang, Guisen Li, Li Wang, Yi Li
Bioinformatics analysis showed that these significant proteins were mainly involved in placenta blood vessel development and cell adhesion molecule binding. Curtis et al. identified that conditional deletion of Smarca4 had revealed its importance role in the embryonic vascular development [15]. They further revealed that in the course of embryonic vascular development, Smarca4 promoted venous specification by remodeling the COUP-TFII (chicken ovalbumin upstream promoter transcription factor 2, also known as NR2F2) promoter [16]. In addition, Smarca4 can also bind to cell adhesion molecules. For example, it interacted with and was recruited to the CAM promoters, its over-expression also promoted transactivation of adhesion molecules and leukocyte adhesion induced by inflammatory signals [17]. Based on the results of bioinformatics analysis, we chose Smarca4 for further validation.
Augmented angiogenic transcription factor, SOX18, is associated with asthma exacerbation
Published in Journal of Asthma, 2021
Jisu Hong, Pureun-Haneul Lee, Yun-Gi Lee, George D. Leikauf, An-Soo Jang
Prospero homeobox 1 (PROX1) is one of the key transcription factors driving the fate and specification of lymphatic endothelial cells (21). PROX1 and its regulators COUP-TFII (Chicken ovalbumin upstream promoter transcription factor 2 COUP-TFII aka NR2F2) and SOX18 drive lymphatic endothelial cell (LEC) specification in mice (22). LECs form the basis of the lymphatic vasculature, and absolutely require transient SOX18 and COUP-TFII activity to induce Prox1 transcription (22–24).