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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.
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) has been identified as a master regulator of lymphangiogenesis associated with metastasis including small cell lung cancer (21). COUP-TFII aka NR2F2 is associated with numerous forms of cancer, including gastric, prostate, colon and lung cancer (51). PROX1 and its regulators COUP-TFII and SOX18 drive lymphatic endothelial cell (LEC) specification in mice (21). SOX18 is coexpressed with COUP-TFII and drives the expression of Prox1 in a subset of endothelial cells lining the wall of the cardinal vein (CV). These LECs form the basis of the lymphatic vasculature, and absolutely require transient SOX18 and COUP-TFII activity to induce Prox1 transcription (21–23). In this study, PROX1 and COUP-TFII protein were increased in the lung of mouse model of asthma, indicating that transcription factor PROX1 and COUP-TFII be involved in asthma angiogenesis in collaboration with SOX18.