Disease relevance of DDX4

• Furthermore, these findings suggest that VASA is likely to serve as a useful and highly specific biomarker for germ cell tumors, particularly classic and spermatocytic seminoma/dysgerminoma, including their precursor stages [1].
• We investigated the presence of VASA mRNA and protein in a series of germ cell tumors of different histologic subtypes and anatomic location, as well as in nongerm cell tumors such as testicular lymphomas and Leydig cell tumors [1].
• No VASA mRNA or protein was detectable in nonseminomatous germ cell tumors (such as embryonal carcinoma, teratoma, and yolk sac tumor) and derived cell lines, or nongerm cell tumors such as lymphoma or Leydig cell tumor [1].
• We detected VASA mRNA (by quantitative RT-PCR) and protein (by immunohistochemical staining) in normal spermatogenesis, seminoma (both classic and spermatocytic), carcinoma in situ (the precursor of classic seminoma and nonseminoma), dysgerminoma, and gonadoblastoma [1].
• In addition, there were mesoaortitis with obliterative endarteritis of the vasa vasorum and fibrosis of the aortic cusps with separation of the commissures [2].

High impact information on DDX4

• The most motile sperm were found in the proximal epididymis, at or near the vasa efferentia [3].
• Sperm from the proximal caput epididymidis and even sperm from the vasa efferentia (which have never passed through the epididymis) can fertilize the human oocyte in vitro and result in pregnancy with live birth [3].
• Vasa vasorum in coronary-artery disease [4].
• Treatments to arrest acid wood hydrolysis of the Vasa and other wooden marine-archaeological artefacts should therefore focus on the removal of sulphur and iron compounds [5].
• T induces the Wolffian ducts to differentiate into epididymides, vasa deferens, and seminal vesicles [6].

Chemical compound and disease context of DDX4

• Therapeutic Angiogenesis Inhibits or Rescues Chemotherapy-induced Peripheral Neuropathy: Taxol- and Thalidomide-induced Injury of Vasa Nervorum is Ameliorated by VEGF [7].
• Carbon monoxide acts both by inducing hypoxemia and shifting the oxyhemoglobin equilibrium curve, with these effects acting on the oxygen transport system from both the luminal blood and the vasa vasorum [8].
• In all cases, immunofluorescent deposits of hepatitis B surface antigen, immunoglobulin and C3 complement were detected in the vasa nervorum [9].
• Torsion/detorsion of the spermatic cord did not alter exogenously applied noradrenaline-induced contractions in both vasa deferentia [10].
• Important intrarenal compensatory actions of the renin-angiotensin system include support of glomerular filtration, enhancement of vasa recta-mediated counter-current exchange, sustained urea excretion and maintenance of renal artery pressure distal to the stenosis [11].

Biological context of DDX4

• Cell damage to mTALs included mitochondrial swelling, nuclear pyknosis, and cytoplasmic disruption with superimposed calcification; these changes were most severe in the deepest areas of the outer medulla, away from vasa recta in zones remote from oxygen supply [12].
• During maximal vasodilation induced by infusion of adenosine, flow through vasa was 3- to 8-fold greater in atherosclerotic than in normal monkeys [13].
• Early vasa nervorum functional changes are caused by the metabolic insults of diabetes, the balance between vasodilation and vasoconstriction is altered [14].
• Hyperglycemia-induced endothelial dysfunction is mediated by increased oxidative stress, a promoter of adventitial inflammation and vasa vasorum neovascularization in experimental models of diabetic atherosclerosis [15].
• It is expressed at high levels during early oogenesis, but no detectable vasa RNA and little Vasa protein are present in mature unlaid eggs [16].

Anatomical context of DDX4

• DDX4 shows specific expression in germ cells [17].
• We show by Northern analysis of fetal and adult tissues that expression of the human VASA gene is restricted to the ovary and testis and is undetectable in somatic tissues [18].
• Expression of various germ cell markers, such as Vasa, growth differentiation marker 9 and SSEA-1, increased in the clonal cell line, and OLCs showed additionally expression of meiosis-specific markers SCP3 and DMC1 [19].
• This may result from intracellular polymerization of sickle hemoglobin (HbS) in erythrocytes, leading to microvascular occlusion, in the vasa recta of the renal medulla [20].
• In nonatherosclerotic arteries, ACE immunoreactivity was found in luminal and adventitial vasa vasorum endothelium [21].

Associations of DDX4 with chemical compounds

• We generated polyclonal antibodies that bind to the VASA protein in formalin-fixed, paraffin-embedded tissue and characterized VASA protein expression in human germ cells at various stages of development [18].
• Infusion of phenylephrine or serotonin did not alter flow through vasa in normal monkeys [22].
• During infusion of adenosine, blood flow to vasa was fourfold greater in atherosclerotic monkeys than after regression of atherosclerosis [22].
• We conclude that vasa vasorum in atherosclerotic coronary arteries respond to vasoconstrictor stimuli and that there is loss of vasa vasorum and a large decrease in blood flow through vasa to intima-media of coronary arteries after regression of atherosclerosis [22].
• The Kidd (JK) blood group locus encodes a urea transporter that is expressed on human red cells and on endothelial cells of the vasa recta in the kidney [23].

Other interactions of DDX4

• We found that addition of recombinant human BMP4 increased the expression of the germ cell-specific markers VASA and SYCP3 during differentiation of hES cells to embryoid bodies (EBs) [24].

Analytical, diagnostic and therapeutic context of DDX4

• Immunization of BALB/c mice with cDDX4 conjugated with a multiple-antigen peptide (cDDX4-MAP) induced conformational epitope-specific antibodies, and monoclonal antibody IA2-F9 reacted with cDDX4, but not with linear DDX4, as determined by real-time biomolecular interaction analysis using surface plasmon resonance [25].
• This study was performed to determine whether there is increased perfusion of the aortic wall by vasa vasorum in atherosclerosis [13].
• Blood flow to vasa vasorum was measured with microspheres [22].
• Immunocytochemistry studies of the kidney showed gp-Fy in the endothelium of glomeruli, peritubular capillaries, vasa recta, and the principal cells (epithelial) of collecting ducts [26].
• This finding suggests that loss of vessels, not constriction of existing vessels, accounts for the decrease in flow through vasa in intima-media after regression of atherosclerosis [22].

References