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  • br Thy nephritis is one of the most commonly

    2019-10-24


    Thy1.1 nephritis is one of the most commonly used models to study the course of immunoglobulin A and other mesangioproliferative nephropathies. To date, most of the studies have focused on mesangial and, to a lesser extent, endothelial cell recovery following capillary damage, whereas data concerning the podocyte response are still scarce. Podocytes are terminally differentiated epithelial cells with a distinctive morphology. Their foot processes and the slit membrane are localized at the basolateral site, while a well-developed Nicotine faces the urinary space. Proteins located at the basolateral site have been extensively studied owing to their involvement in maintaining podocyte attachment to the basement membrane and barrier function against proteinuria. It is, however, not unusual for apically expressed proteins to regulate the function of foot processes and overall podocyte homeostasis. Therefore, alterations in apical membrane domains are one of the events leading to podocyte degeneration. Nicotine Unlike endothelial and mesangial cells, podocytes have very limited capability of self-renewal, making their injury a critical step in the pathogenesis of nephropathies. Recently ephrinB1, a ligand of the EphB family of receptor tyrosine kinases, has emerged as yet another protein located at the glomerular slit membrane. The specific feature of these versatile molecules is the possibility of bidirectional signaling, where not only the Eph receptor (forward signaling) but also the membrane-bound ephrin ligand (reverse signaling) can convey an intracellular signal. Eph/ephrins have previously attracted a lot of attention owing to their crucial involvement in the development of the vascular and nervous systems. Among Eph/ephrins, EphB4 and its ligand ephrinB2 were first described as critical molecules regulating vascular development, where EphB4-expressing venous endothelial cells assemble with ephrinB2-expressing arterial endothelium to form functional vasculature. As the EphB4/ephrinB2 pair acts in this setting as reciprocal signaling partners, their loss causes similar phenotypes in mouse embryos. Also, there is evidence that EphB4/ephrinB2 control bone homeostasis as well as vascular biology in the adult organism. Eph/ephrins are also expressed in the adult kidney; however, their involvement in glomerular recovery from acute glomerulonephritis has not been addressed. RESULTS
    DISCUSSION
    MATERIALS AND METHODS
    ACKNOWLEDGMENTS This research was supported by grants 3100A0-1183691 of the Swiss National Science Foundation to Uyen Huynh-Do and 31003A-116243 to Valentin Djonov. We greatly acknowledge the technical support from Brigitte Scolari, Regula Buergy, Clemens Weber, and Werner Graber. We thank Felix Frey, Brigitte Frey, Mathias Gugger, and Meike Mevissen for the helpful discussions. We also would like to acknowledge Sue Quaggin and Vera Eremina for providing reagents and for help with the in situ hybridization protocol.
    Introduction Blood vessels form via two distinct processes, vasculogenesis and angiogenesis [1], [2]. Vasculogenesis involves in the differentiation of endothelial cells (ECs) from mesodermal angioblasts, which differentiate into endothelial cords [3]. In the angiogenesis, new blood vessels arise from the preexisting vasculature by proliferation and migration of endothelial cells. In the adult, angiogenesis is accompanied in the ovulation, placental development, and wound healing, and in the pathological processes such as tumor growth and metastasis, diabetic retinopathy, and rheumatoid arthritis [4], [5]. The Eph receptors, which are a class of endothelial receptor tyrosine kinases, were implicated in the control of blood vessel formation [2], [6], [7]. An assembly of endothelial cells into capillary-like structures by promotion of EphrinB2 indicates that EphrinB2 may be involved in the angiogenesis [8]. These findings are supported by in vivo evidence that several disruptive embryogenic vasculature in the Ephrins-B2-deficient mice were observed [9]. In addition, the endothelial cell expression of EphB4 receptor suggested that EphB4 may mediate EphrinB2 signaling in the vascular development [9]. These evidences indicate clearly that Eph receptors and their Ephrin ligands are involved in the control of developing vasculature.