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Embryology of the Female Urogenital System and Clinical Applications
Published in Linda Cardozo, Staskin David, Textbook of Female Urology and Urogynecology - Two-Volume Set, 2017
Figure 22.7 VisuAlizAtion of the three stAges of ureter mAturAtion in vivo in Hoxb7-GFP mice thAt express green fluorescent protein in epitheliA of the fetAl excretory system. (A–c) ureterAl bud formAtion And outgrowth: The distAl ureter (ur) remAins AttAched to the WolffiAn duct (wd). The distAl ureter stArts to sepArAte from the primitive blAdder (ugs) by A terminAl WolffiAn duct segment, the common nephric duct (cnd). (d–f) VerticAl displAcement: The distAl ureter descends And contActs the urogenitAl sinus. The yellow Arrow indicAtes the common nephric duct. broken yellow Arrow shows the downwArd movement of the ureter towArd the urogenitAl sinus. Yellow And green Arrows indicAte the finAl position of the distAl ureter And WolffiAn duct. (g–i) LAterAl displAcement: The distAl ureter sepArAtes from the WolffiAn duct And moves to the finAl position At blAdder bAse. Yellow And green Arrows mArk the position of the distAl ureter And WolffiAn duct before And After sepArAtion. Double-heAded yellow Arrow indicAtes epitheliAl wedge, An epitheliAl outgrowth, which fAcilitAtes the sepArAtion. Color code for (c, f, i): WolffiAn duct And trigonAl wedge, green; urogenitAl sinus, grey; MülleriAn duct, pink; common nephric duct, red; kidney And ureter, blue. (With permission from bAtourinA e et Al., NAt Genet, 32, 109, 2002.)
Intestinal macrophages in defense of the mucosa
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Lesley E. Smythies, Phillip D. Smith
In the bone marrow, pluripotent stem cells are exposed sequentially to combinations of growth factors, hormones, and cytokines that regulate cell maturation and differentiation into common lymphoid progenitor cells and common myeloid progenitor cells. The cytokines interleukin (IL)-1, IL-3, and IL-6 together stimulate pluripotent stem cells to lose their capacity for self-renewal and become myeloid progenitor cells capable of differentiation into monocytic, granulocytic, megakaryocytic, or erythroid lineages. Myeloid progenitor cells become committed to a granulocyte/monocyte lineage and lose their ability to differentiate into the other myeloid lineages under the continued influence of IL-1 and IL-3. Further exposure to this combination of cytokines plus granulocyte-macrophage colony-stimulating factor (GM-CSF) induces the proliferation of both granulocyte and monocyte precursors. Exposure to IL-1, IL-3, GM-CSF, and then macrophage CSF (M-CSF), induces the sequential differentiation of monocyte precursors, monoblasts, promonocytes, and finally monocytes, which are released from the bone marrow and enter the circulation. Under homeostatic conditions, the same precursors can differentiate into monocytes, DCs, or polymorphonuclear neutrophils, but differentiation can be redirected in appropriate circumstances. In addition to the cytokine growth factors mentioned earlier, each stage of this differentiation pathway may be influenced by constitutive and inducible transcription factors, including PU.1 and AML1, which direct the expression of myeloid-specific genes involved in monocyte differentiation. PU.1 is particularly important because it regulates the expression of the receptor for M-CSF, which is critical for M-CSF-dependent differentiation. The transcription factors GATA-2, SCL, and Myb regulate myeloid cell survival. Additional transcription factors, including CCAAT-enhancer-binding protein-β (C/EBP-β), HOXB7, and c-Myc, regulate the intermediate stages of myeloid differentiation, whereas C/EBPβ, EBR-1, IRF-1, NF-Y, and some Jun/Fos and STAT proteins regulate monocyte maturation.
Construction of a novel microRNA-based signature for predicting the prognosis of glioma
Published in International Journal of Neuroscience, 2023
Gaoxin Liu, Xiaoming Rong, Xinrou Lin, Hongxuan Wang, Lei He, Ying Peng
It has been shown in previous studies that miR-196b-5p can promote lung cancer cell proliferation targeting the tumor suppressor FAS [23]. Also, MiR-196b-5p can regulate the metastasis and migration of colorectal cancer cells by interacting with HOXB7 and GALNT [24]. The miR-196b-5p plays a pro-carcinogenic role in glioma cells. Over-expression of miR-196b-5p can promote proliferation, migration, invasion, and reduced apoptosis of glioma cell lines. In glioma cells, miR-196b-5p targets VSNL1. A previous study found that VSNL1 was highly expressed in TCL2 MBEN (medulloblastoma with extensive nodularity) than in TCL1 MBEN, and TCL2 MBEN type had better clinical regression [25]. Suppression of VSNL1 expression counteracts the effect of miR-196b-5p downregulation on glioma development. Moreover, downregulation of VSNL1 abolishes the influence of miR-196b-5p downregulation on glioma cell apoptosis to a certain extent and promotes the apoptosis of glioma cells.
MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
Published in Upsala Journal of Medical Sciences, 2018
Katarina Zeljic, Ivan Jovanovic, Jasmina Jovanovic, Zvonko Magic, Aleksandra Stankovic, Gordana Supic
The activity of other meta-signature miRNAs was also examined in oral cancer. In a study investigating miRNA expression in oral cancer patients with and without metastasis, mir-135b was suggested to be a promising down-regulated biomarker of oral cancer progression (32). It was found that down-regulated miR-376c-3p suppresses the cancer phenotype by targeting homeobox B7 (HOXB7) in oral cancer tissue as well as in cell lines (33). In addition, in head and neck cancer, down-regulated miR-376c-3p leads to runt-related transcription factor 2 gene (RUNX2) deregulation and is associated with lymph node metastasis (34). Poor prognosis of head and neck cancer patients was associated with up-regulated expression of mir-93 (35) and mir-18a (25). Mir-34b has been found to be one of the consistently up-regulated miRNAs in head and neck cancer in a majority of studies as well (36). A recent study reported that in oral cancer miR-424-5p directly targets supressor of cytokine signaling gene (SOCS2) and modulates STAT5 signaling, expression of matrix metalloproteinase, cell migration, and invasion (37). It has been reported that miR-455-3p up-regulation is controlled by the TGF-beta pathway, consequently down-regulating ubiquitin conjugating enzyme E2B gene (UBE2B), which results in oral cancer proliferation (38).
Connection of ES Cell-derived Collecting Ducts and Ureter-like Structures to Host Kidneys in Culture
Published in Organogenesis, 2021
The eUBs for the experiments we describe here were therefore made by exactly the same procedure as in our report of urothelial differentiation,10 the ‘Taguchi protocol’, first described by the Nishinakamura laboratory at Kumamato University, Japan.11 Briefly, the Hoxb7-GFP mouse ESC line was maintained on ES maintenance medium11 for several days and then differentiated into GFP-eUBs using the sequence of medium changes in the Taguchi protocol.11 At day 10, the ES cells formed UB-like tubules that expressed the UB marker hoxb7-GFP (Figure S1 A, B). These structures showed the ability to branch in 3D gel supplemented with branch inducing factors (Figure S1 C, D), as expected from published work.10,11