Luteinizing hormone-releasing hormone (LHRH) neurons originate in the olfactory placode and vomeronasal organ and migrate to the brain from embryonic day 14 (E14) in the rat. We investigated the development of the vomeronasal nerve and its role as a guide for migrating LHRH neurons. Using fluorescent, lipophilic dye tracing methods, we observed axons that emerge from the vomeronasal organ and cross the nasal septum as several large fascicles. At E14-15, these fascicles converge as they enter the region of the cribriform plate and subsequently disperse, projecting dorsally and caudally across the olfactory bulb and rostral forebrain. At E16, the dorsal branch of the vomeronasal nerve forms a more tightly fasciculated projection; the caudal fibers remain dispersed, extending along the medial forebrain. The number of caudally directed axons decreases during development, leaving four or five present at postnatal day 4 (P4). Immunohistochemical studies indicate that the vomeronasal nerve can be divided into four spatially distinct subpopulations of fibers. One subset, composed of caudal fibers that terminate in the lamina terminalis, selectively expresses TAG-1, a transient axonal surface glycoprotein and PSA-N-CAM, a highly polysialated form of neural cell adhesion molecule. The extension and subsequent retraction of this branch of the vomeronasal nerve corresponds spatially and temporally with the migration of LHRH neurons from the nasal cavity to the brain. Our studies show that between E14 and E18, LHRH neurons migrate in contact with the TAG-1+, PSA-N-CAM+ caudal branch of the vomeronasal nerve.
Cirrhosis is a chronic liver disease that impairs hepatic function and causes advanced fibrosis. Mesenchymal stem cells have gained recent popularity as a regenerative therapy since they possess immunomodulatory functions. We found that injected adipose tissue‐derived stem cells (ADSCs) reside in the liver. Injection of ADSCs also restores albumin expression in hepatic parenchymal cells and ameliorates fibrosis in a nonalcoholic steatohepatitis model of cirrhosis in mice. Gene expression analysis of the liver identifies up‐ and down‐regulation of genes, indicating regeneration/repair and anti‐inflammatory processes following ADSC injection. ADSC treatment also decreases the number of intrahepatic infiltrating CD11b+ and Gr‐1+ cells and reduces the ratio of CD8+/CD4+ cells in hepatic inflammatory cells. This is consistent with down‐regulation of genes in hepatic inflammatory cells related to antigen presentation and helper T‐cell activation. Conclusion: These results suggest that ADSC therapy is beneficial in cirrhosis, as it can repair and restore the function of the impaired liver. (Hepatology 2013;53:1133–1142)
Copper(II) terephthalate absorbs a large amount of gases such as N2, Ar, O2, and Xe. The maximum amounts of absorption of gases were 1.8, 1.9, 2.2, and 0.9 mole per one mole of the copper(II) salt for N2, Ar, O2, and Xe, respectively, indicating that the gases were not adsorbed on the surface but occluded within the solid. The porous structure of copper(II) terephthalate, in which the gas is occluded, is deduced from the temperature dependence of magnetic susceptibilities and the linear structure of terephthalate.
Luteinizing hormone-releasing hormone (LHRH) neurons migrate from the olfactory placode to the forebrain in association with vomeronasal nerves (VNN) that express the polysialic acid-rich form of the neural cell adhesion molecule (PSA-NCAM). Two approaches were used to investigate the role of PSA-NCAM: injection of mouse embryos with endoneuraminidase N, followed by the analysis of LHRH cell positions, and examination of LHRH cell positions in mutant mice deficient in the expression of NCAM or the NCAM-180 isoform, which carries nearly all PSA in the brain. The enzymatic removal of PSA at embryonic day 12 significantly inhibited the migration of nearly half of the LHRH neuron population, without affecting the VNN tract itself. Surprisingly, the absence of NCAM or NCAM-180 did not produce this effect. However, a shift in the route of migration, resulting in an excess number of LHRH cells in the accessory olfactory bulb, was observed in the NCAM-180 mutant. Furthermore, it was found that PSA expressed by the proximal VNN and its distal branch leading to the accessory bulb, but not the branch leading to the forebrain, was associated with the NCAM-140 isoform and thus was retained in the NCAM-180 mutant. These results provide two types of evidence that PSA-NCAM plays a role in LHRH cell migration: promotion of cell movement along the VNN tract that is sensitive to acute (enzymatic), but not chronic (genetic), removal of PSA-NCAM, and a preference of a subset of migrating LHRH cells for a PSA-positive axon branch over a PSA-negative branch in the NCAM-180 mutant.
Although mitogenic and differentiating factors often activate a number of common signaling pathways, the mechanisms leading to their distinct cellular outcomes have not been elucidated. In a previous report, we demonstrated that mitogen-activated protein (MAP) kinase (ERK) activation by the neurogenic agents fibroblast growth factor (FGF) and nerve growth factor is dependent on protein kinase C␦ (PKC␦), whereas MAP kinase activation in response to the mitogen epidermal growth factor (EGF) is independent of PKC␦ in rat hippocampal (H19-7) and pheochromocytoma (PC12) cells. We now show that EGF activates MAP kinase through a PKC-dependent pathway involving phosphatidylinositol 3-kinase and PDK1 in H19-7 cells. PKC, like PKC␦, acts upstream of MEK, and PKC can potentiate Raf-1 activation by EGF. Inhibition of PKC also blocks EGF-induced DNA synthesis as monitored by bromodeoxyuridine incorporation in H19-7 cells. Finally, in embryonic rat brain hippocampal cell cultures, inhibitors of PKC or PKC␦ suppress MAP kinase activation by EGF or FGF, respectively, indicating that these factors activate distinct signaling pathways in primary as well as immortalized neural cells. Taken together, these results implicate different PKC isoforms as determinants of growth factor signaling specificity within the same cell. Furthermore, these data provide a mechanism whereby different growth factors can differentially activate a common signaling intermediate and thereby generate biological diversity.
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