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  • Urotensin II modulates hepatic fibrosis and portal hemodynamic alterations in rats. 19797237

    The influence of circulating urotensin II (UII) on liver disease and portal hypertension is unknown. We aimed to evaluate whether UII executes a pathogenetic role in the development of hepatic fibrosis and portal hypertension. UII was administered by continuous infusion over 4 wk in 20 healthy rats divided into three treatment groups, controls (saline, n = 7), low dose (UII, 1 nmol.kg(-1).h(-1), n = 8), and high dose (UII, 3 nmol.kg(-1).h(-1), n = 5). Hemodynamic parameters and morphometric quantification of fibrosis were assessed, and profibrotic cytokines and fibrosis markers were assayed in hepatic tissue. UII induced a significant dose-dependent increase in portal venous pressure (5.8 +/- 0.4, 6.4 +/- 0.3, and 7.6 +/- 0.7, respectively, P = 0.03). High-dose UII infusion was associated with an increase in hepatic transcript for transforming growth factor-beta (P 0.05) and platelet-derived growth factor-beta (P = 0.06). Liver tissue hydroxyproline was elevated in the high-dose group (P 0.05). No systemic hemodynamic alterations were noted. We concluded that UII infusion elevates portal pressure and induces hepatic fibrosis in normal rats. This response-05-be mediated via induction of fibrogenic cytokines. These findings have pathophysiological implications in human liver disease where increased plasma UII levels have been observed.
    Document Type:
    Reference
    Product Catalog Number:
    AB755P
    Product Catalog Name:
    Anti-Rat Collagen Type I Antibody

  • The urotensin-II receptor antagonist palosuran improves pancreatic and renal function in diabetic rats. 16267137

    Urotensin-II (U-II) is a cyclic peptide that acts through a specific G-protein-coupled receptor, UT receptor. Urotensin-II and UT receptors have been described in pancreas and kidney, but their function is not well understood. We studied the effects of chronic treatment of diabetic rats with the orally active selective U-II receptor antagonist palosuran. Streptozotocin treatment causes pancreatic beta-cell destruction and leads to the development of hyperglycemia, dyslipidemia, and renal dysfunction. Long-term treatment of streptozotocin-induced diabetic rats with palosuran improved survival, increased insulin, and slowed the increase in glycemia, glycosylated hemoglobin, and serum lipids. Furthermore, palosuran increased renal blood flow and delayed the development of proteinuria and renal damage. The U-II system is unique in that it plays a role both in insulin secretion and in the renal complications of diabetes. Urotensin receptor antagonism might be a new therapeutic approach for the treatment of diabetes.
    Document Type:
    Reference
    Product Catalog Number:
    RI-13K
    Product Catalog Name:
    Rat Insulin RIA

  • Pro-angiogenic activity of Urotensin-II on different human vascular endothelial cell populations. 19362580

    Urotensin-II (U-II), along its receptor UT, is widely expressed in the cardiovascular system, where it exerts regulatory actions under both physiological and pathological conditions. In the present study, human vascular endothelial cells (EC) from one arterious and three venous vascular beds were used to investigate in vitro their heterogeneity in terms of expression of U-II and UT and of angiogenic response to the peptide. Real-time PCR and immunocytochemistry demonstrated the expression of UT, as mRNA and protein, in all the EC populations investigated. U-II, on the contrary, was detectable only in EC from aorta and umbilical vein. U-II did not affect the proliferation rate of adult human EC, but induced a moderate proliferative effect on EC from human umbilical vein. When tested in the Matrigel assay, however, all EC exhibited a strong angiogenic response to the peptide, comparable to that of fibroblast growth factor-2 (FGF-2) and it was not associated to an increased expression of vascular endothelial growth factor (VEGF) and/or its receptors. The angiogenic effect of U-II was abolished by the UT antagonist palosuran. Overall, these data suggest that U-II, in addition to the well known role in the regulation of cardiovascular function, also exert a specific angiogenic activity.
    Document Type:
    Reference
    Product Catalog Number:
    AP132C
    Product Catalog Name:
    Goat Anti-Rabbit IgG Antibody, Cy3 conjugate

  • Lesions of cholinergic pedunculopontine tegmental nucleus neurons fail to affect cocaine or heroin self-administration or conditioned place preference in rats. 24465410

    Cholinergic input to the ventral tegmental area (VTA) is known to contribute to reward. Although it is known that the pedunculopontine tegmental nucleus (PPTg) provides an important source of excitatory input to the dopamine system, the specific role of PPTg cholinergic input to the VTA in cocaine reward has not been previously determined. We used a diphtheria toxin conjugated to urotensin-II (Dtx::UII), the endogenous ligand for urotensin-II receptors expressed by PPTg cholinergic but not glutamatergic or GABAergic cells, to lesion cholinergic PPTg neurons. Dtx::UII toxin infusion resulted in the loss of 95.78 (±0.65)% of PPTg cholinergic cells but did not significantly alter either cocaine or heroin self-administration or the development of cocaine or heroin conditioned place preferences. Thus, cholinergic cells originating in PPTg do not appear to be critical for the rewarding effects of cocaine or of heroin.
    Document Type:
    Reference
    Product Catalog Number:
    AB144P
    Product Catalog Name:
    Anti-Choline Acetyltransferase Antibody

  • Neurotensin in the rat parabrachial region: ultrastructural localization and extrinsic sources of immunoreactivity. 3522659

    We sought to determine (1) the ultrastructural localization and (2) the extrinsic sources of neurotensin-like immunoreactivity (NTLI) in the parabrachial region (PBR). The brains from untreated adult male rats and from others that received intraventricular injections of colchicine (100 micrograms/7.5 microliters saline) 24 hours prior to death were fixed by perfusion with acrolein or glutaraldehyde and paraformaldehyde. Coronal sections were immunocytochemically labeled with a polyclonal rabbit antiserum to neurotensin and the PAP method. Western dot-blots and immunocytochemical labeling with adsorbed antiserum revealed significant cross-reaction only against NT, NT8-13, and glutamine (Gln)4-NT. In the ultrastructural study, the most numerous labeled profiles were axons and axon terminals in both colchicine-treated and control animals. The terminals containing NTLI were characterized by a mixed population of small, clear and large, dense core vesicles; asymmetric junctions principally with unlabeled dendrites; and a few synaptic specializations with unlabeled axon terminals. Compared to axon terminals, relatively few perikarya or dendrites had detectable levels of NTLI in either untreated or colchicine-treated animals. The labeled perikarya measured 8-10 microns in longest cross-sectional diameter, contained NTLI throughout a narrow rim of cytoplasm, and received a few somatic synapses from unlabeled terminals. From the relative density of axon terminals and sparsity of perikarya and dendrites, we conclude that the NTLI in the PBR is principally derived from extrinsic neurons. However, the intrinsic neurons with NTLI may also contribute to the immunoreactivity in the axon terminals of the PBR. We sought to determine the precise location of the extrinsic neurons that contribute to the NTLI in axon terminals in the PBR. Following unilateral injections of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP), dual labeling was most evident in a large population of neurons located in the dorsal, medial and commissural nuclei of the solitary tracts, ipsilateral to the side of the injection. However, a few perikarya containing both the retrogradely transported WGA-HRP and immunocytochemical labels for NT were also detected in the caudal ventrolateral reticular formation, the locus coeruleus, and the paraventricular and lateral hypothalamic nuclei. We conclude that (1) NT or a closely related peptide is present in intrinsic neurons and multiple afferent pathways to the PBR; and (2) the axon terminals with NTLI have synaptic interactions with dendrites of intrinsic neurons and with axon terminals that may have either extrinsic or intrinsic origins.
    Document Type:
    Reference
    Product Catalog Number:
    AB5496

  • Neurotensin terminals form synapses primarily with neurons lacking detectable tyrosine hydroxylase immunoreactivity in the rat substantia nigra and ventral tegmental area ... 1351897

    A light and electron microscopic double antigen localization technique was employed to examine the fine structural relationship between neurotensin-containing axon terminals and dopaminergic neurons in the substantia nigra and ventral tegmental area of the rat. At the light microscopic level, neurotensin-immunoreactive terminals were densely distributed throughout the substantia nigra pars compacta and ventral tegmental area in close proximity to tyrosine hydroxylase-immunoreactive somata and dendrites. On electron microscopic examination, direct synaptic connections were identified between neurotensin-immunoreactive axon terminals and tyrosine hydroxylase-immunopositive perikarya and dendrites. However, only 8.2% and 8.8% of the neurotensin-immunoreactive axonal profiles detected in the substantia nigra and ventral tegmental area, respectively, were found in direct apposition with tyrosine hydroxylase-immunostained elements. In turn, only 9.3% and 10.0% of tyrosine hydroxylase immunoreactive dendrites sampled from the substantia nigra and ventral tegmental area, respectively, were seen in contact with neurotensin immunopositive axon terminals. However, neurotensin-immunoreactive and tyrosine hydroxylase-immunolabelled elements were frequently identified in close anatomical proximity (less than 5 microns) to one another. These results are interpreted in light of the selective association of neurotensin receptors with dopaminergic neurons in the substantia nigra and ventral tegmental area to suggest a predominantly parasynaptic mechanism of action for neurotensin in the ventral midbrain.
    Document Type:
    Reference
    Product Catalog Number:
    AB5496

  • Neurotensin: immunohistochemical localization in rat central nervous system. 333458

    Neurotensin immunofluorescence was examined in the rat central nervous system using a well-characterized antiserum directed against this tridecapeptide. Morphological characteristics of the fluorescence indicate its association with neuronal cell bodies and processes in the brain and with cells of the anterior pituitary. Fluorescence is seen in many brain areas, with notable densities in the substantia gelatinosa zones of the spinal cord and trigeminal nucleus, central amygdaloid nucleus, anterior pituitary, median eminence, and preoptic and basal hypothalamic areas.
    Document Type:
    Reference
    Product Catalog Number:
    AB5496

  • Neurotensin in the human brain. 3670596

    The localization of neurotensin-immunoreactive sites in the adult human brain was investigated by the indirect immunoperoxidase method of Sternberger [Sternberger (1979) Immunocytochemistry. Wiley, New York]. Our results demonstrate a widespread, albeit uneven occurrence of neurotensin-immunoreactive cells and processes throughout the central nervous system. Immunoreactive cells are prominent in the medial hypothalamus and in various regions of the limbic system, including the amygdaloid body, septal area, bed nucleus of the stria terminalis and piriform cortex. A few cells were also found in the dorsal synencephalon, superior colliculus, periaqueductal grey and spinal trigeminal nucleus. The distribution of immunoreactive fibres corresponds well with that reported for rodents. Areas with the highest concentration of neurotensin-immunoreactive processes included all the areas where immunoreactive neurons were found and, in addition, periventricular thalamic nuclei, the sublenticular region, lateral parts of the brainstem reticular formation and the vagus-solitarius complex. Comparison mapping studies of melanin-containing neurons on sections treated with neurotensin antiserum revealed an anatomical relation between almost all the catecholaminergic cell clusters with peptide-containing fibres.
    Document Type:
    Reference
    Product Catalog Number:
    AB5496