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Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Adenosine A1 receptors and vascular reactivity

ACTA PHYSIOLOGICA, Issue 2 2010
Y. Wang
Abstract Aim:, Blood pressure is higher in A1 receptor knock-out (A1R,/,) mice than in wild type litter mates (A1R+/+) and we have examined if this could be related to altered vascular functions. Methods:, Contraction of aortic rings and mesenteric arteries were examined. To examine if the adenosine A1 receptor-mediated contraction of aortic muscle was functionally important we examined pulse pressure (PP) and augmentation index (AIX) using a sensor that allows measurements of rapid pressure transients. Results:, Contraction of aortic rings to phenylephrine and relaxation to acetylcholine were similar between genotypes. The non-selective adenosine receptor agonist N -ethyl carboxamido adenosine (NECA) enhanced the contractile response, and this was eliminated in aortas from A1R,/, mice. However, in mesenteric arteries no contractile response was seen and adenosine-mediated relaxation was identical between studied genotypes. A2B adenosine receptors, rather than A2A receptors, may be mainly responsible for the vasorelaxation induced by adenosine analogues in the examined mouse vessels. PP was higher in A1R,/, mice, but variability was unaltered. AIX was not different between genotypes, but the NECA-induced fall was larger in A1R,/, mice. Conclusions:, The role of adenosine A1 receptors in regulating vessel tone differs between blood vessels. Furthermore, contractile effects on isolated vessels cannot explain the blood pressure in A1 knock-out mice. The A1 receptor modulation of blood pressure is therefore mainly related to extravascular factors. [source]

Electrical stimulation promotes peripheral axon regeneration by enhanced neuronal neurotrophin signaling

DEVELOPMENTAL NEUROBIOLOGY, Issue 2 2007
Arthur W. English
Abstract Electrical stimulation of cut peripheral nerves at the time of their surgical repair results in an enhancement of axon regeneration. Regeneration of axons through nerve allografts was used to evaluate whether this effect is due to an augmentation of cell autonomous neurotrophin signaling in the axons or signaling from neurotrophins produced in the surrounding environment. In the thy-1-YFP-H mouse, a single 1 h application of electrical stimulation at the time of surgical repair of the cut common fibular nerve results in a significant increase in the proportion of YFP+ dorsal root ganglion neurons, which were immunoreactive for BDNF or trkB, as well as an increase in the length of regenerating axons through allografts from wild type litter mates, both 1 and 2 weeks later. Axon growth through allografts from neurotrophin-4/5 knockout mice or grafts made acellular by repeated cycles of freezing and thawing is normally very poor, but electrical stimulation results in a growth of axons through these grafts, which is similar to that observed through grafts from wild type mice after electrical stimulation. When cut nerves in NT-4/5 knockout mice were electrically stimulated, no enhancement of axon regeneration was found. Electrical stimulation thus produces a potent enhancement of the regeneration of axons in cut peripheral nerves, which is independent of neurotrophin production by cells in their surrounding environment but is dependent on stimulation of trkB and its ligands in the regenerating axons themselves. © 2006 Wiley Periodicals, Inc. Develop Neurobiol 67: 158,172, 2007. [source]

Microglial colonization of the developing mouse brain: the effect of CD11b deletion

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2002
J. K. Jeetle
Introduction:, Microglia are resident mononuclear phagocytes of the central nervous system, which colonize the brain both prenatally and after birth. It is proposed that they enter the brain initially via the surrounding mesenchyme, via ventricles and later through blood vessels, but the mechanisms of entry and signals used for migration are still to be established. Previous studies have shown that ligands for some integrin adhesion molecules expressed on blood vessels in the developing nervous system (particularly ICAM-1 and ICAM-2 which bind CD11a/LFA-1 and CD11b/Mac-1), may act as potential recruiting signals for microglial precursors. This study addressed whether CD11b is influential on the migration of microglial precursors into the developing CNS. Material and methods:,Ricinus communis agglutinin-1 (RCA-1) lectin histochemistry was employed to anatomically map the distribution of amoeboid and ramified microglia from embryonic day 15 (E15) to birth. Embryonic mouse brains from CD11b knockout (,/,) (n = 42), and heterozygote (+/,) (n = 52) mice generated on a C57/BL6 background (Melo et al. Cell Immunol 2000; 205: 13,23) and wild-type (+/+) (n = 37) litter mates were fixed in Bouin's solution, processed to paraffin wax and serially sectioned at 15,40 µm. To investigate further potential signals for recruiting microglial precursors, brains were immunochemically screened for integrins CD11a, CD11b, CD18, ,X, VLA-4 and the chemokine MCP-1. Results:, Microscopic analysis revealed the morphological transition of microglia from predominantly amoeboid forms at E15,E16 to a flourishing population of ramified cells at E19,E20. RCA-1 histochemistry showed no clear differences in microglial distribution or timing of colonization between CD11b (,/,) and wild-type mice from E15 to birth. Although CD11b deletion did not influence the timing of microglial ramification, there appeared to be fewer ramified cells in (,/,) mice within comparative brain regions. This requires further quantitative morphometric analysis. Of the integrins investigated, none were restricted to microglia and only VLA-4 and ,X showed reactivity within the CNS. However, MCP-1 was notably localized to the cortical plate within all genotypes, consistent with previous findings in human foetal CNS (Rezaie & Male. Microsc Res Tech 1999; 45: 359,382). Conclusion:, The results suggest that CD11b has little influence on the timing or regional distribution of microglia in the developing murine CNS. It is more likely that CD11b is only one of several factors that influence the migration and differentiation of these cells. [source]

Suppression of experimental lupus nephritis by aberrant expression of the soluble E-selectin gene

PATHOLOGY INTERNATIONAL, Issue 3 2002
Satoru Takahashi
Circulating leukocytes, particularly neutrophils and monocytes, are important effector cells in the induction of many forms of glomerulonephritis. Adhesion molecules, especially selectins, are also thought to be critical for the development of this disease. We examined the possible suppressive effect of soluble E-selectin on the development of experimental lupus nephritis induced by the injection of a hybridoma clone (2B11.3) derived from an MRL/MpJ- lpr/lpr lupus mouse. This clone produces IgG3 antibodies that induce severe proliferative glomerulonephritis resembling lupus nephritis when injected into normal mice. Transgenic mice with a soluble E-selectin gene were injected intraperitoneally with the hybridoma cells and histopathologically examined on day 15. As a result, the development of glomerulonephritis was significantly suppressed. This suppression was characterized by fewer inflammatory cell infiltrates, compared with non-transgenic litter mates, despite the fact that there were no remarkable differences in immunoglobulin deposits or expression of E-selectin between the two groups. These findings suggest that by controlling inflammatory cell infiltration, soluble E-selectin plays a preventative role in the development of a particular type of lupus nephritis. [source]