Cheung, BMY

Lan, HY

Li, YY

Tang, F

Wong, LYF

Hong Kong Medical Journal

HKU Scholars Hub

TitleAdrenomedullin suppresses migration inhibitory factorproduction and cytokine response of rat macrophages tolipopolysaccharideAuthor(s) Wong, LYF; Cheung, BMY; Li, YY; Tang, F; Lan, HYCitationThe 8th Medical Research Conference Abstracts, Hong KongMedical Journal, Hong Kong, China, 25-26 January 2003, v. 9 n. 1Supp 1, p. 29Issued Date 2003URL http://hdl.handle.net/10722/48478Rights Creative Commons: Attribution 3.0 Hong Kong LicenseHKMJ Vol 9 No 1 February 2003 Supplement      29Adrenomedullin suppresses migration inhibitory factor production and cytokineresponse of rat macrophages to lipopolysaccharideLYF Wong, BMY Cheung, YY Li,1 F Tang,1 HY Lan2Department of Medicine & Department of Physiology,1 The University of Hong Kong; Baylor College of Medicine, Texas, US2Introduction: Adrenomedullin (AM) is a vasorelaxant peptide that is also involved in inflammation. Macrophagemigration inhibitory factor (MIF) is released from pituitary and macrophages and is an important regulator ofinflammation. We investigated the interaction between AM and MIF in cultured rat macrophages.Method: Rat macrophages (NR8383) were activated by LPS in the absence and presence of AM at 1ng/mL to 1µg/mL.MIF, TNF-alpha, IL-6 and IL-1beta were measured by ELISA at 0, 1, 3, 6, and 24-hours. The effect of AM oncytokine response from resting macrophages was determined from cell cultures containing RPMI medium and AMalone.Results: AM increased release of MIF from resting macrophage dose-dependently in the first hour by 36.3 % to 75.7 %(compared to control with no AM) while further production in subsequent 24 hours was not significantly affectedby the presence of AM. For LPS-stimulated macrophages, AM also increased MIF secretion dose-dependently inthe first hour by 13.5% to 35.4% (compared to control containing LPS but no AM), but reduced further productionof MIF by 22.6±6.8% at 24 hours. The suppressive effect was observed even at 1 ng/mL of AM. The presence ofAM also reduced the production of TNF-alpha, IL-6 and IL-1beta from LPS-stimulated cells by 66%, 49 % and 30 %respectively.Conclusion: Our results suggest that AM modulates cytokine secretion from rat macrophages and may have aregulatory role in inflammation.Do you know your mice? A lesson from SM22alpha knockout miceJCL Zhang1,2, BP Helmke3, T Shum4, WW Yu2, MM Lu2, PF Davies3, MS Parmacek2Div. of Cardiology, Queen Mary Hospital,Univ. of Hong Kong, Hong Kong1; Dept. of Medicine2 and Institute of Medical Engineering3, Univ. of Pennsylvania, USA;Dept. of Medicine, Univ. of Chicago, USA4.Introduction: SM22alpha is a 22-kD smooth muscle cell (SMC) lineage restricted protein that physically associ-ates with cytoskeletal actin filament bundles in contractile SMCs. To examine the function of SM22alpha, genetargeting as used to generate SM22alpha -deficient (SM22-/-LacZ) mice.Method: The gene targeting strategy employed resulted in insertion of the bacterial LacZ reporter gene at theSM22alpha initiation codon permitting precise analysis of the temporal and spatial pattern of SM22alpha transcrip-tional activation in the developing mouse. Multidisciplinary approach was taken to characterize the SM22alphaknockout mice from the ultrastructual organization to whole animal cardiovascular physiology.Results: Northern and Western blot analyses confirmed that the gene targeting strategy resulted in a null mutation.Histological analysis of SM22+/-LacZ embryos revealed detectable beta-galactosidase activity in the unturned E8.0embryo in the layer of cells surrounding the paired dorsal aortae concomitant with its expression in the primitiveheart tube, cephalic mesenchyme and yolk sac vasculature. Subsequently, during postnatal development, beta-galactosidase activity was observed exclusively in arterial, venous and visceral SMCs. SM22alpha -deficient miceare viable and fertile. Their blood pressure and heart rate do not differ significantly from their control SM22alpha +/- andSM22alpha +/+ littermates. Cardiac echocardiography revealed preserved systolic function and no significant differencesin chamber sizes. The vasculature and SMC-containing tissues of SM22alpha-deficient mice develop normally andappear histologically similar to those of their control littermates. Deconvolution microscopy confirms thecolocalization of SM22alpha to actin filaments. However, electron microscopy revealed a subtle ultra structuraldefect in the actin filament organization.Conclusion: Taken together, these data demonstrate that SM22alpha is not required for basal homeostatic functionsmediated by vascular and visceral SMCs in the developing mouse. These data also suggest that signalling pathwaysthat regulate SMC specification and differentiation from local mesenchyme are activated earlier in the angiogenicprogram than previously recognized.CVS-21CVS-22

Adrenomedullin suppresses migration inhibitory factor production and cytokine response of rat macrophages to lipopolysaccharide

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Adrenomedullin suppresses migration inhibitory factor production and cytokine response of rat macrophages to lipopolysaccharide

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