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Comptes rendus des séances de la Soci&eacut... 21건

  1. [해외논문]   Généralités sur le vieillissement vasculaire rénal.  

    Schaeverbeke, J
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 955 - 958 , 1995 , 0037-9026 ,

    초록

    Until the last decade, kidney aging was considered to be the result of progressive loss of nephrons associated with development of glomerulosclerosis and thus decrease in glomerular filtration rate, and finally renal deficiency. However this nephropathy can also result of environmental (such as husbandry conditions, diet ...) and genetical factors. So, food restriction can protect glomeruli against hyperfiltration and risks of glomerulosclerosis. Both capillaries and large vessels were modified during aging. Concerning the glomerular capillaries, the main alterations are changes in glomerular hemodynamics and in the composition and structure of the glomerular basement membrane (noticeably thickening and decrease in heparan sulfate proteoglycans and thus in anionic barrier), glycation of both the structural and plasma protein, resulting in increased permeability of the glomerular capillary wall and development of proteinuria.

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  2. [해외논문]   Le vieillissement vasculaire. Rôle du récepteur de l'élastine.  

    Robert, L
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 959 - 966 , 1995 , 0037-9026 ,

    초록

    A distinction is made between atheromatous plaque formation and arteriosclerosis, only this second process is strictly age-dependent. Interactions between lipids and constituents of the vascular wall are however involved in both processes, although by different mechanisms. The progressive increase with age of elastase activity is a second important factor in the age-dependent progression of arteriosclerosis. The fragmentation of elastic fibers produces elastin peptides, present in the circulating blood in microgram/ml conc-s, increasing in several arteriopathies. The constant presence of elastin peptides in the circulation maintains activated the elastin receptor (16) on endothelial cells producing NO* with vasorelaxing activity (18). The simultaneous production of superoxyde leads to the formation of peroxynitrate, neutralized by reduced glutathion. This process, maintained over decades may well impair the antiradical defense mechanisms of the cells and deprive the endothelium from the vasorelaxing activity of NO*. We propose therefore that the maintained activation of the elastin receptor with free radical and lytic enzyme production might well represent the initiating process underlying atherogenesis.

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  3. [해외논문]   Effets du processus de glycation sur la structure macromoléculaire des membranes basales glomérulaires et sur les fonctions glomérulaires au cours du vieillissement et du diabète sucré.  

    Sternberg, M ; Urios, P ; Grigorova-Borsos, A M
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 967 - 985 , 1995 , 0037-9026 ,

    초록

    Three stages can be distinguished during the glycation process: initiation with the formation of Amadori product; spreading with glyco-oxidation reactions; terminal formation of advanced glycation end products (AGEs). Some AGEs have been isolated and characterized: pyrraline linked to one aminoacid, pentosidine linked to two aminoacids and forming a cross-link between peptidic chains. The AGE-induced cross-links alter the biophysical properties of the proteins with increased stiffness of the fibrous proteins and resistance to proteases. Glycation of the glomerular basement membrane (GBM) macromolecules modifies the architecture of the glomerular filtration barrier. Type IV collagen is the major constituent of the GBM and the mesangial matrix and is a substrate for prolonged glycation, due to its long half-life. In the GBM, AGE level (particularly pentosidine level per mg collagen) increases with age; it is higher in diabetic or uremic patients than in age-matched controls. In insulin-dependent diabetes mellitus, a correlation has been shown between the pentosidine level of skin collagen and the severity of vascular complications. Glycation inhibits the homotypic polymerization interactions between two type IV collagen molecules through their NC1 ends. Glycation also affects the heterotypic interactions between different GBM macromolecules: the affinity of glycated fibronectin for type IV collagen is diminished. Besides, glycation modifies the interactions between type IV collagen and adjacent cells: mesangial and endothelial cells are less adherent on a glycated type IV collagen matrix and their morphology modified. GBM treated with dimethylmalonimidate, which induces cross-links between amines as does advanced glycation, are more permeable to proteins.

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  4. [해외논문]   Approache des mécanismes cellulaires de la glomérulosclérose dans un modèle de vieillissement accéléré, le rat Zucker obèse.  

    Chevalier, J ; Masurier, C ; Lavaud, S ; Michel, O ; Bariety, J
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 987 - 1007 , 1995 , 0037-9026 ,

    초록

    With age, the morphological changes which occur in renal glomeruli in the absence of any added pathology are an expansion of the extracellular matrices (ECM)--glomerular basement membrane (GBM) and mesangial matrix--and lesions of focal and segmental glomerular hyalinosis (FSGH). Although the mechanisms involved in these glomerular changes are still unknown, an inflammatory step seems to precede the expansion of the extracellular matrices, but the nature of the cytokines and adhesion molecules has yet to be explored. In order to understand the cellular and molecular events of the FSGH, we used the genetically obese Zucker rat (fa/fa) which develops several early FSGH lesions. We observed that FSGH is the result of a modification of the podocyte: 1) bulging of the podocyte with endocytotic vesicles rich in albumin; 2) detachment from the GBM, collapsing of the capillary loops with a progressive disappearance of capillary cells and formation of hyalin and lipid deposits, synthesis of new ECM components; 3) focal adherence of the GBM and the basement lamina of Bowman's capsule and synthesis of new matrix. The detachment of the podocytes from the GBM appeared to be linked to the disappearance of the alpha 3 beta 1 integrin, major molecule which anchors the epithelial cells to the GBM. By immuno-gold techniques, we showed that the density of alpha 3 moieties significantly diminished when podocytes are spreaded over the GBM. This integrin is probably bound to the laminin in the GBM.

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  5. [해외논문]   Modifications matricielles et cellulaires précoces dans un modèle d'hypertension induite chez le rat (Modèle de Goldblatt). Etude quantitative morphométrique.  

    Appay, M D ; Heudes, D ; Xu, Y C ; Lemoine, R ; Hinglais, N ; Michel, J B ; Bariéty, J
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1009 - 1024 , 1995 , 0037-9026 ,

    초록

    In the two-kidney one-clip hypertensive Goldblatt model of nephrosclerosis, the aim of this study was to detect, during the first twenty-eight days of high blood pressure, interstitial and periarterial (interlobular arterial and arteriolar) kidney changes. Morphometric analysis for type I collagen, in situ hybridization for type I and IV collagen mRNAs and immunohistochemistry for inflammatory cells were used to quantify and localize the following lesions: 1) A very early increase of collagen I proteins and mRNAs soon as the first 3 days and an important influx of inflammatory cells (macrophages and T-helper lymphocytes) were observed concomitantly. Then, these phenomenons decrease until the end of the experiment. 2) The interstitium reacts in the same way but with a lower intensity and with a time shifting. The main interstitial changes were seen after the second week of hypertension. 3) A same periarterial collagen I increase was measured during the first 3 days of hypertension in both clipped kidney and unclipped kidney. This hypertension-independent manifestation in the clipped kidney does not increase in later times of hypertension as it does in the unclipped kidney. A possible explanation is given by the angiotensin II concentration higher in the clipped kidney than in the unclipped kidney, and by direct angiotensin II effects as growth factor. 4) Periarterial fibrosis and macrophages or T-helper lymphocytes infiltration were co-localized. The intensity of both phenomenons is well correlated. These facts suggest that inflammatory cell infiltration and interstitial fibrosis are strongly and early linked.

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  6. [해외논문]   Biologie moléculaire et génétique des NO synthases.  

    Nadaud, S ; Soubrier, F
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1025 - 1038 , 1995 , 0037-9026 ,

    초록

    Nitric oxide is synthesized by three isoenzymes widely distributed in the organism. The three genes encoding these enzymes show structural homology confirming that they are members of a protein family. Isoforms I (neuronal) and III (endothelial) are constitutive but their expression is transcriptionnaly regulated by various factors. NOS I promoter has not been studied yet, but alternative splicing around exons 9 and 10 has been described. SP1 binding on NOS III promoter is critical for its constitutive expression. NOS II isoform is inducible in a large variety of cells and seems also to be present constitutively in some tissues such as kidney. Functional studies of NOS II promoter reveal two important regions for lipopolysaccharides (- 85 - 75) and interferon gamma (- 900 - 975) induction. NOS III polymorphic markers allowed genetic studies which indicate that NOS III gene is not associated with human essential hypertension.

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  7. [해외논문]   Les métalloprotéines, cibles cellulaires du monoxyde d'azote: une revue succincte.  

    Henry, Y ; Guissani, A
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1039 - 1057 , 1995 , 0037-9026 ,

    초록

    In this review we recall the main physical properties of nitric oxide. The irreversible reactions of NO with O2 and O2.-, which yield strongly oxydant and nitrosating, and therefore toxic, species, are described in kinetic terms. Nearly all metalloproteins are potential targets for NO, often detectable by EPR spectroscopy. The case of hemoglobin in vitro and within circulating erythrocytes, especially in pathophysiological cases, is particularly described. A few examples of hemoproteins activated or inhibited by NO are given. Results obtained with cellular systems responding to cytokines are summarized, together with the effects of NO synthesis on [FeS] clusters-containing proteins, on ribonucleotide reductase and on the proteins implicated in iron metabolism.

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  8. [해외논문]   Le monoxyde d'azote: implication dans l'excitotoxicité et l'ischémie cérébrale.  

    Demerlé-Pallardy, C ; Chabrier, P E
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1059 - 1068 , 1995 , 0037-9026 ,

    초록

    In the central nervous system, several cellular types are able to produce nitric oxide (NO). In particular in neuronal cells, the excitatory amino-acid receptor activation induces NO synthesis and release. Since excessive activation of these receptors is responsible of neuronal death in excitotoxicity or cerebral ischemia, the hypothesis of a NO role in neuronal damage has been proposed. The use of NO synthesis inhibitors in excitotoxicity or cerebral focal ischemia models has provided contradictory data. Here we attempt to present the main bibliographic data concerning this controversial research area in order to a better comprehension of NO role in neuronal death.

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  9. [해외논문]   La NO synthase endothéliale.  

    Boulanger, C M
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1069 - 1079 , 1995 , 0037-9026 ,

    초록

    Nitric oxide (NO) may be produced in the vascular wall by different NO synthases. One of the constitutive isoforms, the endothelial NO synthase, contributes to the regulation of vascular tone and may prevent unwanted platelet and leucocyte adhesion to the endothelial surface. The release of NO by the endothelial NO synthase is exquisitely regulated by increases of intracellular free calcium following endothelial receptors activation by shear stress, neuromediators, hormones or platelet products. The immediate and transient release of NO diffuses towards the underlying smooth muscle and contributes to the appropriate response to local changes in blood flow or composition. The endothelial release of NO depends also on the availability of NO synthase cofactors; in addition, several experimental evidences suggest a transcriptional and postranscriptional regulation of the endothelial NO synthase itself. Another isoform of NO synthase insensitive to changes in intracellular calcium may be induced following exposure to cytokines or under some pathological conditions such as sepsis, inflammation or after vessel wall injury. The massive and long-lasting release of NO caused by induction of NO synthase requires a latency period of several hours. The inducible NO synthase may compensate the dysfunction of the endothelial isoform after injury (angioplasty) or in atherosclerosis. However, uncontrolled regulation of inducible NO synthase expression may have deleterious consequences on the vascular wall.

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  10. [해외논문]   NO, effecteur ambivalent de l'immunité non spécifique et de l'inflammation.  

    Drapier, J C
    Comptes rendus des séances de la Société de biologie et des ses filiales v.189 no.6 ,pp. 1081 - 1096 , 1995 , 0037-9026 ,

    초록

    Nitric oxide produced from the amino acid L-arginine is a short-lived free radical produced by many types of cells for a variety of biological functions, including defence against a range of pathogens. NO synthesis via NOS-2 is deeply intertwined in the cytokine network. Thus, expression of NOS-2 is induced by IFN-gamma, TNF and IL-1 as well as microbial products whereas IL-4, IL-10 and TGF-beta down-regulate its synthesis. In spite of this tight regulation, excessive production of NO as a result of immunological stimulation via NOS-2 could have potential toxic effects on hosts. Indeed, large amount of nitric oxide (NO) are produced at sites of inflammation through the action of NOS-2. The role of NO in inflammation is unclear and may depend on the balance between NO and O2-. The somewhat paradoxical effects of NO might indeed be explained by its various chemical forms. Besides, understanding the regulation and function of NOS-2 is likely to lead to therapeutic approaches to treat a number of diseases.

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