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A rat model of progressive chronic renal failure produced by microembolism

AMERICAN JOURNAL OF PATHOLOGY 1999年第4期155卷 1371-1380页

作者： Kimura, M Suzuki, T Hishida, A Univ Shizuoka Sch Nursing Shizuoka 4228526 Japan Hamamatsu Univ Sch Med Dept Med Hamamatsu Shizuoka 43131 Japan

We report a new model of chronic progressive renal failure in rats, produced by a single injection of microspheres (20 to 30 mu m in diameter) into the left renal artery after right nephrectomy, Significant proteinuria appeared after 4 weeks, followed by hypoalbuminemia and hypercholesterolemia, in rats that received approximately 5 x 10(5) microspheres (0.8 mg), Renal function partially recovered by 4 weeks after nephrectomy and injection from postoperative dysfunction, but deteriorated again 12 weeks after operation. In the early stage, histologic examination showed tubules with cuff-like thickening of basement membranes scattered among apparently intact tubules. Many epithelial cells in the atrophic tubuli were immunoreactive for proliferating cell nuclear antigen (PCNA), Dilated tubules became apparent several weeks after development of tubular atrophy, most Likely representing distal tubules. Dilated tubuli were mostly negative for the proliferation marker. These results showed similarity to findings in human chronic renal failure and strongly suggested that tubular atrophy and dilation in chronic tubulointerstitial lesions differ in pathogenesis, This new model of renal failure induced by microembolism should be useful for studying the interaction between normal and diseased tissue elements in histologically heterogenous lesions as well as the pathogenesis of interstitial fibrosis in disturbance of microcirculation.

关键词：白蛋白尿/化学诱导血压胆固醇/血液肌酸酐/血液疾病模型动物栓塞/化学诱导栓塞/并发症栓塞/病理学纤维化/病理学肾皮质/病理学肾功能衰竭慢性/血液肾功能衰竭慢性/病因学肾功能衰竭慢性/病理学肾功能衰竭慢性/尿肾小球/病理学肾小管/病理学微球体坏死大鼠 Wistar 肾循环血清白蛋白/代谢时间因素动物男(雄)性大鼠

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Cyclosporin exerts a direct fibrogenic effect on human tubulointerstitial cells:: Roles of insulin-like growth factor I, transforming growth factor β₁, and platelet-derived growth factor

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 535-542页

作者： Johnson, DW Saunders, HJ Johnson, FJ Huq, SO Field, MJ Pollock, CA Royal N Shore Hosp Univ Sydney Dept Med Sydney NSW 2065 Australia

To assess the direct fibrogenic effects of cyclosporin A (CyA) on the human tubulointerstitium, primary cultures of human renal proximal tubule cells (PTC) and renal cortical fibroblasts (CF) were incubated for 24 h with various concentrations of CyA. Cytotoxicity was confirmed in both cell populations by dose-dependent inhibition of thymidine incorporation, viability, and PTC apical sodium-hydrogen exchange activity (ethylisopropylamiloride-sensitive apical Na-22(+) uptake). Compared with controls, both 500 and 1000 ng/ml CyA significantly stimulated CF collagen synthesis (proline incorporation 4.6 +/- 0.4, 6.5 +/- 0.8, and 7.1 +/- 1.0%, respectively;p <.05) and inhibited matrix metalloproteinase-2 (100%, 85.7 +/- 10.0%, and 38.8 +/- 9.2%) and matrix metalloproteinase-9 activity (100%, 110.6 +/- 19.0%, and 49.9 +/- 12.8%), CyA did not affect CF secretion of transforming growth factor beta(1), but markedly stimulated insulin-like growth factor-I (IGF-I) secretion and inhibited secretion of both IGF-I binding protein-(IGFBP)-3 and IGFBP-2, CyA-induced CF collagen synthesis was abrogated by 5 mu g/ml anti-IGF-I receptor antibody, but not by 5 mu g/ml murine nonimmune globulin. Increasing concentrations of CyA progressively augmented PTC secretion of the fibrogenic cytokines transforming growth factor-beta(1) and platelet-derived growth factor. These results indicate that clinically relevant concentrations of CyA are directly toxic to PTC and CF, irrespective of hemodynamic effects, and promote interstitial fibrosis by inhibiting matrix degradation and stimulating cortical fibroblast collagen synthesis via induction of autocrine IGF-I action. The latter effect may be further accentuated by the ability of CyA to augment secretion of transforming growth factor beta(1) and platelet-derived growth factor by PTCs.

关键词：细胞存活/药物作用细胞培养的胶原/生物合成培养基条件性环孢菌素/毒性纤维化明胶/代谢免疫抑制剂/毒性胰岛素样生长因子Ⅰ/生理学肾皮质/药物作用肾皮质/代谢肾皮质/病理学肾小管/药物作用肾小管/代谢肾小管/病理学肾小管近端/药物作用肾小管近端/病理学金属内肽酶类/代谢血小板源性生长因子/生理学转化生长因子β/生理学女(雌)性人类男(雄)性中年人

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Nephroprotective effect of treatment with calcium channel blockers in spontaneously hypertensive rats

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期294卷 948-954页

作者： Sabbatini, M Vitaioli, L Baldoni, E Amenta, F Univ Camerino Dipartimento Sci Farmacol & Med Sperimentale Sez Anat Umana I-62032 Camerino Italy Univ Camerino Dipartimento Sci Morfol & Biochim Comparate I-62032 Camerino Italy

The influence of hypertension and of treatment with some dihydropyridine-type Ca2+ channel blockers and with the nondihydropyridine-type vasodilator hydralazine on the morphology of kidney was investigated in 26-week-old spontaneously hypertensive rats (SHR) and in age-matched Wistar-Kyoto rats. Fourteen-week-old SHR were treated for 12 weeks with a nonhypotensive dose of lercanidipine or with equihypotensive doses of lercanidipine, manidipine, nicardipine, and hydralazine. In control SHR, systolic pressure values were significantly higher in comparison with Wistar-Kyoto rats. Treatment with the low dose of lercanidipine did not reduce systolic blood pressure in SHR, whereas the higher dose of lercanidipine or other compounds tested significantly decreased systolic pressure values. Glomerular hypertrophy accompanied by signs of glomerulosclerosis, increase of mesangial cells, and convoluted tubules degeneration were observed in control SHR. Hypotensive doses of Ca2+ antagonists countered glomerular injury, the increase of mesangial cells, the reduction of capsular space, and tubular degeneration. Hydralazine, in spite of its hypotensive activity, displayed a slight nephroprotective action. The nonhypotensive dose of lercanidipine countered in part glomerular injury, narrowing of capsular space, and tubular degeneration, and decreased mesangial cell augmentation in SHR. These results suggest that treatment with dihydropyridine-type Ca+2 antagonists counters hypertensive glomerular and tubular changes occurring in SHR. The demonstration of nephroprotection by the nonhypotensive dose of lercanidipine suggests that the renal effects of the compound may be in part unrelated to its hemodynamic activity.

关键词：血压/药物作用钙通道阻滞药/药理学二氢吡啶类/药理学肼苯哒嗪/药理学肾/血液供给肾/药物作用肾/病理学肾皮质/药物作用肾皮质/病理学肾小球/药物作用肾小球/病理学肾小管/药物作用肾小管/病理学尼卡地平/药理学大鼠近交SHR 大鼠近交WKY 血管舒张药/药理学动物男(雄)性大鼠

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In vitro and in vivo expression of endothelial von Willebrand factor and leukocyte accumulation after fractionated irradiation

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RADIATION RESEARCH 2000年第4期154卷 375-381页

作者： van Kleef, E Verheij, M Poele, HT Oussoren, Y Dewit, L Stewart, F Netherlands Canc Inst Div Expt Therapy NL-1066 CX Amsterdam Netherlands Netherlands Canc Inst Div Radiotherapy NL-1066 CX Amsterdam Netherlands

Previous investigations have demonstrated an increased release of von Willebrand factor (VWF;also known as VWF) in endothelial cells after high single-dose irradiation in vitro. We have also found increased levels of Vwf protein in mouse glomeruli after a high single dose of renal irradiation in vivo. In addition, increased numbers of leukocytes were observed in the renal cortex after irradiation in vivo. The aim of the present study was to investigate and quantify these biological processes after clinically relevant fractionated irradiation and to relate them to changes in renal function. A significantly greater increase in release of VWF was observed in cultured human umbilical vein endothelial cells (HUVECs) after fractionated irradiation (20 x 1.0 Gy) than after a single dose of 20 Gy (147% compared to 115% of control, respectively, P < 0.0005). In contrast with the in vitro observations, glomerular Vwf staining was lower after fractionated irradiation in vivo (20 x 2.0 Gy or 10 x 1.6 Gy +/- re-irradiation) than after a single dose of 16 Gy. The number of leukocytes accumulating in the renal cortex was also lower after fractionated in vivo irradiation than after a single radiation dose. The onset of these events preceded renal functional and histopathological changes by approximately 10 weeks. These data indicate that radiation-induced changes in endothelial. VWF expression after in vivo irradiation may be distinct from the in vitro observations. Increased VWF expression may reflect pivotal processes in the pathogenesis of late radiation nephropathy and provide a clue to appropriate timing of pharmacological intervention. (C) 2000 by Radiation Research Society.

关键词：细胞黏附细胞培养的/代谢细胞培养的/辐射效应趋化性白细胞/辐射效应内皮血管/代谢内皮血管/辐射效应肾皮质/代谢肾皮质/病理学肾皮质/辐射效应肾功能试验肾小球/代谢肾小球/病理学肾小球/辐射效应肾小管/代谢肾小管/病理学肾小管/辐射效应白细胞/病理学小鼠近交C3H 肾单位/代谢肾单位/病理学肾单位/辐射效应辐射损伤实验性/代谢辐射损伤实验性/病理学辐射耐受性脐静脉 vonWillebrand因子/生物合成 vonWillebrand因子/遗传学动物女(雌)性人类小鼠

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Age-dependent expression of fibrosis-related genes and collagen deposition in rat kidney cortex

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JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES 2000年第8期55卷 B365-B372页

作者： Gagliano, N Arosio, B Santambrogio, D Balestrieri, MR Padoani, G Tagliabue, J Masson, S Vergani, C Annoni, G Milan Bicocca Univ Osped Maggiore IRCCS Dept Internal Med & Geriatr I-20122 Milan Italy Ist Ric Sigma Tau Milan Italy Ist Ric Farmacol Mario Negri Dept Cardiovasc Res Milan Italy

Because progressive fibrosis is a histological hallmark of the aging kidney, we sought to characterize the course of some fibrosis-related genes [pro-alpha2(I)collagen (COL-I), pro-alpha1(III)collagen (COL-III), and transforming growth Factors beta1 and beta3 (TGF-beta1 and TGF-beta3)] of interstitial collagen accumulation [COL-I and COL-III proteins, hydroxyproline (PRO-OH), histology] and its degradation (matrix metalloproteinase MMP-1 and -2) during maturation and early aging in rats. During the lifespan considered we observed no changes in the mRNA, except that COL-I mRNA tended to be up-regulated from 2 to 19 months of age. However, progressive fibrosis was histologically detectable, with COL-I accumulation (p <.05 and p <.01 in 12-month- and 19-month-old rats vs the youngest), and confirmed by the PRO-OH tissue levels (p =.0001);COL-III seemed to be less involved. The MMP-1 protein level decreased significantly in the cortex of 12-month- and 19-month-old rats (p <.05), whereas MMP-2 protein level and activity remained essentially unchanged. These results show that, during aging of the kidney, (i) renal cortex fibrosis is explained by COL-I accumulation as a consequence of an altered balance between its synthesis and degradation, and (ii) the expression of the pleiotropic factor TGF- in the renal cortex is not modified.

关键词：年龄因素胶原/生物合成胶原/遗传学纤维化基因表达羟脯氨酸/代谢肾皮质/酶学肾皮质/代谢肾皮质/病理学基质金属蛋白酶1/代谢基质金属蛋白酶2/代谢 RNA 信使/生物合成大鼠 Sprague-Dawley 转化生长因子β/生物合成转化生长因子β/遗传学动物男(雄)性大鼠

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Gene expression of CC chemokines in experimental acute tubulointerstitial nephritis

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JOURNAL OF LABORATORY AND CLINICAL MEDICINE 1999年第1期133卷 41-47页

作者： Ou, ZL Natori, Y Natori, Y Int Med Ctr Japan Dept Clin Pharmacol Res Inst Shinjuku Ku Tokyo 1628655 Japan

The infiltration of mononuclear leukocytes into glomeruli or the interstitium is a feature in most forms of glomerular diseases. CC chemokines, mostly chemoattractants for mononuclear leukocytes, are molecules that are potentially responsible for the recruitment of these cells in the kidney. We previously reported that the gene expression of six CC chemokines-MCP-1, MCP-3, MIP-1 alpha, MIP-1 beta, RANTES, and TCA3-was enhanced in a rat model of crescentic glomerulonephritis, the most severe form of glomerulonephritis. In this study we analyzed their gene expression in a model of another type of kidney disease, acute nephrosis accompanied by tubulointerstitial lesions, which is induced by an injection of puromycin aminonucleoside. Because leukocyte infiltration in this model is much more prominent in the interstitium than in glomeruli, we analyzed their gene expression in the renal cortex. On day 3, when the level of urinary protein was slightly but significantly increased but the number of interstitial leukocytes was unchanged, the enhanced expression of mRNAs for MCP-1, MCP-3, and TCA3 was observed. On day 5, the numbers of interstitial monocytes and lymphocytes significantly increased, and the levels of the mRNA expression of the above chemokines were still higher than the control animals, whereas the levels of mRNAs for MIP-1 alpha, MIP-1 beta, and RANTES were not higher or were only slightly higher than the control ones. These results suggest that multiple CC chemokines may play a role in the recruitment of leukocytes in this model and that the expression pattern of CC chemokines depends on the type of kidney injury.

关键词：急性病 CD4阳性T淋巴细胞/病理学 CD8阳性T淋巴细胞/病理学趋化因子 CC/遗传学趋化因子 CC/代谢 DNA引物/化学 DNA探针/化学疾病模型动物基因表达肾皮质/代谢肾皮质/病理学白细胞计数单核细胞/病理学肾炎间质性/化学诱导肾炎间质性/遗传学肾炎间质性/病理学肾病/化学诱导肾病/并发症肾病/遗传学肾病/病理学蛋白尿嘌呤霉素氨基核苷/毒性 RNA 信使/生物合成大鼠 Wistar 逆转录聚合酶链反应动物男(雄)性大鼠

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Heparin-binding EGF-like growth factor is up-regulated in the obstructed kidney in a cell- and region-specific manner and acts to inhibit apoptosis

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AMERICAN JOURNAL OF PATHOLOGY 2000年第3期156卷 889-898页

作者： Nguyen, HT Bride, SH Badawy, AB Adam, RM Lin, JQ Orsola, A Guthrie, PD Freeman, MR Peters, CA Childrens Hosp Dept Urol Urol Lab Boston MA 02115 USA Harvard Univ Sch Med Dept Surg Boston MA 02115 USA

The expression of certain growth factors in the epidermal growth factor (EGF) family is altered in response to renal injury. Recent studies have demonstrated that heparin binding EGF-like growth factor (HB-EGF) expression may be cytoprotective in response to apoptotic signals. The purpose of this study was to investigate the potential role of HB-EGF in the upper urinary tract following unilateral ureteral obstruction. We present evidence that: i) ureteral obstruction induced cell-specific but transient activation of HB-EGF gene expression;ii) HB-EGF expression in renal epithelial cells increased under conditions where mechanical deformation, such as that caused by hydronephrotic distension, induces apoptosis,but HB-EGF expression did not increase in renal pelvis smooth muscle cells under identical conditions;and iii) enforced expression of HB-EGF served to protect renal epithelial cells from stretch-induced apoptosis. These results suggest a potential mechanism by which the kidney protects itself from apoptosis triggered by urinary tract obstruction.

关键词：肌动蛋白类/代谢细胞凋亡细胞培养的 DNA碎片裂 DNA引物/化学疾病模型动物表皮生长因子/遗传学表皮生长因子/代谢上皮细胞/代谢上皮细胞/病理学免疫酶技术胞间信号肽类和蛋白质类角蛋白质类/代谢肾皮质/代谢肾皮质/病理学亮氨酰氨肽酶/代谢肌平滑/代谢肌平滑/病理学 RNA 信使/代谢大鼠 Zucker 逆转录聚合酶链反应转染增量调节输尿管梗阻/代谢输尿管梗阻/病理学 γ-谷氨酰转移酶/代谢动物女(雌)性人类小鼠大鼠

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ACQUIESCENT RENAL INFECTION

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KIDNEY INTERNATIONAL 1975年第6期7卷 413-421页

作者： MILLER, TE NORTH, D BURNHAM, S UNIV AUCKLAND SCH MEDDEPT MEDAUCKLANDNEW ZEALAND

Acquiescent renal infection. The relationship between bacterial infection of the renal parenchyma with Escherichia coli and the establishment of pathologic lesions has been investigated experimentally. Infection was established in one kidney and the bacteriologie, pathologic and immunologic features of infection were compared in the pyelonephritic and contralateral unmanipulated kidney. Whereas active bacterial infection was associated with pathologic changes in the pyelonephritic kidney, a poor correlation was found between bacterial growth and the gross pathology and histopathologic changes in the contralateral kidney. The conclusion from these studies is that infection of the kidney is not always associated with pathologic changes. The term "acquiescent infection" has teen used to describe this host-parasite relationship in which active, persistent, bacterial infection is not associated with pathologic lesions. Evidence is presented that bacteria in the contralateral unmanipulated kidney are present in the renal parenchyma and that bacterial proliferation can be induced following renal trauma. Activation of infection and bacterial proliferation did not always result in histopathologic damage to the kidney and was not associated with an increase in serum antibody.

关键词：大肠杆菌感染/药物疗法大肠杆菌感染/免疫学庆大霉素类/治疗应用免疫肾/免疫学肾浓缩能力肾皮质/病理学肾疾病/微生物学肾疾病/病理学肾髓质/病理学肾小管/药物作用萘啶酸/治疗应用肾盂肾炎/微生物学肾盂肾炎/病理学大鼠近交系动物女(雌)性大鼠

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Tretinoin prevents age-related renal changes and stimulates antioxidant defenses in cultured renal mesangial cells

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 123-132页

作者： Manzano, VM Puyol, MR Puyol, DR Cazaña, FJL Univ Alcala de Henares Fac Med Dept Physiol Madrid Spain

Age-related progressive glomerular sclerosis in the rat is associated with increased expression of tumor necrosis factor-beta(1) and increased protein content in the renal cortex, enhanced production of H2O2, in both renal glomeruli and mesangial cells (MCs) cultured from them, as well as augmented glomerular oxidative damage. We have previously shown that tretinoin-treated old male Fischer 344 rats have 30% lower protein content in the renal cortex than control old rats. Here, we report that this effect may depend on the inhibition of the expression of tumor necrosis factor-beta(1), a matrigenic cytokine, and osteopontin, a protein with cell adhesive and chemotactic properties. In addition, we show that tretinoin prevents the cytotoxicity of H2O2 in cultured human MCs by increasing both the catalase activity and the reduced glutathione content, which are dose- and time-dependent changes. These increases were not dependent on each other: when these effects were previously inhibited with 3-amino-1,2,4-atriazole or L-buthionine-(S,R)-sulfoximine, respectively, tretinoin still induced the increase of the other noninhibited antioxidant defense. An enhanced gene transcription is the most likely mechanism involved in the tretinoin-induced stimulation of MC antioxidant defense systems because 1) preincubation of MCs with actinomycin D or cycloheximide fully abolished it;2) tretinoin-incubated MCs showed increased levels of catalase mRNA and gamma-glutamyl-cysteine synthetase (catalytic subunit) mRNA, the latter being the rate-limiting step in de novo reduced glutathione synthesis;and 3) the stability of both mRNA was unchanged by tretinoin. These results show one strategy of protecting renal cells from H2O2-mediated injury based on increasing their antioxidant defenses.

关键词：衰老/病理学抗氧化剂/代谢过氧化氢酶/生物合成细胞存活/药物作用细胞培养的细胞因子类/生物合成膳食肾小球膜/药物作用肾小球膜/代谢肾小球膜/病理学谷胱甘肽/代谢过氧化氢/拮抗剂和抑制剂肾皮质/药物作用肾皮质/病理学骨桥蛋白质氧化剂/拮抗剂和抑制剂 RNA 信使/生物合成大鼠近交F344 唾液糖蛋白类/生物合成转化生长因子β/生物合成维甲酸/药理学动物人类男(雄)性大鼠

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RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy

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AMERICAN JOURNAL OF PATHOLOGY 2003年第4期162卷 1123-1137页

作者： Wendt, TM Tanji, N Guo, JC Kislinger, TR Qu, W Lu, Y Bucciarelli, LG Rong, LL Moser, B Markowitz, GS Stein, G Bierhaus, A Liliensiek, B Arnold, B Nawroth, PP Stern, DM D'Agati, VD Schmidt, AM Columbia Univ Coll Phys & Surg Dept Surg New York NY 10032 USA Columbia Univ Coll Phys & Surg Dept Pathol New York NY 10032 USA Columbia Univ Coll Phys & Surg Dept Physiol New York NY 10032 USA Columbia Univ Coll Phys & Surg Dept Cellular Biophys New York NY 10032 USA Columbia Univ Coll Phys & Surg Dept Med New York NY 10032 USA Univ Jena Dept Internal Med 4 D-6900 Jena Germany Heidelberg Univ Dept Med 1 Heidelberg Germany German Canc Res Ctr Dept Mol Immunol Div Tumor Immunol D-6900 Heidelberg Germany

Diabetic nephropathy ensues from events involving earliest changes in the glomeruli and podocytes, followed by accumulation of extracellular matrix in the mesangium. Postulated mechanisms include roles for vascular endothelial growth factor (VEGF), produced by podocytes and contributing to enhanced excretion of urinary albumin and recruitment/activation of inflammatory cells, and transforming growth factor-beta (TGF-beta), elicited largely from mesangial cells and driving production of extracellular matrix. RAGE, a receptor for advanced glycation endproducts (AGES) and S100/calgranulins, displays enhanced expression in podocytes of genetically diabetic db/db mice by age 13 weeks. RAGE-bearing podocytes express high levels of VEGF by this time, in parallel with enhanced recruitment of mononuclear phagocytes to the glomeruli;events prevented by blockade of RAGE. By age 27 weeks, soluble RAGE-treated db/db mice displayed diminished albuminuria and glomerulosclerosis, and improved renal function. Diabetic homozygous RAGE null mice failed to develop significantly increased mesangial matrix expansion or thickening of the glomerular basement membrane. We propose that activation of RAGE contributes to expression of VEGF and enhanced attraction/activation of inflammatory cells in the diabetic glomerulus, thereby setting the stage for mesangial activation and TGF-beta production;processes which converge to cause albuminuria and glomerulosclerosis.

关键词：白蛋白尿/病理学细胞分化细胞培养的糖尿病肾病/病理学疾病模型动物疾病恶化糖基化终产物高级/代谢肾皮质/病理学小鼠突变型受体免疫/生理学尿道上皮/病理学动物男(雄)性小鼠

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