Nitric oxide modulates expression of matrix metalloproteinase-9 in rat mesangial cells

Eberhardt, W.; Beeg, T.; Beck, Karl‐Friedrich; Walpen, Sebastian; Gauer, Stefan; Böhles, Hansjosef; Pfeilschifter, Josef

doi:10.1046/j.1523-1755.2000.00808.x

Cited by 143 publications

(140 citation statements)

References 25 publications

(5 reference statements)

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“…Moreover, we considered the activity and expression of two proteins (iNOS and MMP2) as playing an important role in nephrotoxicity (Eberhardt et al 2000;Khanna et al 2002;Rezzani et al 2003;Buffoli et al 2005) and found an induction of these proteins after CsA treatment. Of note, it seems that these data underlie an increase of these proteins in apical membrane of Henle loops.…”

Section: Discussionmentioning

confidence: 99%

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Protective Role of Polyphenols in Cyclosporine A-induced Nephrotoxicity During Rat Pregnancy

Rezzani

Rodella

Tengattini

et al. 2006

J Histochem Cytochem.

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The aim of this study was to evaluate the adverse effects of cyclosporine A (CsA) toward renal morphogenesis and to test the renoprotective natural antioxidants such as provinol (PV). Pregnant rats were divided into four groups. Group I was injected SC with olive oil. Group II was treated with oral administration of PV and was used as control. Group III animals were injected SC daily with CsA, and group IV animals were injected daily with CsA and PV for 21 days of pregnancy. Five pups per litter were killed and the kidneys removed and treated by morphological and immunohistochemical (IHC) methods. IHC analysis considered two proteins responsible for nephrotoxicity in adult rats: inducible nitric oxide (iNOS) and matrix metalloproteinase-2 (MMP2). Pregnancy outcomes among CsA-treated rats demonstrated a reduced number of pups. Pups that were exposed antenatally to CsA presented several pathologic findings in all immature parenchyma and an increase in iNOS and MMP2 expression. These side effects were not observed in kidney of litters born from CsA + PV-treated mothers. Our study indicates that CsA induces morphological alterations in renal parenchyma of neonates and that PV plays a protective role against these side effects.

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Section: Discussionmentioning

confidence: 99%

“…To help to address these questions we studied the activity and expression of two proteins responsible for CsA nephrotoxicity in adult rats: inducible nitric oxide synthase (iNOS, NOS2) (Rezzani et al 2003;Buffoli et al 2005) and matrix metalloproteinase-2 (MMP2) (Eberhardt et al 2000;Khanna et al 2002).…”

mentioning

confidence: 99%

Protective Role of Polyphenols in Cyclosporine A-induced Nephrotoxicity During Rat Pregnancy

Rezzani

Rodella

Tengattini

et al. 2006

J Histochem Cytochem.

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“…Assessment of gelatinolytic MMP-9 content of proteins from cellular supernatants was performed as described previously [22]. Proteins with gelatinolytic content were visualized as areas of lytic activity on an otherwise blue gel [23].…”

Section: Sds-page Zymographymentioning

confidence: 99%

“…cDNA inserts for rat MMP-9 and TIMP-1 were generated as described previously [22]. A cDNA insert from mouse 18S rRNA was from Ambion (Austin, TX, USA).…”

Section: Cdna Clones and Plasmidsmentioning

confidence: 99%

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Differential modulation of the cytokine-induced MMP-9/TIMP-1 protease–antiprotease system by the mTOR inhibitor rapamycin

Osman

Akool

Doller

et al. 2011

Biochemical Pharmacology

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The mTOR-inhibitor rapamycin is a potent drug used in many immunosuppressive and antiinflammatory therapeutic regimes. In renal transplantation despite its benefical roles rapamycin in some cases can promote renal fibrosis in the kidney but the underlying mechanisms are unknown. In this study, we tested for possible modulatory effects of rapamycin on the cytokine-triggered matrix metalloproteinase 9 (MMP-9)/ tissue inhibitor of metalloproteinase (TIMP)-1 protease-antiprotease system which is critically involved in renal inflammation and fibrosis. Treatment of rat mesangial cells (MC) with rapamycin dosedependently reduced the interleukin 1 (IL-1-triggered increase in gelatinolytic levels as demonstrated by zymography. The reduction in the extracellular MMP-9 content by rapamycin coincided with an attenuation in cytokine-induced steady-state MMP-9 mRNA levels. Conversely, rapamycin caused a dose-dependent increase in cytokine-evoked TIMP-1 expression in a Smad binding element (SBE) -dependent manner. Surprisingly, the attenuation of MMP-9 mRNA levels by rapamycin is accompanied by a potentiation of IL-1-induced MMP-9 promoter activity in which the stimulatory effects by rapamycin are mainly attributed to a proximal AP-1 binding site. Furthermore, the rapamycin-dependent potentiation of MMP-9 expression is accompanied by an amplification of cytokine-triggered activities of nuclear factor B (NF-B) and activator protein 1 (AP-1) transcription factors. Importantly, rapamycin-triggered increase in MMP-9 promoter activity is fully impaired when we used a MMP-9 reporter construct which is under the additional control of the 3´untranslated region (3´-UTR) of MMP-9. Collectively, these data imply that rapamycin inhibits the cytokineinduced MMP-9 mainly through posttranscriptional events and thereby exerts profibrotic activities.

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The Hepatic Sinusoidal Endothelial Cell: Morphology, Function, and Pathobiology

DeLeve

2009

The Liver

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Nitric oxide modulates expression of matrix metalloproteinase-9 in rat mesangial cells

Cited by 143 publications

References 25 publications

Protective Role of Polyphenols in Cyclosporine A-induced Nephrotoxicity During Rat Pregnancy

Protective Role of Polyphenols in Cyclosporine A-induced Nephrotoxicity During Rat Pregnancy

Differential modulation of the cytokine-induced MMP-9/TIMP-1 protease–antiprotease system by the mTOR inhibitor rapamycin

The Hepatic Sinusoidal Endothelial Cell: Morphology, Function, and Pathobiology

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