scholarly journals Role of interleukin-6 in mediating mesangial cell proliferation and matrix production in vivo

1997 ◽  
Vol 51 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Frank Eitner ◽  
Ralf Westerhuis ◽  
Michael Burg ◽  
Birgit Weinhold ◽  
Hermann-Josef Gröne ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Interleukin 6 ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Matrix Production

scholarly journals Anti-angiogenic compound (TNP-470) inhibits mesangial cell proliferation in vitro and in vivo

1997 ◽  
Vol 51 (6) ◽  
pp. 1838-1846 ◽  
Author(s):  
Masashi Haraguchi ◽  
Mikio Okamura ◽  
Masayo Konishi ◽  
Yoshio Konishi ◽  
Nobuo Negoro ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Proliferation In Vitro

Effect of interleukin-6 receptor blockage on renal injury in apolipoprotein E-deficient mice

2009 ◽  
Vol 297 (3) ◽  
pp. F679-F684 ◽  
Author(s):  
Mari Tomiyama-Hanayama ◽  
Hiromi Rakugi ◽  
Masaharu Kohara ◽  
Toru Mima ◽  
Yasuo Adachi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Apolipoprotein E ◽  
Interleukin 6 ◽  
Renal Injury ◽  
Mesangial Cell ◽  
Organ Damage ◽  
Glomerular Injury ◽  
Mesangial Cell Proliferation ◽  
Matrix Expansion ◽  
Interleukin 6 Receptor

Hyperlipidemia has been demonstrated to be associated with renal disease, yet the mechanism of renal injury is still poorly understood. Inflammation that occurs with the hyperlipidemia has been considered to play an important role in development of glomerular injury. In the present study, we investigated the role of interleukin-6 (IL-6), a key inflammatory molecule, on renal injury in apolipoprotein E-deficient (ApoE−/−) mice with severe hypercholesterolemia. The 6-wk-old mice were fed a high-fat diet and administered weekly rat anti-IL-6 receptor monoclonal antibody (MR16-1), control rat IgG, or saline for a total of 4 wk. We examined histopathological changes in the kidney and urinary excretion of protein and albumin. Saline- and IgG-treated mice showed remarkable proteinuria at 10 wk of age, whereas MR16-1-treated mice exhibited significantly lower levels. Renal histopathology of saline- and IgG-treated mice revealed striking lipid deposits and foam cells in the glomerular tuft, juxtaglomerular area, and arteriolar wall along with range of mesangial cell proliferation and matrix expansion. Notably, the severity of lipid deposits and mesangial cell proliferation were significantly reduced in MR16-1-treated mice. Immunohistochemistry demonstrated that mesangial IL-6 expression was dramatically reduced in MR16-1-treated mice compared with IgG-treated mice. Blocking the IL-6 receptor prevented progression of proteinuria and renal lipid deposit, as well as the mesangial cell proliferation associated with severe hyperlipoproteinemia. These results clearly demonstrate that IL-6 plays an essential role in the pathogenesis of hyperlipidemia-induced glomerular injury in ApoE−/− mice and suggests the usefulness of anti-IL-6 receptor antibody in treatments for hyperlipidemia-induced organ damage.

scholarly journals A positive feedback loop involving Erk5 and Akt turns on mesangial cell proliferation in response to PDGF

2014 ◽  
Vol 306 (11) ◽  
pp. C1089-C1100 ◽  
Author(s):  
Amit Bera ◽  
Falguni Das ◽  
Nandini Ghosh-Choudhury ◽  
Xiaonan Li ◽  
Sanjay Pal ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dna Synthesis ◽  
Cyclin D1 ◽  
Positive Feedback ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Pi3 Kinase ◽  
Dominant Negative ◽  
Mesangial Cell Proliferation

Platelet-derived growth factor BB and its receptor (PDGFRβ) play a pivotal role in the development of renal glomerular mesangial cells. Their roles in increased mesangial cell proliferation during mesangioproliferative glomerulonephritis have long been noted, but the operating logic of signaling mechanisms regulating these changes remains poorly understood. We examined the role of a recently identified MAPK, Erk5, in this process. PDGF increased the activating phosphorylation of Erk5 and tyrosine phosphorylation of proteins in a time-dependent manner. A pharmacologic inhibitor of Erk5, XMD8-92, abrogated PDGF-induced DNA synthesis and mesangial cell proliferation. Similarly, expression of dominant negative Erk5 or siRNAs against Erk5 blocked PDGF-stimulated DNA synthesis and proliferation. Inhibition of Erk5 attenuated expression of cyclin D1 mRNA and protein, resulting in suppression of CDK4-mediated phosphorylation of the tumor suppressor protein pRb. Expression of cyclin D1 or CDK4 prevented the dominant negative Erk5- or siErk5-mediated inhibition of DNA synthesis and mesangial cell proliferation induced by PDGF. We have previously shown that phosphatidylinositol 3-kinase (PI3-kinase) contributes to PDGF-induced proliferation of mesangial cells. Inhibition of PI3-kinase blocked PDGF-induced phosphorylation of Erk5. Since PI3-kinase acts through Akt, we determined the role of Erk5 on Akt phosphorylation. XMD8-92, dominant negative Erk5, and siErk5 inhibited phosphorylation of Akt by PDGF. Interestingly, we found inhibition of PDGF-induced Erk5 phosphorylation by a pharmacological inhibitor of Akt kinase and kinase dead Akt in mesangial cells. Thus our data unfold the presence of a positive feedback microcircuit between Erk5 and Akt downstream of PI3-kinase nodal point for PDGF-induced mesangial cell proliferation.

scholarly journals C-type natriuretic peptide inhibits mesangial cell proliferation and matrix accumulation in vivo

1998 ◽  
Vol 53 (5) ◽  
pp. 1143-1151 ◽  
Author(s):  
Sima Canaan-Kühl ◽  
Tammo Ostendorf ◽  
Kerstin Zander ◽  
Karl-Martin Koch ◽  
Jürgen Floege
Keyword(s):  
Cell Proliferation ◽  
Natriuretic Peptide ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation ◽  
Matrix Accumulation

scholarly journals Inhibition of mesangial cell proliferation by E2F decoy oligodeoxynucleotide in vitro and in vivo.

1998 ◽  
Vol 101 (11) ◽  
pp. 2589-2597 ◽  
Author(s):  
Y Maeshima ◽  
N Kashihara ◽  
T Yasuda ◽  
H Sugiyama ◽  
T Sekikawa ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Mesangial Cell ◽  
Mesangial Cell Proliferation
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