Interleukin-6: An autocrine regulator of mesangial cell growth

Coleman, David L.; Ruef, C.

doi:10.1038/ki.1992.91

Cited by 99 publications

(53 citation statements)

References 11 publications

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“…IL-6 has been shown to be an autocrine growth factor for mesangial cells. This cytokine has been found increased in a number of mesangial proliferative types of human nephritis and urinary IL-6 concentrations have been correlated with the activity of the disease [10,30,31,32,33,34]. In this study significant uptake of 3 H-thymidine was observed at 96 h in ETB/ETBP-treated mesangial cell cultures, suggesting cellular proliferation.…”

Section: Discussionsupporting

confidence: 50%

“…The mitogenic effect of IL-6 on cultured mesangial cells is less potent and requires more time than other stimulatory cytokines (PDGF or bFGF) [10]. The available data indicate that IL-6 acts as a competence factor stimulating cells in G o to enter G 1 and requiring additional progression factors to induced mesangial cell replication [33, 34]. In addition to the mitogenic effect of IL-6 on mesangial cells, this cytokine has been identified as an antigen-nonspecific B cell differentiation factor that induces the final maturation of B cells into antibody-producing cells [35].…”

Section: Discussionmentioning

confidence: 99%

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Increased IL-6 in Supernatant of Rat Mesangial Cell Cultures Treated with Erythrogenic Toxin Type B and Its Precursor Isolated from Nephritogenic Streptococci

Pedreáñez

Viera²,

Rincón³

et al. 2006

Am J Nephrol

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Background/Aims: Previous reports have shown the presence of streptococcal erythrogenic toxin type B (ETB), IL-8, transforming growth factor-β (TGF-β) and glomerular proliferation in renal biopsies from patients with acute poststreptococcal glomerulonephritis (APSGN). In addition, increased levels of plasma IL-6 and tumor necrosis factor-α (TNFα) and urinary IL-6 have also been reported in this disease. To determine the effect of ETB in mesangial cell cytokine production and proliferation, the concentration of several cytokines (IL-6, IL-1β, TNFα, IL-10, IL-4, RANTES), soluble TNF receptor I (STNFR-I), soluble TNF receptor II (STNFR-II) and proliferation were measured in rat mesangial cells cultures after treatment with ETB or its precursor (ETBP). Methods: To analyze the levels of cytokines and production of soluble receptors as well as proliferation, rat mesangial cells were cultured with ETB or ETBP (50 µg/ml). After 24, 48 and 96 h of incubation, culture supernatants were assessed for cytokines and receptors by ELISA and for proliferation by incorporation of radioactive thymidine. Results: A significant increase in IL-6 levels was found in mesangial cell cultures treated with either ETBP or ETB when compared with controls. Streptococcal proteins treated mesangial cells also showed elevated levels of proliferation at 96 h. Increased production of IL-6 was not correlated with proliferation. A polyclonal anti-ETB antibody abolished the IL-6 stimulatory effect of ETB on mesangial cells. ETB/ETBP failed to increase the levels of other cytokines and cytokine soluble receptors. Conclusion: Streptococcal ETB/ETBP is capable of inducing increased production of IL-6 and proliferation on mesangial cells. These findings could be relevant in a possible early interaction of streptococcal proteins with mesangial cells and during the course of APSGN.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Increased IL-6 in Supernatant of Rat Mesangial Cell Cultures Treated with Erythrogenic Toxin Type B and Its Precursor Isolated from Nephritogenic Streptococci

Pedreáñez

Viera²,

Rincón³

et al. 2006

Am J Nephrol

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“…In the kidney, cytokines induce expression of reactive oxygen/nitrogen species (16), bioactive lipids (17), and adhesion molecules (18,19). They also promote aberrant matrix metabolism (20,21), proliferation of resident cells (22), and procoagulant activity of endothelium in the kidney (23). In the Beaver Dam Chronic Kidney Disease Study, a population-based cohort of 4926 predominantly white participants from Wisconsin, circulating levels of IL-6 and TNF-a receptor 2 were associated with incident CKD (24).…”

Section: Discussionmentioning

confidence: 99%

Inflammation and Progression of CKD: The CRIC Study

Amdur¹,

Feldman²,

Gupta³

et al. 2016

CJASN

327

256

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Background and objectives CKD is a global public health problem with significant mortality and morbidity.Design, setting, participants, & measurements We examined the multivariable association of plasma levels of IL-1, IL-1 receptor antagonist, IL-6, TNF-a, TGF-b, high-sensitivity C-reactive protein, fibrinogen, and serum albumin with progression of CKD in 3430 Chronic Renal Insufficiency Cohort study participants.Results Over a median follow-up time of 6.3 years, 899 participants reached the composite end point of $50% decline in eGFR from baseline or onset of ESRD. Elevated plasma levels of fibrinogen, IL-6, and TNF-a and lower serum albumin were associated with a greater decline in eGFR over time. After adjusting for demographics, BP, laboratory variables, medication use, and baseline eGFR, hazard ratios for the composite outcome were greater for the patients in the highest quartile of fibrinogen (hazard ratio, 2.05; 95% confidence interval, 1.64 to 2.55; P,0.001), IL-6 (hazard ratio, 1.44; 95% confidence interval, 1.17 to 1.77; P,0.01), and TNF-a (hazard ratio, 1.94; 95% confidence interval, 1.52 to 2.47; P,0.001) compared with those in the respective lowest quartiles. The hazard ratio was 3.48 (95% confidence interval, 2.88 to 4.21; P,0.001) for patients in the lowest serum albumin quartile relative to those in the highest quartile. When also adjusted for albuminuria, the associations of fibrinogen (hazard ratio, 1.49; 95% confidence interval, 1.20 to 1.86; P,0.001), serum albumin (hazard ratio, 1.52; 95% confidence interval, 1.24 to 1.87; P,0.001), and TNF-a (hazard ratio, 1.42; 95% confidence interval, 1.11 to 1.81; P,0.001) with outcome were attenuated but remained significant.Conclusions Elevated plasma levels of fibrinogen and TNF-a and decreased serum albumin are associated with rapid loss of kidney function in patients with CKD.

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“…Several investigators have previously reported that some cytokines could play an important role in the pathophysiology of human renal diseases [1, 2, 3, 4, 5, 6]. Studies using cultured mesangial cells or experimental models of glomerulonephritis have shown that mesangial expansion with cell proliferation might be affected with cytokines.…”

Section: Introductionmentioning

confidence: 99%

“…Studies using cultured mesangial cells or experimental models of glomerulonephritis have shown that mesangial expansion with cell proliferation might be affected with cytokines. As an example, transforming growth factor-β (TGF-β) accentuates the accumulation of extracellular matrix [1, 7, 8, 9], and other cytokines such as platelet-derived growth factor (PDGF) [2, 9, 10, 11], tumor necrosis factor-α (TNF-α) [4], interleukin (IL)-1 [3]or IL-6 [5, 12, 13]promote the proliferation of mesangial cells. Using an immunoperoxidase or immunofluorescent method, the expression of TGF-β [14], PDGF [15], TNF-α [16, 17, 18], IL-1 [16, 17, 18]or IL-6 [12, 16, 18, 19]has been demonstrated in the mesangial region of glomeruli, as well as in the glomerular resident or infiltrating cells from the patients with mesangial proliferative glomerulonephritis, antineutrophil cytoplasmic autoantibody-positive glomerulonephritis or focal glomerular sclerosis.…”

Section: Introductionmentioning

confidence: 99%

Immunogold Labelling of Cytokines in Glomeruli in Children with Various Renal Diseases

Nakajima

Kawahara²,

Sakagami³

et al. 1999

Nephron

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Precise localization of cytokines such as transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interleukin (IL)-1 and IL-6 was observed in glomeruli using immunogold electron microscopy in 21 children with various types of renal diseases. The distribution pattern of these cytokines, as well as immunoglobulins, C3c and fibrinogen (Fg), was essentially confined to the electron-dense deposits (EDDs) regardless of their location. Frequency of positive labelling of each cytokine was different among various types of renal disorder, that is, TGF-β was found mainly in lupus nephritis (LN), membranous nephropathy and IgA nephropathy, TNF-α in LN, and IL-1 in Henoch-Schönlein purpura nephritis. IL-6 was detected only in 1 case of LN. TNF-α was also found in the cytoplasm of glomerular epithelial cells. Furthermore, in order to evaluate the relation of cytokines to mesangial expansion, extracellular matrix components such as type IV collagen, laminin and fibronectin were stained. The result was that there was no significant correlation between the signal intensity or distribution pattern of cytokines and that of extracellular matrix components. These findings indicate that these cytokines could be associated with the formation of EDDs together with immunoglobulins, C3c and Fg. The involvement of each cytokine in renal pathophysiology might also depend upon the type of renal disease. They also raise the possibility that the glomerular epithelial cells might produce or absorb TNF-α. However, these results did not show significant correlation between cytokine involvement and mesangial expansion.

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Interleukin-6: An autocrine regulator of mesangial cell growth

Cited by 99 publications

References 11 publications

Increased IL-6 in Supernatant of Rat Mesangial Cell Cultures Treated with Erythrogenic Toxin Type B and Its Precursor Isolated from Nephritogenic Streptococci

Increased IL-6 in Supernatant of Rat Mesangial Cell Cultures Treated with Erythrogenic Toxin Type B and Its Precursor Isolated from Nephritogenic Streptococci

Inflammation and Progression of CKD: The CRIC Study

Immunogold Labelling of Cytokines in Glomeruli in Children with Various Renal Diseases

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