Chemokines, osteopontin, ICAM-1 gene expression in cultured rat mesangial cells

Lee, Sang-Koo; Park, Joo-Yeol; Chung, Shi-Jung; Yang, Weon-Suk; Kim, Soon-Bae; Park, Su-Kil; Park, Jungsik

doi:10.3346/jkms.1998.13.2.165

Cited by 8 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reportedly, SPP1 expression is induced by IL-1 α or IL-1 β as well (28, 29). SPP1 is an extracellular glycoprotein, belonging to the integrin superfamily (30).…”

Section: Resultsmentioning

confidence: 99%

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

et al. 2012

View full text Add to dashboard Cite

Among several peroxisomal neurodegenerative disorders, the pseudoneonatal adrenoleukodystrophy (P-NALD) is characterized by the acyl-coenzyme A oxidase 1 (ACOX1) deficiency, which leads to the accumulation of very-long-chain fatty acids (VLCFA) and inflammatory demyelination. However, the components of this inflammatory process in P-NALD remain elusive. In this study, we used transcriptomic profiling and PCR array analyses to explore inflammatory gene expression in patient fibroblasts. Our results show the activation of IL-1 inflammatory pathway accompanied by the increased secretion of two IL-1 target genes, IL-6 and IL-8 cytokines. Human fibroblasts exposed to very-long-chain fatty acids exhibited increased mRNA expression of IL-1α and IL-1β cytokines. Furthermore, expression of IL-6 and IL-8 cytokines in patient fibroblasts was down-regulated by MAPK, p38MAPK, and Jun N-terminal kinase inhibitors. Thus, the absence of acyl-coenzyme A oxidase 1 activity in P-NALD fibroblasts triggers an inflammatory process, in which the IL-1 pathway seems to be central. The use of specific kinase inhibitors may permit the modulation of the enhanced inflammatory status.

show abstract

“…Reportedly, SPP1 expression is induced by IL-1 α or IL-1 β as well (28, 29). SPP1 is an extracellular glycoprotein, belonging to the integrin superfamily (30).…”

Section: Resultsmentioning

confidence: 99%

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Furthermore, glucocor-found in interstitial cell infiltrates of human renal transplants [15], these data may be relevant to human trans-ticoid treatment of the lupus nephritis resulted in a prompt reduction in urinary CCL2/MCP-1 levels consis-plant rejection also. The strongest support for this hypothesis comes from a recent multicenter case control study tent with in vitro results on the inhibitory effect of glucocorticoids on renal cell production of CCL2/MCP-1 [89].…”

Section: Chemokines Mediate Inflammation Functional Studies In Animal Models and In Patients During The Progression Of With Renal Diseasementioning

confidence: 99%

Chemokines and chemokine receptors are involved in the resolution or progression of renal disease

Anders

Vielhauer

Schlöndorff

2003

Kidney International

235

206

View full text Add to dashboard Cite

Locally secreted chemokines mediate leukocyte recruitment during the initiation and amplification phase of renal inflammation. In turn, the infiltrating leukocytes contribute to renal damage by releasing inflammatory and profibrotic factors. Rapid down modulation of the chemokine signal will support resolution of acute inflammation, whereas progression occurs if ongoing or repeated renal injury maintains continuous local chemokine secretion and leukocyte influx into the glomerulus or the interstitial space. In glomerular injury proteinuria itself as well as glomerular secreted cytokines stimulate downstream tubular epithelial cells to also secrete chemokines. During primary tubular injury, tubular epithelial cells directly become a major site of chemokine production. This in turn supports leukocyte infiltration and activation. Infiltrating leukocytes stimulate fibroblast proliferation and matrix synthesis, leading to widening of the interstitial space. The specific and intricate renal vascular architecture renders the organ susceptible to ischemic damage as interstitial volume increases. Ischemia in turn serves as a stimulus for chemokine and cytokine production and matrix synthesis. The mutual stimulation between fibroblasts and infiltrating leukocytes supports progressive tubular damage, renal fibrosis, and glomerulosclerosis. Potentially this vicious circle leading to progression of chronic nephropathies offers the opportunity for therapeutic intervention. Interfering with the chemokine network that mediates leukocyte recruitment may represent a promising therapeutic option for progressive renal disorders and renal fibrosis. This article summarizes the present data on the role of chemokines in acute and chronic renal disease with special emphasis on their potential role in mediating resolution or progression of renal disease as well as on therapeutic options.

show abstract

“…can induce mesangial cells to express ICAM-1 and VCAM-1 and to secrete MCP-1, IL-8, RANTES, CINC, MIP-2, and IP-10 [21,76,77]. A variety of stimuli (IL-1, TNF, IFN-γ, thrombin, etc.)…”

Section: Mechanisms Of Glomerular Leukocyte Recruitment: Adhesion Molmentioning

confidence: 99%

Resident Kidney Cells and Their Involvement in Glomerulonephritis

Timoshanko¹,

Tipping

2005

CDTIA

View full text Add to dashboard Cite

Each year, worldwide, there is an increasing number of patients with chronic kidney disease that progress to end-stage renal disease. Glomerulonephritis (GN) is the commonest single cause of end-stage renal failure in the world. GN can be a manifestation of primary renal injury or may be a secondary feature of a systemic disease process, for example Systemic Lupus Erythematosus (SLE) and Anti-Neutrophilic Cytoplasmic Antibody (ANCA) associated vasculitis. Understanding of the immunopathogenesis of GN has advanced considerably over the last 25 years, particularly the immune system's role. The injurious role of infiltrating leukocytes and humoral mediators has been emphasised, however, the contribution of intrinsic renal cells has proved difficult to define. Most evidence for the pro-inflammatory capacity of intrinsic renal cells has been derived from in vitro studies. Although cytokine production by intrinsic renal cells has been demonstrated by immunohistochemistry and in situ hybridisation studies in renal tissue during the development of GN, the functional contribution of this cytokine production to renal injury was unknown. Little was known about direct and specific interactions between different glomerular cell types and infiltrating leukocytes in the pathogenesis of GN. The development of mice with genetic deficiencies of pro-inflammatory mediators and cytokines, and the technique of bone marrow transplantation into irradiated recipients to produce chimeric mice with restricted cytokine expression has allowed in vivo assessment of the functional contribution made by intrinsic renal cells. Studies have demonstrated the significant contribution of intrinsic renal cell derived cytokines (e.g. TNF) in mediating GN, whereas others (IL-1beta) have a relatively minor role.

show abstract

Chemokines, osteopontin, ICAM-1 gene expression in cultured rat mesangial cells

Cited by 8 publications

References 0 publications

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

The Inflammatory Response in Acyl-CoA Oxidase 1 Deficiency (Pseudoneonatal Adrenoleukodystrophy)

Chemokines and chemokine receptors are involved in the resolution or progression of renal disease

Resident Kidney Cells and Their Involvement in Glomerulonephritis

Contact Info

Product

Resources

About