Effect of IgA aggregates on transforming growth factor-β1 production in human mesangial cells and the intraglomerular expression of transforming growth factor-β1 in patients with IgA nephropathy

Sang Youb Han, Chun Gyoo Ihm, Dae-Ryong Cha, Young Sun Kang, Kum Hyun Han, Hyoung Kyu Kim, Jee Young Han

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Background: Transforming growth factor-β (TGF-β) stimulates renal fibrosis in various renal diseases including IgA nephropathy. Methods: We examined whether immunoglobulin A (IgA) stimulated TGF-β1 synthesis in human mesangial cells (MCs), and whether this effect was mediated through the protein kinase C (PKC) pathway. We measured the intraglomerular TGF-β mRNA expression by using competitive RT-PCR, and this was compared with various parameters in IgA nephropathy patients. Results: The IgA aggregate increased the TGF-β1 mRNA expression in MCs, while this expression was not affected by the culture media or IgG aggregate. Phorbol 12-myristate 13-acetate and calphostin C did not influence the TGF-β1 mRNA expression that was increased by the IgA aggregate. Intraglomerular TGF-β1 mRNA expression was significantly correlated with creatinine clearance (r=-0.764, p=0.027), daily proteinuria (r=0.781, p=0.022), serum creatinine (r=0.884, p=0.004), and tubulointerstitial changes (r=-0.809, p=0.015). Glomerular TGF-β1 mRNA expression was associated with an increased tendency for glomerulosclerosis (r=0.646, p=0.084). After 4 years, patients with a high expression of intraglomerular TGF-β1 mRNA showed a tendency for an decrease of their renal function. Conclusion: The IgA aggregate increased TGF-β1 mRNA expression in MCs, and this was independent of the PKC pathway. The evaluation of intraglomerular TGF-β1 mRNA expression could be useful in predicting the progression of IgA nephropathy.

Original languageEnglish
Pages (from-to)40-47
Number of pages8
JournalKorean Journal of Internal Medicine
Volume20
Issue number1
Publication statusPublished - 2005 Mar 1

Fingerprint

IGA Glomerulonephritis
Mesangial Cells
Transforming Growth Factors
Immunoglobulin A
Messenger RNA
Kidney
Protein Kinase C
Creatinine
Proteinuria
Culture Media
Acetates
Fibrosis
Immunoglobulin G

Keywords

  • Competitive RT-PCR
  • IgA
  • IgA nephropathy
  • Transforming growth factor beta

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Effect of IgA aggregates on transforming growth factor-β1 production in human mesangial cells and the intraglomerular expression of transforming growth factor-β1 in patients with IgA nephropathy. / Han, Sang Youb; Ihm, Chun Gyoo; Cha, Dae-Ryong; Kang, Young Sun; Han, Kum Hyun; Kim, Hyoung Kyu; Han, Jee Young.

In: Korean Journal of Internal Medicine, Vol. 20, No. 1, 01.03.2005, p. 40-47.

Research output: Contribution to journalArticle

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abstract = "Background: Transforming growth factor-β (TGF-β) stimulates renal fibrosis in various renal diseases including IgA nephropathy. Methods: We examined whether immunoglobulin A (IgA) stimulated TGF-β1 synthesis in human mesangial cells (MCs), and whether this effect was mediated through the protein kinase C (PKC) pathway. We measured the intraglomerular TGF-β mRNA expression by using competitive RT-PCR, and this was compared with various parameters in IgA nephropathy patients. Results: The IgA aggregate increased the TGF-β1 mRNA expression in MCs, while this expression was not affected by the culture media or IgG aggregate. Phorbol 12-myristate 13-acetate and calphostin C did not influence the TGF-β1 mRNA expression that was increased by the IgA aggregate. Intraglomerular TGF-β1 mRNA expression was significantly correlated with creatinine clearance (r=-0.764, p=0.027), daily proteinuria (r=0.781, p=0.022), serum creatinine (r=0.884, p=0.004), and tubulointerstitial changes (r=-0.809, p=0.015). Glomerular TGF-β1 mRNA expression was associated with an increased tendency for glomerulosclerosis (r=0.646, p=0.084). After 4 years, patients with a high expression of intraglomerular TGF-β1 mRNA showed a tendency for an decrease of their renal function. Conclusion: The IgA aggregate increased TGF-β1 mRNA expression in MCs, and this was independent of the PKC pathway. The evaluation of intraglomerular TGF-β1 mRNA expression could be useful in predicting the progression of IgA nephropathy.",
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AU - Han, Sang Youb

AU - Ihm, Chun Gyoo

AU - Cha, Dae-Ryong

AU - Kang, Young Sun

AU - Han, Kum Hyun

AU - Kim, Hyoung Kyu

AU - Han, Jee Young

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N2 - Background: Transforming growth factor-β (TGF-β) stimulates renal fibrosis in various renal diseases including IgA nephropathy. Methods: We examined whether immunoglobulin A (IgA) stimulated TGF-β1 synthesis in human mesangial cells (MCs), and whether this effect was mediated through the protein kinase C (PKC) pathway. We measured the intraglomerular TGF-β mRNA expression by using competitive RT-PCR, and this was compared with various parameters in IgA nephropathy patients. Results: The IgA aggregate increased the TGF-β1 mRNA expression in MCs, while this expression was not affected by the culture media or IgG aggregate. Phorbol 12-myristate 13-acetate and calphostin C did not influence the TGF-β1 mRNA expression that was increased by the IgA aggregate. Intraglomerular TGF-β1 mRNA expression was significantly correlated with creatinine clearance (r=-0.764, p=0.027), daily proteinuria (r=0.781, p=0.022), serum creatinine (r=0.884, p=0.004), and tubulointerstitial changes (r=-0.809, p=0.015). Glomerular TGF-β1 mRNA expression was associated with an increased tendency for glomerulosclerosis (r=0.646, p=0.084). After 4 years, patients with a high expression of intraglomerular TGF-β1 mRNA showed a tendency for an decrease of their renal function. Conclusion: The IgA aggregate increased TGF-β1 mRNA expression in MCs, and this was independent of the PKC pathway. The evaluation of intraglomerular TGF-β1 mRNA expression could be useful in predicting the progression of IgA nephropathy.

AB - Background: Transforming growth factor-β (TGF-β) stimulates renal fibrosis in various renal diseases including IgA nephropathy. Methods: We examined whether immunoglobulin A (IgA) stimulated TGF-β1 synthesis in human mesangial cells (MCs), and whether this effect was mediated through the protein kinase C (PKC) pathway. We measured the intraglomerular TGF-β mRNA expression by using competitive RT-PCR, and this was compared with various parameters in IgA nephropathy patients. Results: The IgA aggregate increased the TGF-β1 mRNA expression in MCs, while this expression was not affected by the culture media or IgG aggregate. Phorbol 12-myristate 13-acetate and calphostin C did not influence the TGF-β1 mRNA expression that was increased by the IgA aggregate. Intraglomerular TGF-β1 mRNA expression was significantly correlated with creatinine clearance (r=-0.764, p=0.027), daily proteinuria (r=0.781, p=0.022), serum creatinine (r=0.884, p=0.004), and tubulointerstitial changes (r=-0.809, p=0.015). Glomerular TGF-β1 mRNA expression was associated with an increased tendency for glomerulosclerosis (r=0.646, p=0.084). After 4 years, patients with a high expression of intraglomerular TGF-β1 mRNA showed a tendency for an decrease of their renal function. Conclusion: The IgA aggregate increased TGF-β1 mRNA expression in MCs, and this was independent of the PKC pathway. The evaluation of intraglomerular TGF-β1 mRNA expression could be useful in predicting the progression of IgA nephropathy.

KW - Competitive RT-PCR

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