NF-kappa B involved in transcription enhancement of TGF-beta 1 induced by Ox-LDL in rat mesangial cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>To determine the binding activity of nuclear factor-kappa B (NF-kappa B) and the transcription of transforming growth factor-beta 1 (TGF-beta 1) induced by oxidized low density lipoprotein (Ox-LDL) in rat mesangial cells and to elucidate the mechanism of renal injury of Ox-LDL.</p><p><b>METHODS</b>NF-kappa B binding activity was measured by gel shift assay in mesangial cells with or without inducement of Ox-LDL. Protein kinase inhibitors and activators were then used to determine the signal transduction pathways. In this course I kappa B protein expression was analyzed by Western blot assay. TGF-beta 1 mRNA was measured in mesangial cells exposed to Ox-LDL by RT-PCR assay. TGF-beta 1 promoter from -1551 to +57 were constructed into a pGL3-Basic vector with a luciferase reporting gene. A putative binding site of NF-kappa B was mutated. The wild and mutant promoters activity was analyzed by transfection into mesangial cells.</p><p><b>RESULTS</b>NF-kappa B was activated by Ox-LDL persistently and rebounded in the early period. Ox-LDL induced NF-kappa B activation in a dose dependent way. It also induced I kappa B degradation in 2 hours and resumed to normal levels. NF-kappa B activation was not alleviated by inhibitors of protein kinase A (PKA), extracellular signal-regulated kinase (ERK), and p38 MAP kinase (p38MAPK). Inhibitors of protein kinase C (PKC) and proteinsome inhibited the enhancement of NF-kappa B binding activity. Ox-LDL induced the transcription of TGF-beta1 in a time and dose dependent manner. Mutation of the putative binding site of NF-kappa B reduced the activity of TGF-beta1 promoter.</p><p><b>CONCLUSION</b>Ox-LDL induced activation of NF-kappa B persistently. It was probably regulated by the degradation of I kappa B mediated by PKC pathway. NF-kappa B may be involved in the enhancement of TGF-beta 1 induced by Ox-LDL in rat mesangial cells.</p>

Role of hepatitis B virus infection in pathogenesis of IgA nephropathy / 中华预防医学杂志

<p><b>OBJECTIVE</b>To clarify the relationship between hepatitis B virus (HBV) infection and IgA nephropathy (IgAN).</p><p><b>METHODS</b>HBV antigen (HBAg) in renal tissues of the patients with IgAN was detected by immunohistochemical technique, the carrier status and localization of HBV DNA in renal tissues were determined by Southern blot analysis and in situ hybridization.</p><p><b>RESULTS</b>Serum HBsAg was detected in 18 of the 100 patients with IgAN (18%), HBAg was detected in 31 of 100 patients (31%) in their renal tissue and in 20 of 31 patients (65%) in their glomeruli, and both HBsAg and HBcAg were detected in 10 of 31 patients (32%), respectively. HBcAg was also found in tubular epithelia (45%, 14/31) and renal interstitium (6%, 2/31), respectively. Five of six cases were proved to be positive of integrated-form HBV DNA in their renal tissue by Southern blot analysis. In situ hybridization demonstrated that HBV DNA was 8/8 and 6/8 positive in their renal tubules and glomeruli of all eight specimens, localized in the nucleus of tubular epithelial cells, glomerular mesangial cells, as well as infiltrated interstitial lymphocytes.</p><p><b>CONCLUSION</b>HBV infection closely related with IgAN and HBV infection might be involved in pathogenesis of IgAN.</p>