27
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      Call for Papers: Green Renal Replacement Therapy: Caring for the Environment

      Submit here before July 31, 2024

      About Blood Purification: 3.0 Impact Factor I 5.6 CiteScore I 0.83 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found

      Apolipoprotein E regulates primary cultured human mesangial cell proliferation.

      Nephron. Experimental Nephrology
      Apolipoprotein E2, Apolipoprotein E3, Apolipoprotein E4, Apolipoproteins B, pharmacology, Apolipoproteins E, physiology, Apoptosis, drug effects, Cell Proliferation, Cells, Cultured, Drug Combinations, Glomerular Mesangium, cytology, Humans, Time Factors

      Read this article at

      ScienceOpenPublisherPubMed
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The role of apolipoprotein (apo) E in kidney disease is still unclear. Animal studies have been performed, but it is doubtful if the conclusions are applicable to human beings. The objective of this study was to determine how apo E acts on human kidneys using primary cultured normal human mesangial cells (NHMCs) rather than animals used in previous studies. apo E and its isoforms E2, E3 and E4, or combinations with apo B were cocultured with primary NHMCs in serum-free medium. Premix WST-1 Cell Proliferation Assay System and DNA-Prep Reagent System were used to measure the proliferation and apoptosis of NHMCs, respectively. (1) apo E itself increased NHMC proliferation at 24 h of culture, while it inhibited this proliferation after 48 h. (2) At 72 h of culture, apo E alone inhibited NHMC proliferation at concentrations higher than 0.78 microg/ml in concentration-dependent manner. (3) When co-cultured with both apo E and apo B, NHMC proliferation was higher than that with apo E alone and lower than that with apo B alone. (4) At 72 h of culture, apo E2, E3 and E4 inhibited NHMC proliferation at different intensities, with no proliferative effect observed. (5) Neither apo E nor apo B caused NHMC apoptosis. apo E regulates primary NHMC proliferation by (1) inhibiting NHMC proliferation or reducing NHMC proliferation induced by apo B, which implies that apo E has a protective effect on the kidney, and (2) increasing the proliferation under certain conditions.

          Related collections

          Most cited references14

          • Record: found
          • Abstract: not found
          • Article: not found

          Apolipoprotein B and apolipoprotein A-I: risk indicators of coronary heart disease and targets for lipid-modifying therapy

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Apolipoprotein E modulates immune activation by acting on the antigen-presenting cell.

            Apolipoprotein E (ApoE) is synthesized by a variety of cells including macrophages. These cells activate T lymphocytes by antigen presentation, while the T-cell cytokine, interferon-gamma, inhibits macrophage ApoE expression. ApoE inhibits T-cell proliferation in culture but its role in immune responses has been unclear. The ApoE-deficient (E0) mouse permits an evaluation of the immunological role of ApoE. We have analysed T-cell responses to an exogenous antigen (ovalbumin) and polyclonal mitogen (concanavalin A) in E0 and ApoE+/+ mice. Macrophages of E0 mice stimulated T-cell activation more effectively as antigen-presenting cells than macrophages from ApoE+/+ mice. Both proliferation and interferon-gamma secretion were enhanced in T cells activated in the context of antigen-presenting cells from E0 mice. Since the macrophage-T-cell interaction depends on interactions between cell surface molecules, we assessed the expression of such molecules after in vivo stimulation with interferon-gamma. This treatment caused an increased expression of the co-stimulatory surface proteins CD40 and CD80, and also of the major histocompatibility complex class II molecules I-Ab on macrophages of E0 mice compared with ApoE+/+. Our data suggest that ApoE inhibits T-cell activation by reducing the density of immune stimulatory proteins on antigen-presenting cells.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Apolipoprotein E genetic polymorphism, remnant lipoproteins, and nephropathy in type 2 diabetic patients.

              We previously showed that the apolipoprotein (apo) Eepsilon2 allele is associated with the progression of diabetic nephropathy. The aim of the present study is to further investigate the association between apo E genetic polymorphism, plasma lipid levels (particularly remnant lipoproteins), and diabetic nephropathy. One hundred fifty-eight patients with type 2 diabetes who had a duration of diabetes longer than 10 years were divided into the three apo E groups: apo E2 (n = 22), E3/3 (n = 102), and E4 (n = 34). Plasma levels of lipids and remnant lipoproteins were measured. The effect of apo E2 triglyceride (TG)-rich lipoproteins, including remnant lipoproteins, on the accumulation of cholesteryl esters by human mesangial cells (HMCs) was estimated by measuring the stimulation of radioactive carbon-labeled oleate incorporation into cholesteryl esters. The frequency of overt nephropathy was significantly greater in apo E2 patients with diabetes (59.1%) than apo E3/3 (34.3%) or apo E4 patients (8.8%), and the frequency of normoalbuminuria was significantly greater in apo E4 patients with diabetes (67.6%) than apo E3/3 (34.3%) or apo E2 patients (4.5%). Logistical regression analysis showed that odds ratios of apo E2 and apo E4 genotypes for the presence of overt nephropathy were 10.179 (P = 0.0349) and 0.129 (P = 0.0028), respectively. Plasma TG and remnant-like lipoprotein particle cholesterol levels were significantly greater in apo E2 patients and significantly lower in apo E4 patients than apo E3/3 patients. Apo E2 TG-rich lipoproteins stimulated the accumulation of cholesteryl esters by HMCs significantly more than apo E3/3 or apo E4 TG-rich lipoproteins. Apo E2 is a positive factor and apo E4 is a negative factor for diabetic nephropathy. Apo E2 TG-rich lipoproteins, including remnant lipoproteins, affected HMCs. Remnant lipoproteins may have an important role in the progression of diabetic nephropathy. Copyright 2002 by the National Kidney Foundation, Inc.
                Bookmark

                Author and article information

                Comments

                Comment on this article