Glucose regulation of β-defensin-1 mRNA in human renal cells

Malik, Afshan N.; Al‐Κafaji, Ghada

doi:10.1016/j.bbrc.2006.12.037

Cited by 33 publications

(30 citation statements)

References 31 publications

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“…The regulation of hBD-1 and hBD-4 synthesis is less well understood; hBD-1 has been largely considered a constitutively expressed defensin, but a recent observation of a relatively low degree of induction in epidermal cultures, suggests some sort of regulation by LPS and supernatants from stimulated mononuclear blood leukocytes [11]. Moreover, hBD-1 upregulation by albumin, arginine and isoleucine has been observed in human colon tumor cells, by a pathway involving c-myc [31], and induction by glucose has been reported in human renal cells [32]. Similar to hBD-2 and -3, hBD-4 expression is induced by Ca 2+ , TNFa, IL-1b, phorbol 12-myristate 13-acetate and heat-killed P. aeruginosa in primary keratinocytes [10].…”

Section: Defensins Expression Can Be Induced In Response To Bacterialmentioning

confidence: 95%

Defensins in the immunology of bacterial infections

Menéndez

Finlay

2007

Current Opinion in Immunology

115

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Section: Defensins Expression Can Be Induced In Response To Bacterialmentioning

confidence: 95%

Defensins in the immunology of bacterial infections

Menéndez

Finlay

2007

Current Opinion in Immunology

115

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“…These results suggested that the role of innate immunity, especially in regards to HBD-1, was a primary process in the development of DM. Malik et al found that the increased expression of HBD-1 mRNA in high glucose suggested a role for HBD-1 in the molecular pathways induced during hyperglycemia [21]. Further, the high serum HBD-1 levels in DM patients might contribute to the development of DN.…”

Section: Discussionmentioning

confidence: 99%

Proflie of Human β-Defensins 1,2 and Proinflammatory Cytokines (TNF-α, IL-6) in Patients with Chronic Kidney Disease

Kim²,

Lee³

et al. 2013

Kidney Blood Press Res

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Background/Aim: Our aim was to determine whether altered human β-defensin (HBD), pro-inflammatory cytokines including interleukin (IL)-6 and tumor necrotic factor (TNF)-α could increase the risk of developing and exacerbation of chronic kidney disease (CKD), especially for patients with diabetic nephropathy (DN). Methods: Serum samples were obtained from 338 CKD patients and 88 sex, age-matched healthy controls. The concentrations of HBD-1 were assayed using an RIA kit. Serum levels of HBD-2, IL-6 and TNF-α were assayed using an ELISA kit. Results: Serum levels of HBD-1, IL-6 and TNF-α were significantly higher in CKD patients compared to healthy controls (P<0.05). HBD-1 levels were inversely related to estimated glomerular filtration rate (eGFR), which was the coefficient factor (β = -0.357, P = 0.035) explaining the variability in HBD-1 in CKD. Diabetic nephropathy (DN) patients at stage 3-5 had significantly higher serum HBD-1 levels than non DN patients (P=0.00). Conclusion: Our data support the view that there is increased inflammation in CKD and DN. The inverse correlation between eGFR and serum HBD-1 which we observed is suggestive of a relationship between innate immunity and renal function and should be further investigated.

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“…The GK rat and control Wistar rat kidneys (Institute of Nephrology, University of Wales College of Medicine, Cardiff, UK) used in this study have been previously described [13][14][15]. GK rats are normoglycaemic at 6 weeks (6 mmol/l), have slightly raised blood glucose at 16 weeks (7-8 mmol/l) and by 26 weeks are hyperglycaemic (13 mmol/l) [21].…”

Section: Biological Materialsmentioning

confidence: 99%

“…Oligonucleotide primers (electronic supplementary material [ESM] Table 1) were designed using the universal probe library (Roche), and synthesised (Sigma-Aldrich). Real-time quantitative PCR (qPCR) was carried out using SYBR green (Qiagen, Crawley, UK) [13][14][15] in the Roche LC480 Light Cycler. Copy number values were expressed as relative to GAPDH.…”

Section: Rna Extraction and Real-time Pcrmentioning

confidence: 99%

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Elevated levels of renal and circulating Nop-7-associated 2 (NSA2) in rat and mouse models of diabetes, in mesangial cells in vitro and in patients with diabetic nephropathy

et al. 2011

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Aims/hypothesis We previously found that Nop-7-associated 2 (NSA2), which is involved in ribosomal biogenesis in yeast and is a putative cell cycle regulator in mammalian cells, is elevated in the kidney of Goto-Kakizaki (GK) rat, a spontaneous model of type 2 diabetes. Here we tested the hypothesis that elevated NSA2 is involved in diabetic nephropathy (DN). Methods We examined Nsa2/NSA2 expression and NSA2 production in two rodent models of diabetes, in cultured renal glomerular cells, and in diabetic patients with and without nephropathy. Patients with nephropathy who had a history of albuminuria were further divided as responders (DN-NA; DN patients normoalbuminuric at the time of this study with a history of albuminuria) and non-responders (DN-A; diabetic nephropathy patients with albuminuria) to current treatment for albuminuria. Results Renal Nsa2/NSA2 mRNA increased in tandem with hyperglycaemia in GK rats, in a streptozotocin-induced mouse model of diabetes, and in human mesangial cells (HMCs) grown in high glucose (p<0.05). In the mouse model of diabetes, hyperglycaemia resulted in increased Nsa2 expression and NSA2 levels in tubular and glomerular cells and in circulating cells; this increase was normalised by diabetes treatment. Circulating NSA2 mRNA levels were elevated in patients with DN independently of body weight (BMI), glycaemic (HbA 1c ) and haemodynamic (blood pressure) control, and showed an inverse correlation with renal function (GFR, p<0.05). NSA2 levels were the only variable that showed a significant difference between patients with albuminuria (DN-A) compared with nonalbuminuric patients (DN-NA) and diabetic controls (p< 0.05), this increase being independent of all other variables, including GFR. Conclusion We show for the first time that renal and circulating NSA2/NSA2 levels are increased in hyperglycaemia in experimental models of diabetes, and that circulating NSA2 is elevated in DN patients with albuminuria. Further studies will be required to assess whether NSA2 plays a role in the pathogenesis of DN.

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Glucose regulation of β-defensin-1 mRNA in human renal cells

Cited by 33 publications

References 31 publications

Defensins in the immunology of bacterial infections

Defensins in the immunology of bacterial infections

Proflie of Human β-Defensins 1,2 and Proinflammatory Cytokines (TNF-α, IL-6) in Patients with Chronic Kidney Disease

Elevated levels of renal and circulating Nop-7-associated 2 (NSA2) in rat and mouse models of diabetes, in mesangial cells in vitro and in patients with diabetic nephropathy

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