Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani, Parisa; Halabian, Raheleh; Rouhbakhsh, Mahdi; Roushandeh, Amaneh Mohammadi; Masroori, Nasser; Ebrahimi, Majid; Samadikuchaksaraei, Alí; Shokrgozar, Mohammad Ali; Roudkenar, Mehryar Habibi

doi:10.1007/s12192-009-0154-5

Cited by 54 publications

(45 citation statements)

References 39 publications

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“…We found that HO-1 decreased 24 h after glycerol treatment and remained decreased through 72 h and that suramin up-regulated renal HO-1 at 72 h after glycerol treatment. One possible explanation for this observation could involve NGAL, because NGAL was shown previously to confer a cytoprotective and survival benefit in response to diverse forms of cellular stress by inducing HO-1 (Mori et al, 2005;Schmidt-Ott et al, 2007;Bahmani et al, 2010;Johnson et al, 2010). Consistent with this idea, we …”

Section: Untreated E 72 H After Glycerol + Suramin D 72 H After Glysupporting

confidence: 88%

Recovery from Glycerol-Induced Acute Kidney Injury Is Accelerated by Suramin

Korrapati

Shaner²,

Schnellmann³

2012

J Pharmacol Exp Ther

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Acute kidney injury (AKI) is a common and potentially lifethreatening complication after ischemia/reperfusion and exposure to nephrotoxic agents. In this study, we examined the efficacy and mechanism(s) of suramin in promoting recovery from glycerol-induced AKI, a model of rhabdomyolysis-induced AKI. After intramuscular glycerol injection (10 ml of 50% glycerol per kilogram) into male Sprague-Dawley rats, serum creatinine maximally increased at 24 to 72 h and then decreased at 120 h. Creatinine clearance (CrCl) decreased 75% at 24 to 72 h and increased at 120 h. Suramin (1 mg/kg i.v.) administered 24 h after glycerol accelerated recovery of renal function as demonstrated by increased CrCl, decreased renal kidney injury molecule-1, and improved histopathology 72 h after glycerol injection. Suramin treatment decreased interleukin-1␤ (IL-1␤) mRNA, transforming growth factor-␤ 1 (TGF-␤ 1 ), phospho-p65 of nuclear factor-B (NF-B), and cleaved caspase-3 at 48 h compared with glycerol alone. Suramin treatment also decreased glycerol-induced activation of intracellular adhesion molecule-1 (ICAM-1) and leukocyte infiltration at 72 h. Urinary/ renal neutrophil gelatinase-associated lipocalin 2 (NGAL) levels, hemeoxygenase-1 expression, and renal cell proliferation were increased by suramin compared with glycerol alone at 72 h. Mechanistically, suramin decreases early glycerol-induced proinflammatory (IL-1␤ and NF-B) and growth inhibitory (TGF-␤ 1 ) mediators, resulting in the prevention of late downstream inflammatory effects (ICAM-1 and leukocyte infiltration) and increasing compensatory nephrogenic repair. These results support the hypothesis that delayed administration of suramin is effective in abrogating apoptosis, attenuating inflammation, and enhancing nephrogenic repair after glycerol-induced AKI.

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Section: Untreated E 72 H After Glycerol + Suramin D 72 H After Glysupporting

confidence: 88%

Recovery from Glycerol-Induced Acute Kidney Injury Is Accelerated by Suramin

Korrapati

Shaner²,

Schnellmann³

2012

J Pharmacol Exp Ther

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“…It has also been reported that NGAL may play a role in renal adaptation to diabetes, probably as a defensive mechanism to mitigate tubular injury (Bolignano et al, 2009b). NGAL has also been reported to have antioxidant properties (Roudkenar et al, 2007(Roudkenar et al, , 2008(Roudkenar et al, , 2011Bahmani et al, 2010). Of interest, in our study, renal NGAL increased in diabetic rats, and suramin intervention further increased renal NGAL.…”

Section: Downloaded Fromsupporting

confidence: 64%

Diabetes-Induced Renal Injury in Rats Is Attenuated by Suramin

Korrapati

Shaner²,

Neely³

et al. 2012

J Pharmacol Exp Ther

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Progression of hyperglycemia-induced renal injury is a contributing factor for diabetic nephropathy (DN)-induced end-stage renal disease (ESRD), and development of novel therapeutic strategies that act early to prevent progression of DN and ESRD are important. We examined the efficacy and mechanism(s) of suramin on hyperglycemia-induced renal injury before development of overt histological damage. Two groups of male Sprague-Dawley rats received streptozotocin (STZ) and one group received saline. Three weeks later, one STZ group received suramin (10 mg/kg). All animals were euthanized 1 week later (4 weeks). Although there was a decrease in creatinine clearance between control and STZ Ϯ suramin rats, there was no difference in creatinine clearance between STZ rats Ϯ suramin intervention. Liquid chromatography-tandem mass spectroscopy-based analysis revealed increases in urinary proteins that are early indicators of DN (e.g., cystatin C, clusterin, cathepsin B, retinol binding protein 4, and peroxiredoxin-1) in the STZ group, which were blocked by suramin. Endothelial intracellular adhesion molecule-1 (ICAM-1) activation, leukocyte infiltration, and inflammation; transforming growth factor-␤1 (TGF-␤1) signaling; TGF-␤1/SMAD-3-activated fibrogenic markers fibronectin-1, ␣-smooth muscle actin, and collagen 1A2; activation of proinflammatory and profibrotic transcription factors nuclear factor-B (NF-B) and signal transducer and activator of transcription factor-3 (STAT-3), respectively, were all increased in STZ rats and suramin blocked these changes. In conclusion, delayed administration of suramin attenuated 1) urinary markers of DN, 2) inflammation by blocking NF-B activation and ICAM-1-mediated leukocyte infiltration, and 3) fibrosis by blocking STAT-3 and TGF-␤1/ SMAD-3 signaling. These results support the potential use of suramin in DN.

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“…This suggests that neutrophils, the primary effectors of acute inflammatory response in the body, require NGAL to home in to the target organs (in this case the transplanted heart). The latter role is suggested from observations made in both Chinese hamster ovary (CHO) and human embryonic kidney (HEK) cells that an aberrant expression of 24p3/Ngal leads to a significant upregulation in the expression of the antioxidant enzymes superoxide dismutase (SOD) and heme oxygenase (HO) (Bahmani et al, 2010;Roudkenar et al, 2007;Roudkenar et al, 2008c;Roudkenar et al, 2008a;Roudkenar et al, 2008b). NGAL also appears to play a role in wound healing.…”

Section: Functions Of Ngalmentioning

confidence: 99%