Heme oxygenase-1 is induced by thyroid hormone and involved in thyroid hormone preconditioning-induced protection against renal warm ischemia in rat

Li, Fēi; Lu, S Y; Zhu, Ruixia; Zhou, Zhongxin; Ma, Lingdi; Cai, Leiming; Liu, Zhiyuan

doi:10.1016/j.mce.2011.03.019

Cited by 22 publications

(27 citation statements)

References 45 publications

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“…These HO-1 enzyme-generated products exhibit free radical scavenging, vasodilating, anti-inflammatory, and anti-apoptotic proprieties. 1,38,39 Indeed, it has been demonstrated that HO-1 induction by pharmacologic preconditioning can prevent cold I/R induced injury in renal graft. 38 Li Volti and his coworkers 39 demonstrated that pharmacologic induction of HO-1 attenuates renal warm I/R injury via inhibiting apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

et al. 2014

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Renal ischemia reperfusion (I/R) injury, which occurs during renal surgery or transplantation, is the major cause of acute renal failure. Trimetazidine (TMZ), an anti-ischemic drug, protects kidney against the deleterious effects of I/R. However its protective mechanism remains unclear. The aim of this study is to examine the relevance of Akt, endothelial nitric oxide synthase (eNOS), and hypoxia inducible factor-1a (HIF-1a) on TMZ induced protection of kidneys against I/R injury. Wistar rats were subjected to 60 min of warm renal ischemia followed by 120 min of reperfusion, or to intraperitoneal injection of TMZ (3 mg/kg) 30 min before ischemia. In sham operated group renal pedicles were only dissected. Compared to I/R, TMZ treatment decreased lactate dehydrogenase (845 ± 13 vs. 1028 ± 30 U/L). In addition, creatinine clearance and sodium reabsorption rates reached 105 ± 12 versus 31 ± 11 mL/min/g kidney weight and 95 ± 1 versus 68 ± 5%, respectively. Besides, we noted a decrease in malondialdehyde concentration (0.33 ± 0.01 vs. 0.59 ± 0.03 nmol/mg of protein) and an increase in glutathione concentration (2.6 ± 0.2 vs. 0.93 ± 0.16 mg GSH/mg of protein), glutathione peroxidase (95 ± 4 vs. 61 ± 3 mg GSH/min/mg of protein), and superoxide dismutase (25 ± 3 vs. 11 ± 2 U/mg of protein) and catalase (91 ± 12 vs. 38 ± 9 mmol/min/mg of protein) activities. Parallely, we noted a significant increase in p-Akt, eNOS, nitrite and nitrate (18 ± 2 vs. 8 ± 0.1 pomL/mg of protein), HIF-1a (333 ± 48 vs. 177 ± 14 mg/mg of protein) and heme oxygenase-1 (HO-1) levels regarding I/R. TMZ treatment improves renal tolerance to warm I/R. Such protection implicates an activation of Akt/eNOS signaling pathway, HIF-1a stabilization and HO-1 activation.

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Section: Discussionmentioning

confidence: 99%

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

et al. 2014

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“…For example, hydrogen peroxide increases DHCR24 expression in human-derived neuroblastoma cells 25 and induces HO-1 expression in human dental pulp cells. 26 Thyroid hormones 27 and estrogen 28 increase DHCR24 expression in human fetal neuroepithelial cells and also enhance HO-1 expression in the rat kidney 29 and intestine. 30 However, high dietary intake of the trace metal selenium reduces DHCR24 expression in the rat prostate, 31 whereas bovine aortic endothelial cells cultured in selenium-deficient medium have increased expression of HO-1.…”

Section: Discussionmentioning

confidence: 99%

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

Chen

Shrestha

et al. 2013

Circulation Research

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Rationale: Lipid-free apolipoprotein (apo) A-I and discoidal reconstituted high-density lipoproteins (rHDL) containing apoA-I, (A-I)rHDL, inhibit vascular inflammation by increasing 3β-hydroxysteroid-Δ24 reductase (DHCR24) expression. Objective: To determine whether the lipid-free apoA-I–mediated and (A-I)rHDL-mediated increase in DHCR24 expression induces the cytoprotective and potentially cardioprotective enzyme, heme oxygenase-1 (HO-1). Methods and Results: In vivo: A single intravenous infusion of lipid-free apoA-I (8 mg/kg) administered 24 hours before inserting a nonocclusive periarterial carotid collar into New Zealand White rabbits decreased collar-induced endothelial vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression, reduced intima/media neutrophil infiltration, and increased DHCR24 and HO-1 mRNA levels. Knockdown of vascular DHCR24 and HO-1 and systemic administration of tin-protoporphyrin-IX, an HO inhibitor, abolished these anti-inflammatory effects. In vitro: Preincubation of human coronary artery endothelial cells with (A-I)rHDL before activation with tumor necrosis factor-α increased DHCR24 and HO-1 mRNA levels and inhibited cytokine-induced vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression. Transfection of the cells with DHCR24 and HO-1 small interfering RNA and tin-protoporphyrin-IX treatment abolished these effects. The (A-I)rHDL-mediated induction of HO-1 was reduced in human coronary artery endothelial cells transfected with DHCR24 small interfering RNA. Transfection of human coronary artery endothelial cells with HO-1 small interfering RNA and tin-protoporphyrin-IX treatment did not inhibit the (A-I)rHDL-mediated increase in DHCR24 expression. Inhibition of phosphatidylinositol 3-kinase/Akt reduced the (A-I)rHDL-mediated increase in HO-1, but not DHCR24 expression. The activation of phosphatidylinositol 3-kinase/Akt by (A-I)rHDL was decreased in human coronary artery endothelial cells that were transfected with DHCR24 small interfering RNA. Conclusions: Lipid-free apoA-I and (A-I)rHDL inhibit inflammation by increasing DHCR24 expression, which, in turn, activates phosphatidylinositol 3-kinase/Akt and induces HO-1.

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“…Ancak Fernandez ve arkadaşları (25) T3 ile oluşan oksidatif stresin geçici ve geri dönüşümlü olduğunu bildirmektedirler. Ayrıca T3 önkoşullanmasının kalpte oksidatif stres artışı ile ısı şok proteini 70 (heat shock protein 70, hsp 70) ve hsp27 yapımına neden olduğu (14) ve böbrek iskemisinde ise heme oksijenaz-1 (HO-1) yapımı ile koruycu etki gösterdiği saptanmıştır (11). Bu proteinlerin yapımı hücrede oksidatif stres gibi durumlarda artmakta ve antiapoptotk, antioksidant ve antiinflamatuar etkiler ile koruyucu olduğu bildirilmektedir (11).…”

Section: Discussionunclassified

“…Ayrıca T3 önkoşullanmasının kalpte oksidatif stres artışı ile ısı şok proteini 70 (heat shock protein 70, hsp 70) ve hsp27 yapımına neden olduğu (14) ve böbrek iskemisinde ise heme oksijenaz-1 (HO-1) yapımı ile koruycu etki gösterdiği saptanmıştır (11). Bu proteinlerin yapımı hücrede oksidatif stres gibi durumlarda artmakta ve antiapoptotk, antioksidant ve antiinflamatuar etkiler ile koruyucu olduğu bildirilmektedir (11). Ayrıca hepatik İ/R'da T3 önkoşullanmasının nötrofil infiltrasyonu, proinflamatuar sitokin ve adezyon moleküllerinin yapımını azalttığı da gösterilmiştir (13 Sonuç olarak intesinal İ/R hasarında T3 önkoşullanmasının ileum ve akciğer dokularında histopatolojik olarak koruyucu etki gösterdiği saptanmıştır.…”

Section: Discussionunclassified

“…Tiroid hormon büyüme, gelişme ve metabolizmanın fizyolojik kontrolünde rol oynamasının yanısıra iskemik dokularda tiroid hormonunun koruycu etkileri son dönemlerde ortaya konmuştur. Tiroid hormon öntedavisi pek çok dokunun iskemik direncini artırarak I/R hasarına karşı koruycu etkili olduğu gösterilmiştir (11). Deneysel I/R hasarı modellerinde gerek l-3,3′,5-tri-idotironin(T3) gerekse l-tiroksin (T4) önkoşullanmasının hepatik (12,13), miyokardiyal (14), böbrek (10,11) …”

Section: Introductionunclassified

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İntestinal İskemi/Reperfüzyon Modelinde Tiroid Hormon Ön Koşullanmasının İnce Bağırsak Ve Akciğer Hasarı Üzerine Etkisi

TURAN¹,

Özaçmak²,

Barut³

et al. 2017

MJWBS

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Heme oxygenase-1 is induced by thyroid hormone and involved in thyroid hormone preconditioning-induced protection against renal warm ischemia in rat

Cited by 22 publications

References 45 publications

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

Effects of trimetazidine on the Akt/eNOS signaling pathway and oxidative stress in anin vivorat model of renal ischemia-reperfusion

High-Density Lipoproteins Inhibit Vascular Endothelial Inflammation by Increasing 3β-Hydroxysteroid-Δ24 Reductase Expression and Inducing Heme Oxygenase-1

İntestinal İskemi/Reperfüzyon Modelinde Tiroid Hormon Ön Koşullanmasının İnce Bağırsak Ve Akciğer Hasarı Üzerine Etkisi

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