Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling

Li, Ping Chia; Yang, Chi‐Rei; Hsu, Shih Ping; Chien, Chiang Ting

doi:10.1016/j.jvs.2011.11.062

Cited by 15 publications

(15 citation statements)

References 38 publications

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“…Recent studies have showed that PI3K/AKT signal pathway was involved in the induction of HSP70 expression [29,30]. This regulation might rely on the fact that the activation of AKT inhibited GSK-3β [31], and the inhibition of GSK-3β could activate HSF1.…”

Section: Discussionmentioning

confidence: 99%

Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70

Fang

Jiang

et al. 2013

Cancer Cell Int

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Up-regulation of heat shock protein 70 (HSP70) could be elicited primarily by heat in former studies, and this was proved to be associated with cancer progression. Burkitt's lymphoma is one of highly aggressive B-cell non-Hodgkin’s lymphoma and is one of the fastest growing human tumors. To investigate the effect of HSP70 expression on the sensitivity of human Burkitt lymphoma cells (Raji cells) to chemotherapy and its role in the involvement of PI3K/AKT pathway, we evaluated the effects of LY294002, a PI3K inhibitor, on the expression of HSP70 and cell sensitivity to adriamycin (ADM) or cisplatin (DDP). In present study, expressions of HSP70, AKT and phosphorylated AKT (p-AKT) in Raji cells were measured by Western-Blot. Apoptosis index of Raji cells was examined by flow cytometry. Cytotoxicities of adriamycin (ADM) and cisplatin (DDP) were determined by WST-8 assay. We found that hyperthermia (42 degrees for 1 hour) up-regulated the expression of HSP70 expression and blockade of PI3K/AKT pathway down-regulated HSP70 expression in Raji cells. Compared to cells treated with ADM or DDP alone, hyperthermia protected cells from chemotherapy while LY294002 enhanced sensitivity of Raji cells to chemotherapy. Our results suggested down-regulation of HSP70 expression by blockade of PI3K/AKT pathway maybe responsible for the increased sensitivity of Raji cells to chemotherapy. Targeting PI3K/AKT pathway or inhibiting HSP70 expression may be beneficial for chemotherapy treatment of Burkitt lymphoma patients.

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Section: Discussionmentioning

confidence: 99%

Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70

Fang

Jiang

et al. 2013

Cancer Cell Int

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“…Membranes were then incubated for 1 h at room temperature with anti-rabbit or rabbit anti-sheep IgG antibodies conjugated to horseradish peroxidase (Vector Laboratories, Burlingame, CA, USA), and proteins were visualized using a commercial enhanced chemiluminescence kit (GE Healthcare). Band densities were determined semi-quantitatively by densitometry using an Alpha Innotech image analysis system (San Leandro, CA, USA) [ 50 ].…”

Section: Methodsmentioning

confidence: 99%

The GLP-1 receptor agonists exendin-4 and liraglutide alleviate oxidative stress and cognitive and micturition deficits induced by middle cerebral artery occlusion in diabetic mice

Liu

Jou

et al. 2016

BMC Neurosci

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BackgroundGlucagon-like peptide 1 (GLP-1) analogs protect a variety of cell types against oxidative damage and vascular and neuronal injury via binding to GLP-1 receptors. This study aimed to investigate the effects of the GLP-1 analogs exendin-4 and liraglutide on cerebral blood flow, reactive oxygen species production, expression of oxidative stress-related proteins, cognition, and pelvic sympathetic nerve-mediated bladder contraction after middle cerebral artery occlusion (MCAO) injury in the db/db mouse model of diabetes.ResultsSixty minutes of MCAO increased blood and brain reactive oxygen species counts in male db/db mice, as revealed by dihydroethidium staining. MCAO also increased nuclear factor-κB and intercellular adhesion molecule-1 expression and decreased cerebral microcirculation. These effects were attenuated by treatment with exendin-4 or liraglutide. MCAO did not affect basal levels of phosphorylated Akt (p-Akt) or endothelial nitric oxide synthase (p-eNOS); however, exendin-4 and liraglutide treatments significantly enhanced p-Akt and p-eNOS levels, indicating activation of the p-Akt/p-eNOS signaling pathway. MCAO-induced motor and cognitive deficits and micturition dysfunction, indicated by reduced pelvic nerve-mediated voiding contractions and increased nonvoiding contractions, were also partially attenuated by exendin-4 treatment.ConclusionsThe above data indicate that treatment with GLP-1 agonists exerts protective effects against oxidative, inflammatory, and apoptotic damage in brain areas that control parasympathetic/pelvic nerve-mediated voiding contractions and cognitive and motor behaviors in a diabetic mouse model.

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“…Elevated H 2 O 2 in the impaired arteriovenous fistulas from chronic kidney diseases animals or cell death caused a significant decrease in p-Akt levels and an activated Bax/caspase-3 signaling (7,14). Activation of PI3K/Akt signaling and subsequent enhancement of eNOS, phospho-Ser473-Akt, and phospho-Ser1177-eNOS by several treatments increases NO production, and reduces vascular ROS, oxidative stress, and ICAM-1 expression in the damaged tissue (7,18). Our study also found that the decreased p-Akt/p-eNOS/NO signaling by I/R injury is associated with the reduction of renal microcirculation, the increase of renal H 2 O 2 amount BUN, autophagy and apoptosis consequently leading to proximal tubular injury by the elevation of urinary GST level.…”

Section: Discussionmentioning

confidence: 99%

“…In the endothelial cells, the production of H 2 O 2 , an endothelium-dependent contracting factor, through NAD(P)H oxidase activation causes smooth muscle contraction in the rat renal artery (10). Several preconditioning methods require phosphatidylinositol 3-kinase (PI3K)/Akt signaling for enhancing endothelial nitric oxide synthase (eNOS) expressions, phosphorylation of eNOS (p-eNOS) at Ser-1177, and nitric oxide (NO) production to afford cardiovascular protection (14,18,31). However, H 2 O 2 downregulates PI3K/Akt signaling, p-eNOS expression and NO level and leads to oxidative injury and thrombosis (7,14).…”

Section: Introductionmentioning

confidence: 99%

Effect of Adenoviral Catalase Gene Transfer on Renal Ischemia/Reperfusion Injury in Rats

Yang¹

2015

Chin. J. Physiol.

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Ischemia/reperfusion (I/R) may through overt H₂O₂-induced pathophysiologic mechanisms lead to renal dysfunction. We explore whether catalase (CAT) protein overexpression by adenoviral CAT gene (Adv-CAT) transfection may improve ischemia/reperfusion-induced renal dysfunction. We augmented renal CAT expression by intrarenal arterial Adv-CAT administration with renal venous clamping in avertin-anesthetized female Wistar rats. After Adv-CAT transfection, we examined the CAT expression, location and effects on blood urea nitrogen (BUN) and urinary tubular injury biomarkers by biochemical assays, microcirculation by a laser perfusion imager, renal H₂O₂ amount by a chemiluminescent analyzer and molecular mechanisms including cytosolic cytochrome C leakage, apoptosis, autophagy and phospho- Akt (p-Akt)/phospho-endothelial nitric oxide (p-eNOS)/nitric oxide (NO) signaling by western blotting, immunohistochemistry and immunofluorescence. Adv-CAT enhanced 2.6-fold renal CAT protein expression primarily located in the proximal and distal tubules and renal vessels. Ischemia/reperfusion increased cytosolic cytochrome C leakage, renal H₂O₂-dependent level, autophagic Beclin-1/Atg5-Atg12/LC3 II expression, apoptotic Bax/Bcl-2/caspase 3/poly-(ADP-ribose)-polymerase fragments (PARP) expression and terminal deoxynucleotidyl transferasemediated nick-end labeling (TUNEL) stains and BUN and urinary glutathione S-transferase (GST) levels leading to proximal tubular injury. Ischemia/reperfusion also decreased renal microvascular blood flow associated with the inhibited renal expression of p-Akt and p-eNOS and NO production. Adv-CAT significantly improved the reduction in renal microvascular blood flow, reduced ischemia/reperfusion-enhanced oxidative stress, Beclin-1/Atg5-Atg12/LC3 II-meidated autophagy, Bax/Bcl-2/caspase 3/PARP-mediated apoptotic signaling, TUNEL stains, urinary GST level, and restored the p-Akt/p-eNOS/NO signaling in the kidney. Treatment of phosphatidylinositol 3-kinase inhibitors, wortmannin and LY294002, deleted Adv-CAT-induced p-Akt/p-eNOS/NO protective signaling. In conclusion, our results suggest Adv-CAT gene transfer counteracts H₂O₂-induced ischemia/reperfusion injury through preserving p-Akt/p-eNOS/NO pathway in the rat kidney.

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Repetitive progressive thermal preconditioning hinders thrombosis by reinforcing phosphatidylinositol 3-kinase/Akt-dependent heat-shock protein/endothelial nitric oxide synthase signaling

Abstract: Repetitive PTP is better than single PTP to hinder thrombosis formation via reinforcing PI3K/Akt-dependent Hsp70/eNOS signaling.

Cited by 15 publications

References 38 publications

Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70

Blockade of PI3K/AKT pathway enhances sensitivity of Raji cells to chemotherapy through down-regulation of HSP70

The GLP-1 receptor agonists exendin-4 and liraglutide alleviate oxidative stress and cognitive and micturition deficits induced by middle cerebral artery occlusion in diabetic mice

Effect of Adenoviral Catalase Gene Transfer on Renal Ischemia/Reperfusion Injury in Rats

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