Role of reactive oxygen species in protein degradation in murine myotubes induced by proteolysis-inducing factor and angiotensin II

Russell, Stewart; Eley, Helen L.; Tisdale, Michael J.

doi:10.1016/j.cellsig.2007.04.003

Cited by 80 publications

(75 citation statements)

References 37 publications

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“…5A) [20], formation of ROS (Fig. 5B) [18], and nuclear accumulation of NF-B (Fig. 5C) [21], were all attenuated by AT.…”

Section: Resultsmentioning

confidence: 91%

“…The method has previously been described in detail [18], and measures the conversion of the cell-permeable probe 2,7-dichlorodihydrofluorescein diacetate, to 2,7-dichlorofluorescein upon oxidation by -8 -ROS. Myotubes were incubated with PIF for 30min, washed with PBS and sonicated at 4°C after scraping from the plate.…”

Section: Measurement Of Ros Formation In Myotubesmentioning

confidence: 99%

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Attenuation of skeletal muscle atrophy in cancer cachexia by d-myo-inositol 1,2,6-triphosphate

Russell

Siren²,

Sirén³

et al. 2008

Cancer Chemother Pharmacol

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D-Myo-inositol 1,2,6-triphosphate (alpha trinositol, AT) has been shown to attenuate muscle atrophy in a murine cachexia model through an increase in protein synthesis and a decrease in degradation. The mechanism of this effect has been investigated in murine myotubes using a range of catabolic stimuli, including proteolysis-inducing factor (PIF), angiotensin II (Ang II), lipopolysaccharide, and tumour necrosis factor- / interferon-. At a concentration of 100M AT was found to attenuate both the induction of protein degradation and depression of protein synthesis in response to all stimuli. The effect on protein degradation was accompanied by attenuation of the increased expression and activity of the ubiquitinproteasome pathway. This suggests that AT inhibits a signalling step common to all four agents. This target has been shown to be activation (autophosphorylation) of the dsRNA-dependent protein kinase (PKR) and the subsequent phosphorylation of eukaryotic initiation factor 2 on the -subunit, together with downstream signalling pathways leading to protein degradation. AT also inhibited activation of caspase-3/-8, which is thought to lead to activation of PKR. The mechanism of this effect may be related to the ability of AT to chelate divalent metal ions, since the attenuation of the increased activity of the ubiquitin-proteasome pathway by PIF and Ang II, as well as the depression of protein synthesis by PIF, were reversed by increasing concentrations of Zn 2+. The ability of AT to attenuate muscle atrophy by a range of stimuli suggests that it may be effective in several conditions.

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“…5A) [20], formation of ROS (Fig. 5B) [18], and nuclear accumulation of NF-B (Fig. 5C) [21], were all attenuated by AT.…”

Section: Resultsmentioning

confidence: 91%

Section: Measurement Of Ros Formation In Myotubesmentioning

confidence: 99%

Attenuation of skeletal muscle atrophy in cancer cachexia by d-myo-inositol 1,2,6-triphosphate

Russell

Siren²,

Sirén³

et al. 2008

Cancer Chemother Pharmacol

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“…7 Ang II-induced ROS-formation is attenuated by the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI), suggesting that it is mediated through NADPH Oxidase. 7 In addition, Ang II-induced ROS-formation can also be blocked by losartan, 8 suggesting that AT1R and its downstream pathway are involved.However, the downstream targets of ROS have remained largely unexplored, at least for the regulation of the AT1R. Extracellular administration of nonlethal concentrations of H 2 O 2 has been demonstrated to activate mitogen-activated protein kinase (MAPK) as well as the c-Jun amino-terminal kinase (JNK).…”

mentioning

confidence: 99%

Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons

Gao

Roy

et al. 2008

Circulation Research

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Abstract-We have previously reported that the expression of Angiotensin II (Ang II) type 1 receptors (AT1R) was increased in the rostral ventrolateral medulla (RVLM) of rabbits with chronic heart failure (CHF) and in the RVLM of normal rabbits infused with intracerebroventricular (ICV) Ang II. The present study investigated whether oxidant stress plays a role in Ang II-induced AT1R upregulation and its relationship to the transcription factor activator protein 1 (AP1) in CHF rabbits and in the CATHa neuronal cell line. Key Words: angiotensin ii Ⅲ antioxidant enzymes Ⅲ brain Ⅲ c-jun Ⅲ c-Jun NH2-terminal kinase A ngiotensin II (Ang II), the principle mediator of the renin-angiotensin system, plays a pivotal role in cardiovascular and renal homeostasis. Most of the physiological and pathophysiological effects of Ang II are mediated by the Angiotensin II type 1 receptor (AT1R). The activation of the renin-angiotensin system and the sympathetic nervous system in chronic heart failure (CHF) are critical factors that contribute to the development and progression of CHF in patients. 1,2 Evidence also demonstrates that AT1R blockers, when added to conventional treatment for patients with CHF, are associated with a reduction in morbidity and mortality as well as an improvement in quality of life. 3 Currently, blockade of the renin-angiotensin system has become the primary treatment for patients with CHF. Therefore, a comprehensive understanding of the regulation of the AT1R is necessary for developing new therapies to target this receptor in the setting of CHF.The role of reactive oxygen species (ROS) in the cardiovascular system has been investigated extensively over the past decade. 4 It has been reported that, in the rostral ventrolateral medulla (RVLM), the levels of ROS are elevated in stroke-prone spontaneously hypertensive rats. Scavenging superoxide anion (O 2•Ϫ ) in the RVLM reduces both sympathetic nerve activity and blood pressure. 5 Similar evidence has been provided for rabbits with CHF. 6 Ang II induces a rapid and transient increase in ROS in a wide variety of cell types. 7 Ang II-induced ROS-formation is attenuated by the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI), suggesting that it is mediated through NADPH Oxidase. 7 In addition, Ang II-induced ROS-formation can also be blocked by losartan, 8 suggesting that AT1R and its downstream pathway are involved.However, the downstream targets of ROS have remained largely unexplored, at least for the regulation of the AT1R. Extracellular administration of nonlethal concentrations of H 2 O 2 has been demonstrated to activate mitogen-activated protein kinase (MAPK) as well as the c-Jun amino-terminal kinase (JNK). 9 Endogenous ROS induced by Ang II has also been shown to activate stress activated protein kinase (SAPK), which can be inhibited by treating cells with Original

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“…15-HETE was also shown to cause the nuclear accumulation of NFκB and thus protein degradation [82]. The muscle degradation due to the PIF-induced expression of the ubiquitin-proteasome pathway is also largely reliant on NADPH oxidase and production of ROS [81,83]. Protein kinase C (PKC) is necessary for the activation of NADPH oxidase and may also be dependent on 15-HETE.…”

Section: Proteolysis-inducing Factormentioning

confidence: 99%

Pancreatic Cancer Cachexia: Current Concepts and Clinical Management

Guan¹,

Shinde²,

Hendifar³

2017

Frailty and Sarcopenia - Onset, Development and Clinical Challenges

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There has been great progress over the last decade in understanding the pathophysiology of cachexia associated with pancreatic cancer. However, there is a large need to ind better therapeutic options to successfully manage this complex and challenging condition. Patients with pancreatic cancer have some of the highest prevalence and often the most severe degrees of cachexia, which is described as a multifactorial metabolic syndrome that is associated with unintended weight loss of adipose tissue and skeletal muscle in the seting of anorexia. This chapter will review the current concepts surrounding pancreatic cancer cachexia, its clinical diagnosis, pathophysiology, and its known and proposed therapeutics. A multimodal approach utilizing nutritional support and pharmaceutical therapies is proposed to lead to the most successful management of pancreatic cancer cachexia.Keywords: pancreatic cancer, cachexia, anorexia, metabolic syndrome, catabolism IntroductionIn western countries, pancreatic cancer represents the fourth leading cause of cancer-related death [1]. Among the many complications associated with this disease, cachexia marked by progressive weight loss represents one of the most distressing features related to pancreatic cancer. Cachexia is a multidimensional wasting syndrome that is characterized by unintended loss of both adipose tissue and lean body mass (LBM) that cannot be fully reversed through conventional nutritional support. It is a complex metabolic disorder frequently described in pancreatic cancer and represents a signiicant physical and psychological burden in approximately 80% of pancreatic cancer patients during the disease progression [2]. The complications © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. associated with cachexia, which include immobility, impaired immunity, and severe respiratory muscle impairment leading to cardiopulmonary failure, result in death in up to one-third of pancreatic cancer patients [3]. Cachectic patients are observed to have lower physical function, decreased tolerance to chemotherapy and radiation treatment, and generally worse prognosis than those with stable weight. Poorer outcomes after pancreaticoduodenectomy have also been observed in patients with preoperative signs of cachexia [4].While research over the past decade has provided new insights regarding the pathogenesis of pancreatic cancer cachexia, the mechanistic pathology of this condition is still not entirely understood. In this chapter, we will provide a review of the current concepts, potential therapeutic targets, and management of this signiicant clinical condition. Classiication and progression of cancer cachexiaCachexia has been established to be a common adverse efect of cancer. An international consensus in 2011 deined cachexia as a ...

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Role of reactive oxygen species in protein degradation in murine myotubes induced by proteolysis-inducing factor and angiotensin II

Cited by 80 publications

References 37 publications

Attenuation of skeletal muscle atrophy in cancer cachexia by d-myo-inositol 1,2,6-triphosphate

Attenuation of skeletal muscle atrophy in cancer cachexia by d-myo-inositol 1,2,6-triphosphate

Role of Oxidant Stress on AT1 Receptor Expression in Neurons of Rabbits With Heart Failure and in Cultured Neurons

Pancreatic Cancer Cachexia: Current Concepts and Clinical Management

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