Glutamine's protection against cellular injury is dependent on heat shock factor-1

Morrison, Angela L; Dinges, Martin; Singleton, Kristen D.; Odoms, Kelli; Wong, Hector R.; Wischmeyer, Paul E.

doi:10.1152/ajpcell.00635.2005

Cited by 87 publications

(68 citation statements)

References 34 publications

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“…It plays an important role as a carrier of nitrogen and carbon. Glutamine inhibits protein degradation and is an important precursor for glutathione synthesis (32)(33)(34). Due to the increased glutamine requirement in sepsis, the non-essential amino acid glutamine relatively becomes an essential amino acid.…”

Section: Discussionmentioning

confidence: 99%

Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

et al. 2016

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Background: Electrophysiological studies show that critical illness polyneuromyopathy appears in the early stage of sepsis before the manifestation of clinical findings. The metabolic response observed during sepsis causes glutamine to become a relative essential amino acid. Aims: We aimed to assess the changes in neuromuscular transmission in the early stage of sepsis after glutamine supplementation. Study Design: Animal experimentation. Methods: Twenty male Sprague-Dawley rats were randomized into two groups. Rats in both groups were given normal feeding for one week. In the study group, 1 g/kg/day glutamine was added to normal feeding by feeding tube for one week. Cecal ligation and perforation (CLP) surgery was performed at the end of one week. Before and 24 hours after CLP, compound muscle action potentials were recorded from the gastrocnemius muscle. Results: Latency measurements before and 24 hours after CLP were 0.68±0.05 ms and 0.80±0.09 ms in the control group and 0.69±0.07 ms and 0.73±0.07 ms in the study group (p<0.05). Conclusion: Since enteral glutamine prevented compound muscle action potentials (CMAP) latency prolongation in the early phase of sepsis, it was concluded that enteral glutamine replacement might be promising in the prevention of neuromuscular dysfunction in sepsis; however, further studies are required.

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Section: Discussionmentioning

confidence: 99%

Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

et al. 2016

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“…21 Hamiel et al 22 found that Gln metabolism enhances HSP70 expression by increasing the hexosamine biosynthetic pathway activity, with the O-glycosylation, nuclear translocation, and transcriptional activation of Sp1 and heat shock factor-1 (HSF1) being responsible. Zachara et al 23 reported that stress (including thermal stress) applied to cells rapidly increases the O-glycosylation of intracellular proteins, which is associated with increased HSP70 expression.…”

Section: Discussionmentioning

confidence: 99%

Combined microwave irradiation and intraarticular glutamine administration‐induced HSP70 expression therapy prevents cartilage degradation in a rat osteoarthritis model

Fujita

Nakagawa

Takahashi

et al. 2011

Journal Orthopaedic Research

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The objective of the present study was to investigate the effects of heat stimulation and glutamine (Gln) on the expression of extracellular matrix genes and heat shock protein 70 (HSP70) in rat articular cartilage in vivo and to determine whether HSP70 expression achieved with a combination of microwave (MW) and Gln suppresses osteoarthritis (OA) progression in a rat OA model. Stimulation at 40 W was assumed to be appropriate in the present study, and the effects of heat treatment at this intensity were evaluated. Articular cartilage was collected at 8 h after heat stimulation and/or intraarticular Gln administration, and total RNA was extracted. The expression of HSP70, aggrecan, and type II collagen was quantified using real-time RT-PCR. Cartilage samples from the OA model were subjected to hematoxylin and eosin (HE) and safranin O staining. HSP70 and aggrecan expression was greatest in a group receiving both MW and Gln. In the rat OA model, the severity of OA was significantly milder in a group receiving MW and Gln than in the control group. HSP70, stimulated by the combination of MW heat and Gln, may be involved in the suppression of OA progression. ß

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“…Previous studies have demonstrated that Gln enhances the expression of Hsp (26)(27)(28)(29), which serves a key regulatory role in α-Syn degradation. Therefore, the regulation by Gln on Hsp70 expression in PC12 neuroblastoma cells was investigated.…”

Section: Gln Upregulates Hsp70 Expression In Pc12 Neuroblastoma Cellsmentioning

confidence: 99%

Glutamine promotes Hsp70 and inhibits α-Synuclein accumulation in pheochromocytoma PC12 cells

Wang

Tang

Jiang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Hsp70 regulates α-Synuclein (α-Syn) degeneration in Parkinson's disease (PD), indicating that Hsp70 promotion may be able to prevent or reverse α-Syn-induced toxicity in PD. Additionally, it has been demonstrated that glutamine (Gln) enhances Hsp70 expression. In the present study, Gln-induced Hsp70 promotion in pheochromocytoma was investigated with reverse transcription-quantitative polymerase chain reaction and western blotting methods. Then it was observed whether heat shock factor (HSF)-1 was required for this phenomenon with an RNA interference strategy. The regulatory role of Gln on α-Syn degeneration was also determined in the α-Syn-overexpressed PC12 [PC12 (α-Syn+)] cells, which were treated with or without the proteasomal inhibitor lactacystin (Lac). The results demonstrated that treatment with ≥10 mM Gln significantly increased Hsp70 mRNA and protein levels (P<0.05) and that this promotion was HSF-1-dependent, as HSF-1 knockout with HSF-1-specific small interfering RNA abrogated Hsp70 promotion in PC12 (α-Syn+) cells. Furthermore, Gln treatment markedly upregulated α-Syn degeneration in PC12 (α-Syn+) cells, which was significantly reduced (P<0.05) in the presence of Lac. Therefore, the present study suggests that Gln is able to induce the promotion of Hsp70 expression in PC12 cells in an HSF-1-dependent manner and that Gln-mediated Hsp70 promotion may increase α-Syn degradation even in the presence of proteasomal inhibitor. Thus, glutamine may be a potential therapeutic agent to prevent α-Syn aggregation in PD.

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Glutamine's protection against cellular injury is dependent on heat shock factor-1

Cited by 87 publications

References 34 publications

Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

Neuromuscular Dysfunction in Experimental Sepsis and Glutamine

Combined microwave irradiation and intraarticular glutamine administration‐induced HSP70 expression therapy prevents cartilage degradation in a rat osteoarthritis model

Glutamine promotes Hsp70 and inhibits α-Synuclein accumulation in pheochromocytoma PC12 cells

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