Arginine recycling in endothelial cells is regulated BY HSP90 and the ubiquitin proteasome system

Wu, Xiaomin; Sun, Xutong; Sharma, Shruti; Lu, Qing; Yegambaram, Manivannan; Hou, Yali; Wang, Ting; Fineman, Jeffrey R.; Black, Stephen M.

doi:10.1016/j.niox.2020.12.003

Cited by 5 publications

(2 citation statements)

References 52 publications

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“…MSEA of the endothelial cellular extract revealed that aspects of the urea cycle corresponding to the citrullinearginine cycle in the endothelial cells and arginine/proline metabolism were perturbed. The involvement of the citrulline-arginine cycle in the restoration of arginine levels in endothelial cells was described by Hecker et al and facilitates optimal NO signaling [36,37]. Our experiments showed that NEB was able to inhibit the decrease in arginine due to AA exposure, leading to enhanced eNOS activity and contributing, therefore, to restoring NO bioavailability.…”

Section: Discussionsupporting

confidence: 70%

Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

Antoine

Husson

Yankep

et al. 2022

Toxins

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Aristolochic acids (AAs) are powerful nephrotoxins that cause severe tubulointerstitial fibrosis. The biopsy-proven peritubular capillary rarefaction may worsen the progression of renal lesions via tissue hypoxia. As we previously observed the overproduction of reactive oxygen species (ROS) by cultured endothelial cells exposed to AA, we here investigated in vitro AA-induced metabolic changes by 1H-NMR spectroscopy on intracellular medium and cell extracts. We also tested the effects of nebivolol (NEB), a β-blocker agent exhibiting antioxidant properties. After 24 h of AA exposure, significantly reduced cell viability and intracellular ROS overproduction were observed in EAhy926 cells; both effects were counteracted by NEB pretreatment. After 48 h of exposure to AA, the most prominent metabolite changes were significant decreases in arginine, glutamate, glutamine and glutathione levels, along with a significant increase in the aspartate, glycerophosphocholine and UDP-N-acetylglucosamine contents. NEB pretreatment slightly inhibited the changes in glutathione and glycerophosphocholine. In the supernatants from exposed cells, a decrease in lactate and glutamate levels, together with an increase in glucose concentration, was found. The AA-induced reduction in glutamate was significantly inhibited by NEB. These findings confirm the involvement of oxidative stress in AA toxicity for endothelial cells and the potential benefit of NEB in preventing endothelial injury.

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Section: Discussionsupporting

confidence: 70%

Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

Antoine

Husson

Yankep

et al. 2022

Toxins

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“…It has been verified that HSP90 is the molecular chaperone of ASS and ASL. When it was inhibited, the C-terminus of HSC70-interacting proteins (CHIP) was found to stimulate ASL and ASS degradation via its E3 ligase activities through the proteasome pathway, which regulates L-arginine recycling in endothelial cells [ 133 ].…”

Section: Ubiquitination and Deubiquitination Of Metabolic Enzymesmentioning

confidence: 99%

The Ubiquitin–Proteasome System in Tumor Metabolism

Wang

Xiang

Fan

et al. 2023

Cancers

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Metabolic reprogramming, which is considered a hallmark of cancer, can maintain the homeostasis of the tumor environment and promote the proliferation, survival, and metastasis of cancer cells. For instance, increased glucose uptake and high glucose consumption, known as the “Warburg effect,” play an essential part in tumor metabolic reprogramming. In addition, fatty acids are harnessed to satisfy the increased requirement for the phospholipid components of biological membranes and energy. Moreover, the anabolism/catabolism of amino acids, such as glutamine, cystine, and serine, provides nitrogen donors for biosynthesis processes, development of the tumor inflammatory environment, and signal transduction. The ubiquitin–proteasome system (UPS) has been widely reported to be involved in various cellular biological activities. A potential role of UPS in the metabolic regulation of tumor cells has also been reported, but the specific regulatory mechanism has not been elucidated. Here, we review the role of ubiquitination and deubiquitination modification on major metabolic enzymes and important signaling pathways in tumor metabolism to inspire new strategies for the clinical treatment of cancer.

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Targeting small heat shock proteins to degrade aggregates as a potential strategy in neurodegenerative diseases

Tong

Xiao

et al. 2022

Ageing Research Reviews

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Arginine recycling in endothelial cells is regulated BY HSP90 and the ubiquitin proteasome system

Cited by 5 publications

References 52 publications

Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells

The Ubiquitin–Proteasome System in Tumor Metabolism

Targeting small heat shock proteins to degrade aggregates as a potential strategy in neurodegenerative diseases

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