Facilitatory Roles of Novel Compounds Designed from Cyclopentenone Prostaglandins on Neurite Outgrowth‐Promoting Activities of Nerve Growth Factor

Satoh, Tsuyoshi; Furuta, Kyoji; Tomokiyo, Keiichiro; Nakatsuka, Daisaku; Tanikawa, Motoki; Nakanishi, Makoto; Miura, Maki; Tanaka, Shuuitsu; Koike, Tetsuro; Hatanaka, Hiroshi; Ikuta, Kazuyoshi; Suzuki, Masaaki; Watanabe, Yasuyoshi

doi:10.1046/j.1471-4159.2000.0751092.x

Cited by 58 publications

(44 citation statements)

References 46 publications

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“…These authors also found neuroprotective effects of CDDO methylamide in 3-nitropropionic acid rat and MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) mouse models (Yang et al, 2009). Other intriguing neuroprotective agents that induce Hmox1 expression by this mechanism include the electrophilic neurite outgrowth-promoting prostaglandin compounds (Satoh et al, 2000).…”

Section: Polyphenols and Other Natural Productsmentioning

confidence: 88%

Mitochondrial Quality Control as a Therapeutic Target

2015

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Section: Polyphenols and Other Natural Productsmentioning

confidence: 88%

Mitochondrial Quality Control as a Therapeutic Target

2015

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“…Male ob/+ and ob/ob mice (8 wk old) were anesthetized with Aerane (Baxter) and injected through the penis vein with 10 8 PFU/g BW of Ad β-gal or Ad GRP78 in a final volume of 250 μl sterile physiological serum. Ad GRP78 was constructed as described previously by Satoh et al (55). Adenoviruses were amplified in HEK 293 cells and purified on a cesium chloride gradient.…”

Section: Figure 12mentioning

confidence: 99%

GRP78 expression inhibits insulin and ER stress–induced SREBP-1c activation and reduces hepatic steatosis in mice

Kammoun

Chabanon²,

Hainault³

et al. 2009

J. Clin. Invest.

634

520

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Hepatic steatosis is present in insulin-resistant obese rodents and is concomitant with active lipogenesis. Hepatic lipogenesis depends on the insulin-induced activation of the transcription factor SREBP-1c. Despite prevailing insulin resistance, SREBP-1c is activated in the livers of genetically and diet-induced obese rodents. Recent studies have reported the presence of an ER stress response in the livers of obese ob/ob mice. To assess whether ER stress promotes SREBP-1c activation and thus contributes to lipogenesis, we overexpressed the chaperone glucose-regulated protein 78 (GRP78) in the livers of ob/ob mice using an adenoviral vector. GRP78 overexpression reduced ER stress markers and inhibited SREBP-1c cleavage and the expression of SREBP-1c and SREBP-2 target genes. Furthermore, hepatic triglyceride and cholesterol contents were reduced, and insulin sensitivity improved, in GRP78-injected mice. These metabolic improvements were likely mediated by restoration of IRS-2 expression and tyrosine phosphorylation. Interestingly, GRP78 overexpression also inhibited insulin-induced SREBP-1c cleavage in cultured primary hepatocytes. These findings demonstrate that GRP78 inhibits both insulin-dependent and ER stress-dependent SREBP-1c proteolytic cleavage and explain the role of ER stress in hepatic steatosis in obese rodents.

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“…It is also reported that CDDO-MA has neuroprotective effects in 3-nitropropionic acid (3-NP) rat and MPTP mouse models [87]. Other intriguing neuroprotective agents that induce Hmox1 expression by this mechanism are the electrophilic neurite outgrowth-promoting prostaglandin (NEPP) compounds [88]. …”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Biogenesis: Regulation By Endogenous Gases During Inflammation and Organ Stress

Suliman¹,

Piantadosi

2014

CPD

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The influence of mitochondrial dysfunction on pathological states involving inflammatory and/or oxidative stress in tissues that do not show frank cellular apoptosis or necrosis has been rather difficult to unravel, and the literature is replete with contradictory information. Although such discrepancies have many potential causes related to the type of injurious agent, the severity and duration of the injury, and the particular cells and tissues and the functions involved, it is the successful induction of cellular adaptive responses that ultimately governs the resolution of mitochondrial dysfunction and survival of the cell. Much recent attention has been devoted to unraveling the signaling pathways that activate mitochondrial biogenesis and other processes involved in mitochondrial quality control (QC) during inflammatory and oxidative stress with an eye towards the development of novel targets for therapeutic mitigation of the resultant tissue damage. This review provides a brief overview of this emerging field with an emphasis on the role of signaling through the endogenous gases (NO, CO and H2S) and a redox-based approach that brings transparency to key factors that contribute to the resolution of mitochondrial dysfunction and the maintenance of cell vitality. We make the case that targeted stimulation of mitochondrial biogenesis could be a potentially valuable approach for the development of new therapies for the treatment of diseases for which mitochondrial damage is a major consideration.

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Facilitatory Roles of Novel Compounds Designed from Cyclopentenone Prostaglandins on Neurite Outgrowth‐Promoting Activities of Nerve Growth Factor

Cited by 58 publications

References 46 publications

Mitochondrial Quality Control as a Therapeutic Target

Mitochondrial Quality Control as a Therapeutic Target

GRP78 expression inhibits insulin and ER stress–induced SREBP-1c activation and reduces hepatic steatosis in mice

Mitochondrial Biogenesis: Regulation By Endogenous Gases During Inflammation and Organ Stress

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