Autophagy activation and neuroprotection by progesterone in the G93A-SOD1 transgenic mouse model of amyotrophic lateral sclerosis

Kim, Jean; Kim, Tae Youn; Cho, Kyung-Sook; Kim, Hana; Koh, Jae‐Young

doi:10.1016/j.nbd.2013.07.011

Cited by 69 publications

(58 citation statements)

References 47 publications

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“…It is also delayed disease onset and duration and augmented the life span of ALS model animals, which were concomitant with the activation of autophagy (Fornai et al, 2008a). Moreover, the autophagy inducers XBP-1, PG and Trehalose also delayed the progression of ALS (Hetz et al, 2009;Castillo et al, 2013;Kim et al, 2013). Both lithium and VPA can induce autophagy via downregulation of IP3 levels (Phiel et al, 2001;Sarkar et al, 2005;Sarkar and Rubinsztein, 2006), and the combined treatment with the two agents has a therapeutic effect in ALS mice and patients (Feng et al, 2008;Boll et al, 2014).…”

Section: Discussionmentioning

confidence: 98%

Notch pathway is activated in cell culture and mouse models of mutant SOD1-related familial amyotrophic lateral sclerosis, with suppression of its activation as an additional mechanism of neuroprotection for lithium and valproate

et al. 2015

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Section: Discussionmentioning

confidence: 98%

Notch pathway is activated in cell culture and mouse models of mutant SOD1-related familial amyotrophic lateral sclerosis, with suppression of its activation as an additional mechanism of neuroprotection for lithium and valproate

et al. 2015

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“…Western blot analysis was performed as previously described 22. Cells were lysed in hot 1× sodium dodecyl sulfate sample buffer, and 30 µg samples were loaded into each lane of 4%–12% polyacrylamide gels.…”

Section: Methodsmentioning

confidence: 99%

PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

Liu¹,

Zhang²,

xu-yan³

et al. 2017

OTT

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Endometrial cancer (EC) is now one of the most common malignant tumors in young women. In all, 90% of young patients with EC have a high expression of progesterone recep tor, can be treated with progestin, and have very good prognosis. However, some of the young EC patients are resistant to progestin, the mechanism of which is unclear. To illuminate the mechanism by which endometrial cells acquire progestin resistance, we treated Ishikawa cells by slowly increasing dosage of progestin and established a progestin-resistant cell subline. We show here that progesterone resistant cells acquire increased proliferation rate and interestingly decreased autophagy. To uncover the mechanism by which cells increase proliferation and bypass autophagy, we found higher activation of phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway was necessary to this malignant acquirement by RNAi technique. Further, we elucidated that activation of mTOR was sufficient and necessary for progestin resistance. RAD001, an inhibitor of mTOR, decreased phosphorylation of mTOR and inhibited proliferation of progestin-resistant cancer cells by promoting autophagy. Thus, our results indicated that mTOR can be a target to treat the progestin-resistant EC.

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“…These effects were accompanied both by down-regulation of the activity of S6 kinase, which functions in the mammalian target of rapamycin (mTOR) signaling pathway, and by an increase in the abundance of an autophagic marker LC3 ). In addition, progesterone treatment both delayed motor neuron degeneration and prolonged life span by activating autophagic flux in a SOD1(G93A) mouse model of ALS (Kim et al 2013a).…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 97%

Compromised MAPK signaling in human diseases: an update

2015

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The mitogen-activated protein kinases (MAPKs) in mammals include c-Jun NH2-terminal kinase (JNK), p38 MAPK, and extracellular signal-regulated kinase (ERK). These enzymes are serine-threonine protein kinases that regulate various cellular activities including proliferation, differentiation, apoptosis or survival, inflammation, and innate immunity. The compromised MAPK signaling pathways contribute to the pathology of diverse human diseases including cancer and neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. The JNK and p38 MAPK signaling pathways are activated by various types of cellular stress such as oxidative, genotoxic, and osmotic stress as well as by proinflammatory cytokines such as tumor necrosis factor-α and interleukin 1β. The Ras-Raf-MEK-ERK signaling pathway plays a key role in cancer development through the stimulation of cell proliferation and metastasis. The p38 MAPK pathway contributes to neuroinflammation mediated by glial cells including microglia and astrocytes, and it has also been associated with anticancer drug resistance in colon and liver cancer. We here summarize recent research on the roles of MAPK signaling pathways in human diseases, with a focus on cancer and neurodegenerative conditions.

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Autophagy activation and neuroprotection by progesterone in the G93A-SOD1 transgenic mouse model of amyotrophic lateral sclerosis

Cited by 69 publications

References 47 publications

Notch pathway is activated in cell culture and mouse models of mutant SOD1-related familial amyotrophic lateral sclerosis, with suppression of its activation as an additional mechanism of neuroprotection for lithium and valproate

Notch pathway is activated in cell culture and mouse models of mutant SOD1-related familial amyotrophic lateral sclerosis, with suppression of its activation as an additional mechanism of neuroprotection for lithium and valproate

PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy

Compromised MAPK signaling in human diseases: an update

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