Withdrawal: AMP-activated protein kinase contributes to UV- and H2O2-induced apoptosis in human skin keratinocytes.

Cao, Cong; Lu, Shan; Kivlin, Rebecca; Wallin, Brittany; Card, Elizabeth; Bagdasarian, Andrew; Tamakloe, Tyrone; Chen, Wen-Ming; Guan, Kun‐Liang; Wan, Yinsheng

doi:10.1074/jbc.a109.804144

Cited by 27 publications

(41 citation statements)

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“…AMPK activation has been shown to mediate its procell apoptosis effects primarily through modulating its multiple downstream targets including regulating JNK [14,19,22], p53 [9,23] and inhibiting mTORC1 [7,10,13,24]. For example, it has been reported that sustained AMPK activation leads to JNK activation which is required for the induction of apoptosis in liver cells [19]; our previous study also found that activation of AMPK is involved in vincristine-induced cell apoptosis in B16 melanoma cell by mTORC1 inhibition and p53 induction [25].…”

Section: Introductionmentioning

confidence: 91%

“…AMPK phosphorylates and activates TSC2 (Tuberous sclerosis protein 2), eventually leading to mTORC1 inhibition and cell apoptosis [13,37,41,42]. Therefore, next the possible effects of Doxorubicin on mTOC1 in H9c2 cells are tested.…”

Section: Ampk Activation Is Involved In Doxorubicin-induced Jnk Activmentioning

confidence: 99%

“…Doxorubicin-Induced mTORC1 Inhibition is Dependent on AMPK AMPK activation has been shown to mediate its pro-cell death/apoptosis effects through mTORC1 (mTOR complex 1) inhibition [13,24,40]. AMPK phosphorylates and activates TSC2 (Tuberous sclerosis protein 2), eventually leading to mTORC1 inhibition and cell apoptosis [13,37,41,42].…”

Section: Ampk Activation Is Involved In Doxorubicin-induced Jnk Activmentioning

confidence: 99%

“…Besides balancing of cellular energy, one of the most important outcomes of AMPK activation is to regulate cell apoptosis in response to various stimulations [4][5][6][7][8][9][10][11][12][13][14][19][20][21]. AMPK activation has been shown to mediate its procell apoptosis effects primarily through modulating its multiple downstream targets including regulating JNK [14,19,22], p53 [9,23] and inhibiting mTORC1 [7,10,13,24].…”

Section: Introductionmentioning

confidence: 99%

“…The cardiotoxic effects of Doxorubicin have been linked to DNA damage, oxidative mitochondrial damage, and nuclear translocation of p53, but the exact molecular mechanisms causing Doxorubicin-induced cardiomyopathy are not clear. In the current study, the authors focus on AMP-activated protein kinase (AMPK), a recently discovered protein kinase, which causes cell death and apoptosis in response to various conditions [4][5][6][7][8][9][10][11][12][13][14], in this process.…”

Section: Introductionmentioning

confidence: 99%

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Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

Chen

et al. 2011

Cell Biochem Biophys

104

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Despite its potent antitumor effect, clinical use of Doxorubicin is limited because of serious side effects including myocardial toxicity. Understanding the cellular mechanism involved in this process in a better manner is beneficial for optimizing Doxorubicin treatment. In the current study, the authors focus on the AMP-activated protein kinase (AMPK) in the said process. In this study, the authors discovered for the first time that Doxorubicin induces AMPK activation in cultured rat embryonic ventricular myocardial H9c2 cells. Reactive oxygen species (ROS)-dependent LKB1 activation serves as the upstream signal for AMPK activation by Doxorubicin. Evidence in support of the activation of AMPK contributing to Doxorubicin-induced H9c2 cell death/apoptosis--probably by modulating multiple downstream signal targets, including regulating JNK, p53, and inhibiting mTORC1--is provided in this article.

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Section: Introductionmentioning

confidence: 91%

Section: Ampk Activation Is Involved In Doxorubicin-induced Jnk Activmentioning

confidence: 99%

Section: Ampk Activation Is Involved In Doxorubicin-induced Jnk Activmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

Chen

et al. 2011

Cell Biochem Biophys

104

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20‐O‐β‐d‐Glucopyranosyl‐20(S)‐Protopanaxadiol Suppresses UV‐Induced MMP‐1 Expression Through AMPK‐Mediated mTOR Inhibition as a Downstream of the PKA‐LKB1 Pathway

Shin

Kim

Lim

et al. 2014

J of Cellular Biochemistry

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Various health effects have been attributed to the ginsenoside metabolite 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol (GPD); however, its effect on ultraviolet (UV)-induced matrix metalloproteinase (MMP)-1 expression and the mechanism underlying this effect are unknown. We examined the inhibitory effect of GPD on UV-induced MMP-1 expression and its mechanisms in human dermal fibroblasts (HDFs). GPD attenuated UV-induced MMP-1 expression in HDFs and suppressed the UV-induced phosphorylation of mammalian target of rapamycin (mTOR) and p70(S6K) without inhibiting the activity of phosphatidylinositol 3-kinase and Akt, which are well-known upstream kinases of mTOR. GPD augmented the phosphorylation of liver kinase B1 (LKB1) and adenosine monophosphate-activated protein kinase (AMPK), which are inhibitors of mTOR, to a greater extent than UV treatment alone. Similar to GPD, 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranosyl 5'-monophosphate (AICAR), an activator of AMPK, augmented UV-induced AMPK phosphorylation to a greater extent than UV treatment alone, resulting in the inhibition of MMP-1 expression. AICAR also decreased the phosphorylation of mTOR and p70(S6K). However, compound C, an antagonist of AMPK, increased MMP-1 expression. In HDF cells with AMPK knock-down using shRNA, MMP-1 expression was increased. These results indicate that AMPK activation plays a key role in MMP-1 suppression. Additionally, the cAMP-dependent protein kinase (PKA) inhibitor, H-89, antagonized GPD-mediated MMP-1 suppression via the inhibition of LKB1. Our results suggest that the suppressive activity of GPD on UV-induced MMP-1 expression is due to the activation of AMPK as a downstream of the PKA-LKB1 pathway.

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Parameters of protection against ultraviolet radiation‐induced skin cell damage

Cao

Wan

2009

Journal Cellular Physiology

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Epidemiological and experimental evidence has supported the notion that solar ultraviolet (UV) radiation is the leading cause of skin cell damage and skin cancer. Non-melanoma skin cancer, one of the malignancies with the most rapidly increasing incidence, is suggested to be directly related to the total exposure to solar UV light. Over the past few years, the mechanisms of cellular responses to UV radiation have received unprecedented attention. Understanding how skin cells respond to UV radiation will undoubtedly help decipher what goes wrong in a variety of clinical skin disorders including skin cancer and will facilitate the development of novel therapeutic strategies. In the past decade, studies have established that UV radiation induces multifarious signal transduction pathways, some of which lead to apoptotic cell death, while others protect against this process. In this review, we summarize some of the most recent progresses regarding the involvement of multiple signal pathways in UV radiation-induced apoptosis in skin cells, especially in keratinocytes. These pathways include pro-apoptosis components such as MAPK, AMPK, and p53 as well as pro-survival components, namely, AKT and mTORC complexes.

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Withdrawal: AMP-activated protein kinase contributes to UV- and H2O2-induced apoptosis in human skin keratinocytes.

Cited by 27 publications

References 0 publications

Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

20‐O‐β‐d‐Glucopyranosyl‐20(S)‐Protopanaxadiol Suppresses UV‐Induced MMP‐1 Expression Through AMPK‐Mediated mTOR Inhibition as a Downstream of the PKA‐LKB1 Pathway

Parameters of protection against ultraviolet radiation‐induced skin cell damage

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