Phosphorylated CAV1 activates autophagy through an interaction with BECN1 under oxidative stress

Nah, Jihoon; Yoo, Seung‐Min; Jung, Sunmin; Jeong, Eun Il; Park, Moonju; Kaang, Bong‐Kiun; Jung, Yong‐Keun

doi:10.1038/cddis.2017.71

Cited by 53 publications

(39 citation statements)

References 52 publications

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“…The investigators concluded that autophagy activation following caveolin-1 knockdown might reflect an adaptive response to the marked increase in oxidative stress caused by decreased caveolin-1 protein expression in endothelial cells [80]. However, Nah J et al [81] revealed that the loss of caveolin-1 impairs autophagy and increases the infarct area following cerebral ischemia. Phosphorylated caveolin-1 at tyrosine-14 protects against cerebral ischemic damage by activating autophagy through its binding to the Beclin-1/VPS34 complex under conditions of oxidative stress [82].…”

Section: Crosstalk Between Caveolin and Autophagymentioning

confidence: 99%

Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review

Tian¹,

Popal²,

Huang³

et al. 2020

Aging and disease

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Caveolin, a structural protein of caveolae, play roles in the regulation of endothelial function, cellular lipid homeostasis, and cardiac function by affecting the activity and biogenesis of nitric oxide, and by modulating signal transduction pathways that mediate inflammatory responses and oxidative stress. In this review, we present the role of caveolin in cardiac and vascular diseases and the relevant signaling pathways involved. Furthermore, we discuss a novel therapeutic perspective comprising crosstalk between caveolin and autophagy.

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Section: Crosstalk Between Caveolin and Autophagymentioning

confidence: 99%

Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review

Tian¹,

Popal²,

Huang³

et al. 2020

Aging and disease

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show abstract

“…Oxidative stress, characterized by increased ROS production, plays a key role in the regulation of cells survival [12]. Many drugs exert their negative effects on cancer cells are through increased the production of ROS [13, 14].…”

Section: Introductionmentioning

confidence: 99%

FOXO1, a Potential Therapeutic Target, Regulates Autophagic Flux, Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in Human Cholangiocarcinoma QBC939 Cells

Zhang

Lei

et al. 2018

Cell Physiol Biochem

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Background/Aims: Autophagy is an evolutionarily conserved catabolic mechanism to maintain energy homeostasis and to remove damaged cellular components, which plays an important role in the survival of various cells. Inhibiting autophagy is often applied as a new strategy to halt the growth of cancer cells. Methods: The effect of FOXO1 gene on cellular function and apoptosis and its underlying mechanisms were investigated in cultured QBC939 cells by the methylthiazoletetrazolium (MTT) assay, western blot, DCFDA mitochondrial membrane potential, and ATP content measurement. FOXO1 siRNA was applied to down-regulate FOXO1 expression in QBC939 cells. Results: Here we reported that FOXO1, acetylation of FOXO1 (Ac-FOXO1) and the following interaction between Ac-FOXO1 and Atg7 regulated the basal and serum starvation (SS)-induced autophagy as evidenced by light chain 3 (LC3) accumulation and p62 degration. Either treatment with FOXO1 siRNA or resveratrol, a sirt1 agonist, inhibited autophagic flux, resulting in oxidative stress, mitochondrial dysfunction (MtD) and apoptosis in QBC939 cells, which were attenuated by enhancing autophagy with rapamycin. On the contrary, inhibiting autophagic flux with 3-MA worsened all these effects in QBC939 cells. Conclusions: Taken together, our study for the first time identified FOXO1 as a potential therapeutic target to cure against human cholangiocarcinoma via regulation of autophagy, oxidative stress and MtD.

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“…In addition, in mouse embryonic fibroblasts, Cav-1 knockout promotes lysosomal function and increases LC3B-II expression via the disruption of lipid rafts to promote cell survival under starvation [49]. In contrast, Cav-1 can also function as a positive regulator of 17β-oestradiol mediated autophagy in BT474 human breast cancer cells [50] or autophagy-mediated claudin-5 degradation in oxygen-glucose deprivation-treated endothelial cells [54] and oxidative stress-activated autophagy [55], which involves the Cav-1/HMGB1 pathway [50], the autophagylysosome pathway and an interaction with Beclin-1. Moreover, some components of lipid rafts are reported to promote autophagy [56,57].…”

Section: Discussionmentioning

confidence: 99%

Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

Luo

Mao

et al. 2018

Endocr J

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Hashimoto's thyroiditis (HT) is considered a T helper-type 1 (Th1) cytokine-dominant autoimmune thyroid disease. Caveolin-1 (Cav-1), a part of the thyroxisome multiprotein complex, is localized at the apical pole of thyrocytes and is indispensable for synthesis of thyroid hormones and modulation of oxidative stress in order to avoid cell damage and apoptosis. Reduced autophagy induces thyroid follicular cells (TFC) apoptosis by activating reactive oxygen species (ROS) in HT patients. Nevertheless, whether Cav-1 has roles in the regulation of autophagy remains largely unclear. In this study, we examined Th1 cytokines and Cav-1 expression in HT thyroid tissues, determined the effects of interleukin-1beta (IL-1β) and interferon-gamma (IFN-γ) on Cav-1 and autophagy activity in TFC, and investigated the association between Cav-1 and autophagy activity in vitro. Our results indicate that higher levels of IL-1β and IFN-γ and lower levels of Cav-1 were expressed in thyroid tissues of HT patients than in those of normal controls. Cav-1 mRNA and protein levels were significantly decreased in TFC exposed to IL-1β and IFN-γ, accompanied by decreased expression of autophagy-related protein LC3B-II. Interestingly, small interfering RNA (siRNA)-mediated Cav-1 knockdown in TFC reduced LC3B-II protein expression. Taken together, these results suggest that lack of Cav-1 expression inhibited autophagy activity in TFC exposed to Th1 cytokines (IL-1β and IFN-γ), which might be a novel pathogenetic mechanism of HT.

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Phosphorylated CAV1 activates autophagy through an interaction with BECN1 under oxidative stress

Cited by 53 publications

References 52 publications

Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review

Caveolin as a Novel Potential Therapeutic Target in Cardiac and Vascular Diseases: A Mini Review

FOXO1, a Potential Therapeutic Target, Regulates Autophagic Flux, Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in Human Cholangiocarcinoma QBC939 Cells

Caveolin-1 regulates autophagy activity in thyroid follicular cells and is involved in Hashimoto’s thyroiditis disease

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