Caveolae: Mechanosensing and mechanotransduction devices linking membrane trafficking to mechanoadaptation

Pozo, Miguel Á. del; Lolo, Fidel-Nicolás; Echarri, Asier

doi:10.1016/j.ceb.2020.10.008

Cited by 59 publications

(75 citation statements)

References 97 publications

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“…By contrast, caveolae in neurons are barely detectible, though Cav1 is readily detected and increases with age ( Kang et al, 2006 ). Neurons are in a soft, unstressed mechanical environment, whereas endothelial cells and fibroblasts are mechanically stressed, consistent with a role for caveolae in mechanotransduction ( del Pozo et al, 2020 ). Differential expression of Cav1-interacting molecules is also a likely contributing factor.…”

Section: Caveolae-mediated Endocytosis In Senescencementioning

confidence: 62%

Altered endocytosis in cellular senescence

Shin

Soung

Schwartz³

2021

Ageing Research Reviews

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Cellular senescence occurs in response to diverse stresses (e.g., telomere shortening, DNA damage, oxidative stress, oncogene activation). A growing body of evidence indicates that alterations in multiple components of endocytic pathways contribute to cellular senescence. Clathrin-mediated endocytosis (CME) and caveolae-mediated endocytosis (CavME) represent major types of endocytosis that are implicated in senescence. More recent research has also identified a chromatin modifier and tumor suppressor that contributes to the induction of senescence via altered endocytosis. Here, molecular regulators of aberrant endocytosis-induced senescence are reviewed and discussed in the context of their capacity to serve as senescence-inducing stressors or modifiers.

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Section: Caveolae-mediated Endocytosis In Senescencementioning

confidence: 62%

Altered endocytosis in cellular senescence

Shin

Soung

Schwartz³

2021

Ageing Research Reviews

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“…As a structural component of caveolae, caveolin-1 exerts crucial function in a variety of cellular functions, consisting of cell growth, adhesion, signal transduction, migration, senescence, development, and tumorigenesis (Boscher and Nabi, 2012;Ketteler and Klein, 2018;Volonte and Galbiati, 2020). Caveolin-1 also played an important role in mechanosensing that reflects the response the mechanical forces (extracellular matrix stiffness, vascular shear stress, and muscle stretching) reaching on the plasma membrane and affects the membrane integrity and repair (Dewulf et al, 2019;Del Pozo et al, 2020;Hubert et al, 2020;Liu, 2020;Singh and Lamaze, 2020). Caveolin 1 involves in the EMT in lung cancer (Garnett, 2016;Shi et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial–Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer

Liu

Wang

et al. 2021

DNA and Cell Biology

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PM2.5 plays an important role in the physiological and pathological progression of lung cancer. Lentinan exerts antitumor activity in many kinds of human cancers. Plasmacytoma variant translocation 1 (PVT1) exerts antitumor activity in many kinds of human cancers. However, the role and underlying molecular mechanism of PVT1 in the role of lentinan in PM2.5-exposed lung cancer are still largely unknown. Our study confirmed that PM2.5 exposure induced the production of inflammatory factors, epithelial-mesenchymal transition (EMT) and migration of lung cancer cells. Lentinan exerted antitumor effects by inhibiting the production of inflammatory factors, EMT, and migration of lung cancer cells. Lentinan suppressed PM2.5 exposure-induced cellular progression by inhibiting the PM2.5 exposure-induced elevation of PVT1 expression. PVT1 absorbed miR-199a, and miR-199a inhibited caveolin1 expression and thus formed the PVT1/miR-199a/caveolin1 signaling pathway in lung cancer cells. Our study revealed that silencing of the PVT1/miR-199a/caveolin1 signaling pathway affected the role of lentinan in PM2.5-exposed lung cancer cells. Thus, this study first investigated the role of lentinan in PM2.5-exposed lung cancer cells and further displayed the underlying molecular mechanism, providing a potential treatment for PM2.5-exposed lung cancer.

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“…This is the case, for instance, for autocrine mobility factor (AMF) and cholera toxin [52]. It should be noted that a new role for caveolae has recently been characterized: Caveolae can provide additional membrane upon mechanical stress and reform in an ATP-dependent manner [38,53].…”

Section: Endocytic Mechanisms and Recyclingmentioning

confidence: 99%

The Protein Toxins Ricin and Shiga Toxin as Tools to Explore Cellular Mechanisms of Internalization and Intracellular Transport

Sandvig

Kavaliauskiene

Skotland

2021

Toxins

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Protein toxins secreted by bacteria and found in plants can be threats to human health. However, their extreme toxicity can also be exploited in different ways, e.g., to produce hybrid toxins directed against cancer cells and to study transport mechanisms in cells. Investigations during the last decades have shown how powerful these molecules are as tools in cell biological research. Here, we first present a partly historical overview, with emphasis on Shiga toxin and ricin, of how such toxins have been used to characterize processes and proteins of importance for their trafficking. In the second half of the article, we describe how one can now use toxins to investigate the role of lipid classes for intracellular transport. In recent years, it has become possible to quantify hundreds of lipid species using mass spectrometry analysis. Thus, it is also now possible to explore the importance of lipid species in intracellular transport. The detailed analyses of changes in lipids seen under conditions of inhibited toxin transport reveal previously unknown connections between syntheses of lipid classes and demonstrate the ability of cells to compensate under given conditions.

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Caveolae: Mechanosensing and mechanotransduction devices linking membrane trafficking to mechanoadaptation

Cited by 59 publications

References 97 publications

Altered endocytosis in cellular senescence

Altered endocytosis in cellular senescence

Lentinan Attenuated the PM2.5 Exposure-Induced Inflammatory Response, Epithelial–Mesenchymal Transition and Migration by Inhibiting the PVT1/miR-199a-5p/caveolin1 Pathway in Lung Cancer

The Protein Toxins Ricin and Shiga Toxin as Tools to Explore Cellular Mechanisms of Internalization and Intracellular Transport

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