Membrane Dynamics and Remodelling in Response to the Action of the Membrane-Damaging Pore-Forming Toxins

Lata, Kusum; Singh, Mahendra; Chatterjee, Shamaita; Chattopadhyay, Kausik

doi:10.1007/s00232-022-00227-z

Cited by 11 publications

(6 citation statements)

References 114 publications

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“…Many of these wounds lead to small breaches in the cell cortex that are removed by endocytosis of the membrane region including the lesion (cf. [ 127 ]) or by membrane shedding/cytosolic purging to remove large portions of damaged membrane [ 128 , 129 , 130 , 131 , 132 ]. Some wounds such as chronic ulcers, can become colonized by antibiotic resistant bacteria that release pore-forming toxins (PFTs).…”

Section: Relationship To Diseases and Infectionsmentioning

confidence: 99%

Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair

Hui

Stjepić

Nakamura

et al. 2022

Cells

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To cope with continuous physiological and environmental stresses, cells of all sizes require an effective wound repair process to seal breaches to their cortex. Once a wound is recognized, the cell must rapidly plug the injury site, reorganize the cytoskeleton and the membrane to pull the wound closed, and finally remodel the cortex to return to homeostasis. Complementary studies using various model organisms have demonstrated the importance and complexity behind the formation and translocation of an actin ring at the wound periphery during the repair process. Proteins such as actin nucleators, actin bundling factors, actin-plasma membrane anchors, and disassembly factors are needed to regulate actin ring dynamics spatially and temporally. Notably, Rho family GTPases have been implicated throughout the repair process, whereas other proteins are required during specific phases. Interestingly, although different models share a similar set of recruited proteins, the way in which they use them to pull the wound closed can differ. Here, we describe what is currently known about the formation, translocation, and remodeling of the actin ring during the cell wound repair process in model organisms, as well as the overall impact of cell wound repair on daily events and its importance to our understanding of certain diseases and the development of therapeutic delivery modalities.

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Section: Relationship To Diseases and Infectionsmentioning

confidence: 99%

Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair

Hui

Stjepić

Nakamura

et al. 2022

Cells

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“…Because the macrophage is not dead yet; the inflammasome is actively secreting cytokines of the innate response to effectively initiate activation of the second line of defense of the immune system, such as T cells, but very importantly, the T lymphocytes in charge of generating the specific immune response. In vitro studies like these have shown that the monomeric form of VCC is actually a suitable tool for studying cellular functions [ 29 , 30 , 31 ], such as membrane remodeling and the inhibition of the pore-forming mechanism. With the above reasoning and the results of the present study, we may speculate the following: treated macrophages are setting up a pro-inflammatory response towards the toxin, where an active production of IL-1β is necessary.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Activation of a Pro-Inflammatory Response (NF-κB, AP-1, IL-1β) by the Vibrio cholerae Cytotoxin (VCC) Monomer through the MAPK Signaling Pathway in the THP-1 Human Macrophage Cell Line

Escartín-Gutiérrez

Ponce-Figueroa

Torres-Vega

et al. 2023

IJMS

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This study describes, to some extent, the VCC contribution as an early stimulation of the macrophage lineage. Regarding the onset of the innate immune response caused by infection, the β form of IL-1 is the most important interleukin involved in the onset of the inflammatory innate response. Activated macrophages treated in vitro with VCC induced the activation of the MAPK signaling pathway in a one-hour period, with the activation of transcriptional regulators for a surviving and pro-inflammatory response, suggesting an explanation inspired and supported by the inflammasome physiology. The mechanism of IL-1β production induced by VCC has been gracefully outlined in murine models, using bacterial knockdown mutants and purified molecules; nevertheless, the knowledge of this mechanism in the human immune system is still under study. This work shows the soluble form of 65 kDa of the Vibrio cholerae cytotoxin (also known as hemolysin), as it is secreted by the bacteria, inducing the production of IL-1β in the human macrophage cell line THP-1. The mechanism involves triggering the early activation of the signaling pathway MAPKs pERK and p38, with the subsequent activation of (p50) NF-κB and AP-1 (cJun and cFos), determined by real-time quantitation. The evidence shown here supports that the monomeric soluble form of the VCC in the macrophage acts as a modulator of the innate immune response, which is consistent with the assembly of the NLRP3 inflammasome actively releasing IL-1β.

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“…However, even with such small pores, there may be a necessity for an active wound repair mechanism [80]. Additionally, membrane pores created by pore-forming toxins, despite being nanometer-sized, require an active wound repair mechanism [7,23,81].…”

Section: Spontaneous Self-sealingmentioning

confidence: 99%

Wound Repair of the Cell Membrane: Lessons from Dictyostelium Cells

Yumura

2024

Cells

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The cell membrane is frequently subjected to damage, either through physical or chemical means. The swift restoration of the cell membrane’s integrity is crucial to prevent the leakage of intracellular materials and the uncontrolled influx of extracellular ions. Consequently, wound repair plays a vital role in cell survival, akin to the importance of DNA repair. The mechanisms involved in wound repair encompass a series of events, including ion influx, membrane patch formation, endocytosis, exocytosis, recruitment of the actin cytoskeleton, and the elimination of damaged membrane sections. Despite the absence of a universally accepted general model, diverse molecular models have been proposed for wound repair in different organisms. Traditional wound methods not only damage the cell membrane but also impact intracellular structures, including the underlying cortical actin networks, microtubules, and organelles. In contrast, the more recent improved laserporation selectively targets the cell membrane. Studies on Dictyostelium cells utilizing this method have introduced a novel perspective on the wound repair mechanism. This review commences by detailing methods for inducing wounds and subsequently reviews recent developments in the field.

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Membrane Dynamics and Remodelling in Response to the Action of the Membrane-Damaging Pore-Forming Toxins

Cited by 11 publications

References 114 publications

Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair

Wrangling Actin Assemblies: Actin Ring Dynamics during Cell Wound Repair

Transcriptional Activation of a Pro-Inflammatory Response (NF-κB, AP-1, IL-1β) by the Vibrio cholerae Cytotoxin (VCC) Monomer through the MAPK Signaling Pathway in the THP-1 Human Macrophage Cell Line

Wound Repair of the Cell Membrane: Lessons from Dictyostelium Cells

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