The Ca2+- and phospholipid-binding protein Annexin A2 is able to increase and decrease plasma membrane order

The accelerated acquisition of multidimensional NMR spectra using sparse non-uniform sampling (NUS) has been widely adopted in recent years. The key concept in NUS is that a major part of the data is omitted during measurement, and then reconstructed using, for example, compressed sensing (CS) methods. CS requires spectra to be compressible, that is, they should contain relatively few “significant” points. The more compressible the spectrum, the fewer experimental NUS points needed in order for it to be accurately reconstructed. In this paper we show that the CS processing of similar spectra can be enhanced by reconstructing only the differences between them. Accurate reconstruction can be obtained at lower sampling levels as the difference is sparser than the spectrum itself. In many situations this method is superior to “conventional” compressed sensing. We exemplify the concept of “difference CS” with one such case—the study of alpha-synuclein binding to liposomes and its dependence on temperature. To obtain information on temperature-dependent transitions between different states, we need to acquire several dozen spectra at various temperatures, with and without the presence of liposomes. Our detailed investigation reveals that changes in the binding modes of the alpha-synuclein ensemble are not only temperature-dependent but also show non-linear behavior in their transitions. Our proposed CS processing approach dramatically reduces the number of NUS points required and thus significantly shortens the experimental time.

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“… 2013 ; Varyukhina et al. 2022 ). Membrane curvature modification by aSyn has been suggested (Braun et al.…”

Section: Resultsmentioning

confidence: 99%

Non-uniform sampling of similar NMR spectra and its application to studies of the interaction between alpha-synuclein and liposomes

et al. 2023

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“…Of note, Autophagy is highly dependent on organelle membrane stabilization and integrity [ 38 ]. ANXA2 plays key a role in regulating biological membrane dynamic processes [ 21 ] such as autophagy [ 26 ]. However, the role of ANXA2 in AKI has not been elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…Annexin A2 (ANXA2), a 39-kDa phospholipid-binding protein, belongs to the Annexin family [ 18 ] and plays a key role in membrane organization, traffic, and fusion [ 19 , 20 ]. With the high involvement in dynamic events of membrane events [ 21 , 22 ], ANXA2 plays a crucial role in mediating autophagy [ 23 , 24 ]. Indeed, ANXA2 ablation leads to the defects of phagophore membrane initiation [ 25 ] and the deficiency in autophagy setting [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway

et al. 2022

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Acute kidney injury (AKI) is in high prevalence in the world. However, the therapeutic strategies for AKI are still in mystery. Studies have shown to improve autophagy and lysosomal function could inhibit AKI. But their modulators need to be explored in detail. Annexin A2 (ANXA2) is a phospholipid-binding protein involving in organelle membrane integrity function, suggesting its important role in autophagy and lysosome homeostasis. It implicates ANXA2 potentially protects against AKI. However, this has not been elucidated. Herein, we found that ANXA2 is increased in renal tubules in cisplatin-induced AKI mice. Ectopic expression of ANXA2 improved lysosomal functions and enhanced autophagic flux, further protecting against renal tubular cell apoptosis and kidney injury. Conversely, knockdown of ANXA2 inhibited lysosomal function and autophagy, which aggravated the progression of AKI. Transcriptome sequencing revealed β-catenin signaling is highly responsible for this process. In vitro, we found ANXA2 induced β-catenin activation, further triggering T-cell factor-4 (TCF4)-induced transcription factor EB (TFEB). Furthermore, TFEB promoted lysosome biogenesis to enhance autophagic flux, resulting in the alleviation of AKI. Our new findings underline ANXA2 is a new therapeutic potential for AKI through modulating autophagy and lysosomal function. The underlying mechanism is associated with its inductive effects on β-catenin/TFEB pathway.

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“…The fusion of EVs with plasma membranes or endosomes can also be detected by delivering miRNAs and luciferin to recipient cells 131 . In exocytosis, endocytosis, and cell-cell adhesion, AnxA2 is an essential phospholipid-binding protein 132 . It has been shown that EVs containing AnxA2 are capable of fusing directly with plasma membranes 116 , 133 .…”

Section: Extracellular Vesicles (Evs)mentioning

confidence: 99%

New strategies of neurodegenerative disease treatment with extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs)

Palanisamy,

Pei,

Alugoju

et al. 2023

Theranostics

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Neurodegenerative diseases are characterized by the progressive loss of neurons and intricate interactions between different cell types within the affected regions. Reliable biomarkers that can accurately reflect disease activity, diagnose, and monitor the progression of neurodegenerative diseases are crucial for the development of effective therapies. However, identifying suitable biomarkers has been challenging due to the heterogeneous nature of these diseases, affecting specific subsets of neurons in different brain regions. One promising approach for promoting brain regeneration and recovery involves the transplantation of mesenchymal stem cells (MSCs). MSCs have demonstrated the ability to modulate the immune system, promote neurite outgrowth, stimulate angiogenesis, and repair damaged tissues, partially through the release of their extracellular vesicles (EVs). MSC-derived EVs retain some of the therapeutic characteristics of their parent MSCs, including their ability to regulate neurite outgrowth, promote angiogenesis, and facilitate tissue repair. This review aims to explore the potential of MSC-derived EVs as an emerging therapeutic strategy for neurodegenerative diseases, highlighting their role in modulating disease progression and promoting neuronal recovery. By elucidating the mechanisms by which MSC-derived EVs exert their therapeutic effects, we can advance our understanding and leverage their potential for the development of novel treatment approaches in the field of neurodegenerative diseases.

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The Ca2+- and phospholipid-binding protein Annexin A2 is able to increase and decrease plasma membrane order

Cited by 6 publications

References 64 publications

Non-uniform sampling of similar NMR spectra and its application to studies of the interaction between alpha-synuclein and liposomes

Non-uniform sampling of similar NMR spectra and its application to studies of the interaction between alpha-synuclein and liposomes

Annexin A2 plays a key role in protecting against cisplatin-induced AKI through β-catenin/TFEB pathway

New strategies of neurodegenerative disease treatment with extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs)

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