Matrix metalloproteinases: an emerging role in regulation of actin microfilament system

Bildyug, Natalya

doi:10.1515/bmc-2016-0022

Cited by 13 publications

(15 citation statements)

References 83 publications

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“…The expression of MMPs, enzymes implicated in cell responses to the environmental cues, including cell proliferation, migration, differentiation and in the dynamic process of ECM turnover, with relevant implications in the inflammatory and remodeling phases of healing [33] , suggest that PEMF actuation can modify hTDCs behavior, decreasing the expression of MMPs associated to collagen degradation, which may contribute to inflammatory pain and tendon lesions. As cytoskeleton changes often precede MMP modulation during tissue remodeling, actin dynamics might be linked to the expression of MMP genes [34] . In our study the detection of vinculin and α-actin [ 35 , 36 ] is not compromised by the PEMF stimulation.…”

Section: Discussionmentioning

confidence: 99%

Magnetic responsive materials modulate the inflammatory profile of IL-1β conditioned tendon cells

et al. 2020

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Tendinopathies represent half of all musculoskeletal injuries worldwide. Inflammatory events contribute to both tendon healing and to tendinopathy conditions but the cellular triggers leading to one or the other are unknown. In previous studies, we showed that magnetic field actuation modulates human tendon cells (hTDCs) behavior in pro-inflammatory environments, and that magnetic responsive membranes could positively influence inflammation responses in a rat ectopic model. Herein, we propose to investigate the potential synergistic action of the magnetic responsive membranes, made of a polymer blend of starch with polycaprolactone incorporating magnetic nanoparticles (magSPCL), and the actuation of pulsed electromagnetic field (PEMF): 5 Hz, 4mT of intensity and 50% of duty cycle, in IL-1 β-treated-hTDCs, and in the immunomodulatory response of macrophages. It was found that the expression of pro-inflammatory (TNF α, IL-6, IL-8, COX-2) and ECM remodeling (MMP-1,-2,-3) markers tend to decrease in cells cultured onto magSPCL membranes under PEMF, while the expression of TIMP-1 and anti-inflammatory genes (IL-4, IL-10) increases. Also, CD16 ++ and CD206 + macrophages were only found on magSPCL membranes with PEMF application. Magnetic responsive membranes show a modulatory effect on the inflammatory profile of hTDCs favoring anti-inflammatory cues which is also supported by the anti-inflammatory/repair markers expressed in macrophages. These results suggest that magnetic responsive magSPCL membranes can contribute for inflammation resolution acting on both resident cell populations and inflammatory cells, and thus significantly contribute to tendon regenerative strategies. Statement of significance Magnetically-assisted strategies have received great attention in recent years to remotely trigger and guide cell responses. Inflammation plays a key role in tendon healing but persistent pro-inflammatory molecules can contribute to tendon disorders, and therefore provide a therapeutic target for advanced treatments. We have previously reported that magnetic fields modulate the response of human tendon cells (hT-DCs) conditioned to pro-inflammatory environments (IL-1 β-treated-hTDCs), and that magnetic responsive membranes positively influence immune responses. In the present work, we combined pulsed electromagnetic field (PEMF) and magnetic responsive membranes to guide the inflammatory profile of IL-1 βtreated-hTDCs and of macrophages. The results showed that the synergistic action of PEMF and magnetic membranes supports the applicability of magnetically actuated systems to regulate inflammatory events and stimulate tendon regeneration.

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Section: Discussionmentioning

confidence: 99%

Magnetic responsive materials modulate the inflammatory profile of IL-1β conditioned tendon cells

et al. 2020

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“…We selected Timp1 (induced by TGFβ, Supplementary Fig. 8b), an inhibitor of matrix metalloproteinases, which are known to promote actin-rich structures in invadopodias 41 , and Arhgef6 (inhibited by TGFβ, Supplementary Fig. 8e), which acts as a RAC1 guanine nucleotide exchange factor (GEF) 42 , a crucial regulator of actin cytoskeleton.…”

Section: Inhibition Of Tgfβ Receptor Function Promotes Muscle Cell Fusionmentioning

confidence: 99%

TGFβ signaling curbs cell fusion and muscle regeneration

et al. 2021

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Muscle cell fusion is a multistep process involving cell migration, adhesion, membrane remodeling and actin-nucleation pathways to generate multinucleated myotubes. However, molecular brakes restraining cell–cell fusion events have remained elusive. Here we show that transforming growth factor beta (TGFβ) pathway is active in adult muscle cells throughout fusion. We find TGFβ signaling reduces cell fusion, regardless of the cells’ ability to move and establish cell-cell contacts. In contrast, inhibition of TGFβ signaling enhances cell fusion and promotes branching between myotubes in mouse and human. Exogenous addition of TGFβ protein in vivo during muscle regeneration results in a loss of muscle function while inhibition of TGFβR2 induces the formation of giant myofibers. Transcriptome analyses and functional assays reveal that TGFβ controls the expression of actin-related genes to reduce cell spreading. TGFβ signaling is therefore requisite to limit mammalian myoblast fusion, determining myonuclei numbers and myofiber size.

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“…The interplay of PEBP1 with proteins located from either side of plasma membrane or included in the membrane leaflet, may explain its involvement in the response of the cell to its environment. Particularly, PEBP1 was shown to regulate the expression of several MMPs [7,99], all enzymes that are capable of degrading all kinds of extracellular matrix proteins and that are thought to play a major role in cell proliferation, migration, differentiation, apoptosis and host defense. PEBP1 participates also in sensing the plasma membrane status by acting on internalization of receptors and by controlling the formation of primary cilium that is a sensory organelle.…”

Section: -Pebp1 Interacts With Effectors Regulating Plasma Membrane mentioning

confidence: 99%

PEBP1/RKIP behavior: a mirror of actin-membrane organization

Schoentgen

Jonić

2020

Cell. Mol. Life Sci.

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Phosphatidylethanolamine binding protein 1 (PEBP1), a small 21kDa protein, is implicated in several key processes of the living cell. The deregulation of PEBP1, especially its downregulation, leads to major diseases such as cancer and Alzheimer's disease. PEBP1 was found to interact with numerous proteins, especially kinases and GTPases, generally inhibiting their activity. To understand the basic functionality of this amazing small protein, we have considered several known processes it modulates and we have discussed the role of each molecular target in these processes. Here, we propose that cortical actin organization, associated with membrane changes, is involved in the majority of the processes modulated by PEBP1. Furthermore, based on recent data, we summarize some key PEBP1-interacting proteins, we report their respective functions and focus on their relationships with actin organization. We suggest that, depending on the cell status and environment, PEBP1 is an organizer of the actinmembrane composite material.

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Matrix metalloproteinases: an emerging role in regulation of actin microfilament system

Cited by 13 publications

References 83 publications

Magnetic responsive materials modulate the inflammatory profile of IL-1β conditioned tendon cells

Magnetic responsive materials modulate the inflammatory profile of IL-1β conditioned tendon cells

TGFβ signaling curbs cell fusion and muscle regeneration

PEBP1/RKIP behavior: a mirror of actin-membrane organization

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