Modulation of platelet-derived microparticles to adhesion and motility of human rheumatoid arthritis fibroblast-like synoviocytes

Wang, Wenwen; Liu, Jiahuan; Yang, Bing; Ma, Zhongshuang; Liu, Guiping; Shen, Weishou; Zhang, Yu

doi:10.1371/journal.pone.0181003

Cited by 13 publications

(17 citation statements)

References 26 publications

(27 reference statements)

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“…In addition, PMVs and its active substances can also induce the activation of the NF‐κB factor by activating Erk, the upstream active molecule of NF‐κB, and mediate the adhesion, movement and inflammation of rheumatoid arthritis fibroblast‐like synoviocytes (RA‐FLS). A variety of inflammatory cytokines and chemokines secreted by RA‐FLS have been considered as the key factors to promote the progression of rheumatoid arthritis . NF‐κB can mediate the inflammatory response of various cells mainly because the activation of NF‐κB mediates the formation of inflammatory corpuscle complexes of NLRP3, pro–caspase‐1 and pro–interleukin‐1, which in turn promotes the release of IL‐1β.…”

Section: Mechanism Of Mvs and Its Active Molecules In Exerting Biologmentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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Cell‐derived microvesicles are membrane vesicles produced by the outward budding of the plasma membrane and released by almost all types of cells. These have been considered as another mechanism of intercellular communication, because they carry active molecules, such as proteins, lipids and nucleic acids. Furthermore, these are present in circulating fluids, such as blood and urine, and are closely correlated to the progression of pathophysiological conditions in many diseases. Recent studies have revealed that microvesicles have a dual effect of damage and protection of receptor cells. However, the nature of the active molecules involved in this effect remains unclear. The present study mainly emphasized the mechanism of microvesicles and the active molecules mediating the different biological effects of receptor cells by affecting autophagy, apoptosis and inflammation pathways. The effective ways of blocking microvesicles and its active molecules in mediating cell damage when microvesicles exert harmful effects were also discussed.

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Section: Mechanism Of Mvs and Its Active Molecules In Exerting Biologmentioning

confidence: 99%

The role of microvesicles and its active molecules in regulating cellular biology

Tan

Miao

et al. 2019

J Cellular Molecular Medi

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“…They showed a marked down-regulation with ATRA of CX3CL1 and EPSTI1 together with decreases of MMP1, PTX3, and VCAM1, which are included in the epithelial-mesenchymal transition gene set. All these genes are involved in cell migration and invasion (Li et al, 2014;Tan et al, 2016;Tung et al, 2016;Bernardini et al, 2017;Wang et al, 2017;Kong et al, 2018). In effect, VCAM1 participates in the transendothelial migration of leukocytes (Kong et al, 2018), whereas EPST11 (Li et al, 2014;Tan et al, 2016) and PTX3 (Tung et al, 2016;Chan et al, 2017) contribute to cancer invasion and metastasis.…”

Section: Downloaded Frommentioning

confidence: 99%

“…Even more relevant is downregulation of CX3CL1 and MMP1, because they participate in RA FLS migration. On one side, CX3CL1 is a chemokine ligand that induces FLS proliferation, migration, and pannus formation in an autocrine way (Bernardini et al, 2017), whereas MMP1 contributes to migration and invasion as an extracellular matrix protease (Huang et al, 2017;Wang et al, 2017).…”

Section: Downloaded Frommentioning

confidence: 99%

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

Mosquera

Rodríguez-Trillo

Blanco

et al. 2019

J Pharmacol Exp Ther

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Fibroblast-like synoviocytes (FLSs) are pivotal in inflammation and joint damage of rheumatoid arthritis (RA). They acquire an active and aggressive phenotype, displaying increased migration and invasiveness and contributing to perpetuate synovial inflammation and destruction of cartilage and bone. The main current therapies of RA are focused against inflammatory factors and immune cells; however, a significant percentage of patients do not successfully respond. Combined treatments with drugs that control inflammation and that reverse the pathogenic phenotype of FLS could improve the prognosis of these patients. An unexplored area includes the retinoic acid, the main biologic retinoid, which is a candidate drug for many diseases but has reached clinical use only for a few. Here, we explored the effect of all-trans retinoic acid (ATRA) on the aggressive phenotype of FLS from patients with RA. RA FLSs were treated with ATRA, tumor necrosis factor (TNF), or TNF1ATRA, and cell migration and invasion were analyzed. In addition, a microarray analysis of expression, followed by gene-set analysis and quantitative polymerase chain reaction validation, was performed. We showed that ATRA induced a notable decrease in FLS migration and invasion that was accompanied by complex changes in gene expression. At supraphysiological doses, many of these effects were overridden or reverted by the concomitant presence of TNF. In conclusion, these results have demonstrated the therapeutic potential of retinoic acid on RA FLS provided TNF could be counterbalanced, either with high ATRA doses or with TNF inhibitors.

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“…Platelet-derived microparticles (PMP) are shed from platelet cell surface following activation and constitute the bulk of circulating microparticles in humans [80]. Constitutive activation of platelets and persistently high levels of PMP are thought to characterise autoimmune diseases and affect disease activity, vessel integrity and thrombotic risk [81][82][83][84]. Platelets further contribute to long-term vessel remodelling by releasing growth factors and mitogens [85].…”

Section: Platelets Leukocytes and The Endotheliummentioning

confidence: 99%

Under crossfire: thromboembolic risk in systemic lupus erythematosus

et al. 2018

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Cerebral and cardiovascular ischaemic events are frequent complications of systemic lupus erythematosus (SLE) and constitute primary causes of permanent damage. However, the pathogenic determinants of an increased thromboembolic risk in patients with SLE are only partially understood. Atherosclerosis constitutes a fertile soil for the development of thrombosis and shows disproportionately high prevalence and progression rates in patients with SLE. Antiphospholipid antibodies are independent risk factors for acute thrombosis, but can also prompt long-term vascular inflammation. Aberrant interactions among immune cells and dysfunctions in the deployment of the coagulation cascade have historically less been explored in SLE, but recent evidence suggests they can also play a critical role at the crossroads between inflammation and haemostasis. In this review, we discuss how different pro-thrombotic mechanisms can be prompted by and synergise with SLEspecific pathogenic events and speculate about novel potential directions for research and drug development.

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Modulation of platelet-derived microparticles to adhesion and motility of human rheumatoid arthritis fibroblast-like synoviocytes

Cited by 13 publications

References 26 publications

The role of microvesicles and its active molecules in regulating cellular biology

The role of microvesicles and its active molecules in regulating cellular biology

All-Trans Retinoic Acid Inhibits Migration and Invasiveness of Rheumatoid Fibroblast-Like Synoviocytes

Under crossfire: thromboembolic risk in systemic lupus erythematosus

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