Circulating fibrocytes contribute to the myofibroblast population in proliferative vitreoretinopathy epiretinal membranes

El-Asrar, A M Abu; Struyf, Sofie; Damme, Jo Van; Geboes, Karel

doi:10.1136/bjo.2007.134346

Cited by 60 publications

(30 citation statements)

References 21 publications

(48 reference statements)

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“…11 Among the organs most frequently affected by fibrosis are liver, lungs, kidneys, pancreas, skin and cardiovascular walls, but the phenomenon has also been observed in bile ducts, mammary glandular epithelium, fascias, stomach, ileum, synovium, peritoneal mesothelium, eye structures (e.g., conjunctiva, sclera, lens capsule after glaucoma surgery and in vitreo-retinopathies). 42,43 Although many cell types have been implied in these different tissue fibrosis sites, and numerous recruitment mechanisms were described, a common pathophysiological mechanism appears from recent studies. Most informative have been gene expression profiles with deduction of ''fibrosis signatures,'' and these can be the result of, for example, epigenetic mechanisms, such as histone acetylation, DNA methylation and transcription of noncoding microRNA's.…”

Section: Characterization and Origin Of A Myofibroblastmentioning

confidence: 99%

Stromal myofibroblasts are drivers of invasive cancer growth

Wever¹,

Demetter²,

Mareel³

et al. 2008

Intl Journal of Cancer

625

601

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Tissue integrity is maintained by the stroma in physiology. In cancer, however, tissue invasion is driven by the stroma. Myofibroblasts and cancer-associated fibroblasts are important components of the tumor stroma. The origin of myofibroblasts remains controversial, although fibroblasts and bone marrow-derived precursors are considered to be the main progenitor cells. Myofibroblast reactions also occur in fibrosis. Therefore, we wonder whether nontumorous myofibroblasts have different characteristics and different origins as compared to tumor-associated myofibroblasts. The mutual interaction between cancer cells and myofibroblasts is dependent on multiple invasive growth-promoting factors, through direct cell-cell contacts and paracrine signals. Since fibrosis is a major side effect of radiotherapy, we address the question how the main methods of cancer management, including chemotherapy, hormonotherapy and surgery affect myofibroblasts and by inference the surrogate endpoints invasion and metastasis.

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Section: Characterization and Origin Of A Myofibroblastmentioning

confidence: 99%

Stromal myofibroblasts are drivers of invasive cancer growth

Wever¹,

Demetter²,

Mareel³

et al. 2008

Intl Journal of Cancer

625

601

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“…Fibrocytes contribute to the innate response to injury and tissue remodeling, and these cells also mediate fibrogenesis in a number of systemic and organ-specific fibrosing disorders, such as renal fibrosis, 10 ischemic cardiomyopathy, 11,12 pulmonary fibrosis, 13,14 asthma, [15][16][17][18] and keloid scarring. 19 Recently, Abu El-Asrar et al 20,21 demonstrated that circulating fibrocytes contributed to the population of myofibroblasts in the epiretinal membranes of patients with PDR and iovs.arvojournals.org j ISSN: 1552-5783 proliferative vitreoretinopathy. The authors identified fibrocytes that had undergone local differentiation into myofibroblasts, using double-immunohistochemical staining to detect coexpression of CD45 and a-SMA, and they suggested that myofibroblasts derived from fibrocytes participated in the formation of FVMs in PDR and proliferative vitreoretinopathy patients.…”

mentioning

confidence: 99%

Fibrocytes and Fibrovascular Membrane Formation in Proliferative Diabetic Retinopathy

Tamaki

Usui‐Ouchi

Murakami

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. The purpose of this study was to investigate whether fibrocytes participate in formation of the fibrovascular membrane (FVM) in patients with proliferative diabetic retinopathy (PDR).METHODS. Vitreous fluid and FVM samples were obtained during vitrectomy in patients with PDR. Samples from patients with macular hole or epiretinal membrane were used as controls. Vitreous fluid and FVM samples were subjected to immunohistochemical analysis. In addition, cells isolated from the vitreous fluid of PDR and control patients were cultured in serum-free medium. Fibrocytes were identified among these cells by morphological and immunohistochemical analyses. We examined the number of fibrocytes in PDR patients and control patients. Also, the concentrations of monocyte chemoattractant protein-1 (MCP-1), pentraxin3, and serum amyloid P (SAP) in vitreous fluid samples from PDR patients and control patients were determined by enzyme-linked immunosorbent assay.RESULTS. Fibrocytes were observed in the vitreous and FVM samples from PDR patients. Cells cultured from the vitreous samples of PDR patients were spindle shaped and expressed fibrocyte markers. TGF-b1 induced differentiation of these cells into myofibroblasts. The number of fibrocytes was higher in samples from PDR patients than in samples from control patient. The vitreous fluid concentration of MCP-1 was significantly higher in PDR patients than in controls and showed a significant positive correlation with the number of fibrocytes from the vitreous fluid. Vitreous fluid concentrations of pentraxin3 and SAP were also higher in PDR patients than in control patients.CONCLUSIONS. These findings indicate that fibrocytes may be involved in development of the FVM in PDR.

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“…Myofibroblasts are the cell type that generates and deposits collagen rich pathological extracellular matrix leading to irreversible fibrosis and causing organ dysfunction. There is increasing evidence that CFs contribute to the new population of myofibroblasts that emerge at the tissue site during the process of fibrosis [5,6,15]. Moreover, studies in vitro have reported that LH contributed to modulating the differentiation of progenitor cells, such as endometrial stromal cells and osteoblast [11,12].…”

Section: Discussionmentioning

confidence: 99%

“…Studies have demonstrated that CFs traffic to the site of tissue injury, differentiate into fibroblasts and myofibroblasts, and contribute to collagen deposition and fibrosis [4][5][6]. However, the regulatory processes that govern the differentiation of blood-borne fibrocytes are currently not known.…”

Section: Introductionmentioning

confidence: 99%

Low Molecular Weight Heparin Inhibits Circulating Fibrocytes Differentiation by Modulating Neuronal Nitric Oxide Synthase and TGF-�1/Smad Pathway

Xie

Zhu²,

Fu³

et al. 2012

Cell Physiol Biochem

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Background/Aims: Circulating fibrocytes (CFs) have been placed at the center of a number of fibrosing conditions. Recently, attention has been drawn to the non-anticoagulant activities of low molecular weight heparin (LH), especially its anti-fibrotic effects. The purpose of this study was to investigate the effects of LH on CFs differentiation and possible underlying mechanisms. Methods/Results: CFs were cultured from human peripheral blood mononuclear cells and identified by dual-immunofluorescence staining. Incubation with LH inhibited CFs trans-differentiation by upregulating CD34 and downregulating pro-Collagen I and a-SMA in a concentration- and time-dependent manner, all of which were detected by flow cytometry. Similar effects were observed after incubation with L-NAME, an inhibitor of NOS. NO production was measured by Griess methods and markedly decreased in CFs treated with LH. Three NOS isoforms were assessed by western blot and nNOS was the predominant isoform involved in this process. Additionally, LH and L-NAME had similar down-regulating effects on the expression of TGF-β1 and pSmad2/3, which indicated that TGF-β/Smad pathway might be a downstream signaling of nNOS/NO during LH treatment. Conclusion: These results suggested that LH could exhibit anti-fibrotic effects by inhibiting CFs transdifferentiation, in which the involvement of nNOS/NO and TGF-β/Smad pathway were identified.

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Circulating fibrocytes contribute to the myofibroblast population in proliferative vitreoretinopathy epiretinal membranes

Abstract: Circulating fibrocytes may function as precursors of myofibroblasts in PVR membranes.

Cited by 60 publications

References 21 publications

Stromal myofibroblasts are drivers of invasive cancer growth

Stromal myofibroblasts are drivers of invasive cancer growth

Fibrocytes and Fibrovascular Membrane Formation in Proliferative Diabetic Retinopathy

Low Molecular Weight Heparin Inhibits Circulating Fibrocytes Differentiation by Modulating Neuronal Nitric Oxide Synthase and TGF-�1/Smad Pathway

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