Expression of Matrix Metalloproteases by Fibrocytes

Alba, Carolina García de; Becerril, Carina; Ruiz, Vı́ctor; González, Yolanda; Reyes, Silvia; García, Jorge A.; Selman, Moisés; Pardo, Annie

doi:10.1164/rccm.201001-0028oc

Cited by 106 publications

(83 citation statements)

References 49 publications

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“…Migration of fibrocytes was assessed by using Boyden chambers coated with collagen I, as previously described (26,27). Recombinant human PDGF-AA, PDGF-BB, and SCF were used as the chemoattractants.…”

Section: Phenotype Migration and Differentiation Of Fibrocytesmentioning

confidence: 99%

Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation

Watanabe¹,

Kondo²,

Waseda³

et al. 2017

The Journal of Heart and Lung Transplantation

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Section: Phenotype Migration and Differentiation Of Fibrocytesmentioning

confidence: 99%

Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation

Watanabe¹,

Kondo²,

Waseda³

et al. 2017

The Journal of Heart and Lung Transplantation

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“…Moreover, fibrocytes may ease cell migration and further facilitate the angiogenesis process by secreting a variety of matrix metalloproteinases (MMPs). 31 …”

Section: Ivyspringmentioning

confidence: 99%

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

Xie¹,

Zhao²

2017

J. Biomed

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Pulmonary fibrosis is characterized by excessive deposition of extracellular matrix (ECM) and remodeling of the lung architecture, with clinically irreversible loss of lung function. The exact molecular and cellular mechanisms of pulmonary fibrosis are complicated. Many types of cells are involved in the pathogenic processes. The chemokine (C-X-C motif) ligand 12 (CXCL12) can attract circulating fibrocytes trafficking into lungs via chemokine (C-X-C motif) receptor 4 (CXCR4) to promote tissue repair or impertinently worsen fibrotic lesions. In this review, we briefly summarize the existing experimental and clinical findings about fibrocytes in pulmonary fibrosis and discuss the potential therapeutic target CXCL12/CXCR4 biological axis.

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“…Today the presence of CD45, CD34, or other myeloid antigen like CD11b and CD13 is considered to discriminate fibrocytes from leukocytes. Fibrocytes still do not express large amount of ECM (Chesney et al, 1998), however they produce ECM degrading enzymes, such as MMP9 (García-de-Alba et al, 2010). Fibrocytes can differentiate into myofibroblast in vivo (Mori et al, 2005;Schmidt et al, 2003).…”

Section: Bone Marrow Derived Fibrocytesmentioning

confidence: 99%

Immunological and Molecular Mechanisms Leading to Fibrosis: Origin of Renal Myofibroblasts

Himer¹,

Sziksz²,

Vannay³

2012

Renal Failure - The Facts

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Expression of Matrix Metalloproteases by Fibrocytes

Abstract: Our findings reveal that fibrocytes express a variety of MMPs and that MMP-8 actively participates in the process of fibrocyte migration.

Cited by 106 publications

References 49 publications

Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation

Imatinib ameliorates bronchiolitis obliterans via inhibition of fibrocyte migration and differentiation

Role of CXCL12/CXCR4-Mediated Circulating Fibrocytes in Pulmonary Fibrosis

Immunological and Molecular Mechanisms Leading to Fibrosis: Origin of Renal Myofibroblasts

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