Update on synovitis

Szekanecz, Zoltán; Koch, Alisa E.

doi:10.1007/s11926-001-0051-0

Cited by 53 publications

(64 citation statements)

References 44 publications

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“…PF4 is also released from activated T lymphocytes and mast cells (21). It has been shown to influence numerous other biological properties, including inhibiting endothelial cell proliferation, migration, and angiogenesis (22)(23)(24), inhibiting T cell function by down-modulating cell proliferation and cytokine release (25), and supporting the survival of normal hematopoietic precursors and protecting them from the toxicity of chemotherapeutic agents (26). CTAP-III is an N-terminal cleavage product of PBP, which is synthesized in megakaryocytes.…”

Section: Discussionmentioning

confidence: 99%

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

Vermeulen¹,

Lan²,

Zhang³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Benzene is an important industrial chemical and environmental contaminant that causes leukemia. To obtain mechanistic insight into benzene's mechanism of action, we examined the impact of benzene on the human serum proteome in a study of exposed healthy shoe-factory workers and unexposed controls. Two sequential studies were performed, each using sera from 10 workers exposed to benzene (overall mean benzene air level >30 ppm) and 10 controls. Serum samples were subjected to anion-exchange fractionation and bound to three types of ProteinChip arrays (Ciphergen Biosystems, Fremont, CA) [hydrophobic (H50), metal affinity (IMAC3-Cu), and cation exchange (WCX2)]. Protein-expression patterns were detected by surface-enhanced laser desorption͞ ionization (SELDI)-TOF MS. Three proteins (4.1, 7.7, and 9.3 kDa) were consistently down-regulated in exposed compared with control subjects in both studies. All proteins were highly inversely correlated with individual estimates of benzene exposure (r > 0.75). The 7.7-and 9.3-kDa proteins were subsequently identified as platelet factor (PF)4 and connective tissue activating peptide (CTAP)-III. Initial proteomic results for PF4 and CTAP-III were subsequently confirmed in a single experiment using a ProteinChiparray-based immunoassay(Ciphergen Biosystems). The altered expression of the platelet-derived CXC-chemokines (40% and 63% for PF4 and CTAP-III, respectively) could not be explained by changes in absolute platelet counts. Thus, SELDI-TOF analysis of a limited number of exposed and unexposed subjects revealed that lowered expression of PF4 and CTAP-III proteins is a potential biomarker of benzene's early biologic effects and may play a role in the immunosuppressive effects of benzene.biomarker ͉ leukemia ͉ mass spectrometry ͉ platelet ͉ molecular epidemiology

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Section: Discussionmentioning

confidence: 99%

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

Vermeulen¹,

Lan²,

Zhang³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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“…Angiogenesis is a key event both during physiological and pathological processes and is regulated by factors from the VEGF 1 and fibroblast growth factor families as well as by cytokines and chemokines (1)(2)(3)(4). Chemokines are a family of small polypeptides classified into different subfamilies (C, CC, CXC, and CX3C) and were first described as regulators of leukocyte homing (5).…”

mentioning

confidence: 99%

“…Thus, interleukin-8/CXCL8 (CXC, ELRϩ) is angiogenic (6), whereas monokine induced by interferon-␥ (MIG)/CXCL9 (CXC, ELRϪ) is angiostatic (7). However, other CXC/ELRϪ chemokines such as stromal-derived factor-1/CXCL12 as well as chemokines from other subfamilies such as monocyte-chemoattractant protein-1/CCL2 are also angiogenic (3). Receptors for these chemokines have been reported in ECs (8 -11), but the molecular mechanisms by which they induce or inhibit angiogenesis remain undetermined.…”

mentioning

confidence: 99%

Membrane Type 1-Matrix Metalloproteinase Is Regulated by Chemokines Monocyte-Chemoattractant Protein-1/CCL2 and Interleukin-8/CXCL8 in Endothelial Cells during Angiogenesis

Gálvez¹,

Genı́s²,

Matı́as-Román³

et al. 2005

Journal of Biological Chemistry

100

108

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We have investigated the putative role and regulation of membrane type 1-matrix metalloproteinase (MT1-MMP) in angiogenesis induced by inflammatory factors of the chemokine family. The absence of MT1-MMP from null mice or derived mouse lung endothelial cells or the blockade of its activity with inhibitory antibodies resulted in the specific decrease of in vivo and in vitro angiogenesis induced by CCL2 but not CXCL12. Similarly, CCL2-and CXCL8-induced tube formation by human endothelial cells (ECs) was highly dependent on MT1-MMP activity. CCL2 and CXCL8 significantly increased MT1-MMP surface expression, clustering, activity, and function in human ECs. Investigation of the signaling pathways involved in chemokine-induced MT1-MMP activity in ECs revealed that CCL2 and CXCL8 induced cortical actin polymerization and sustained activation of phosphatidylinositol 3-kinase (PI3K) and the small GTPase Rac. Inhibition of PI3K or actin polymerization impaired CCL2-induced MT1-MMP activity. Finally, dimerization of MT1-MMP was found to be enhanced by CCL2 in ECs in a PI3K-and actin polymerization-dependent manner. In summary, we identify MT1-MMP as a molecular target preferentially involved in angiogenesis mediated by CCL2 and CXCL8, but not CXCL12, and suggest that MT1-MMP dimerization might be an important mechanism of its regulation during angiogenesis.

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“…It is assumed that synovial cells, chondrocytes, and osteoblasts as well as bone marrow cells are also involved in the production of abnormal levels of cytokines (7,8). During the course of inflammation, activated macrophages produce tumor necrosis factor ␣ (TNF-␣), IL-1, and IL-6, and these cytokines, in turn, stimulate the proliferation of synovial cells to form a mass of synovial tissue, called pannus, that degrades bone via the activation of osteoclasts (9)(10)(11)(12)(13).…”

mentioning

confidence: 99%

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice

Yumoto

Ishijima

Rittling

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

194

169

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Rheumatoid arthritis is one of the most critical diseases that impair the quality of life of patients, but its pathogenesis has not yet been fully understood. Osteopontin (OPN) is an extracellular matrix protein containing Arg-Gly-Asp (RGD) sequence, which interacts with ␣v␤3 integrins, promotes cell attachment, and cell migration and is expressed in both synovial cells and chondrocytes in rheumatoid arthritis; however, its functional relationship to arthritis has not been known. Therefore, we investigated the roles of OPN in the pathogenesis of inflammatory process in a rheumatoid arthritis model induced by a mixture of anti-type II collagen mAbs and lipopolysaccharide (mAbs͞LPS). mAbs͞LPS injection induced OPN expression in synovia as well as cartilage, and this expression was associated with joint swelling, destruction of the surface structures of the joint based on scanning electron microscopy, and loss of toluidine blue-positive proteoglycan content in the articular cartilage in wild-type mice. In contrast, OPN deficiency prevented the mice from such surface destruction, loss of proteoglycan in the articular joint cartilage, and swelling of the joints even when the mice were subjected to mAbs͞ LPS injection. Furthermore, mAbs͞LPS injection in wild-type mice enhanced the levels of CD31-positive vessels in synovia and terminal deoxynucleotidyltransferase-mediated UTP end labeling-positive chondrocytes in the articular cartilage, whereas such angiogenesis as well as chondrocyte apoptosis was suppressed significantly in OPNdeficient mice. These results indicated that OPN plays a critical role in the destruction of joint cartilage in the rheumatoid arthritis model in mice via promotion of angiogenesis and induction of chondrocyte apoptosis.

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Update on synovitis

Cited by 53 publications

References 44 publications

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

Decreased levels of CXC-chemokines in serum of benzene-exposed workers identified by array-based proteomics

Membrane Type 1-Matrix Metalloproteinase Is Regulated by Chemokines Monocyte-Chemoattractant Protein-1/CCL2 and Interleukin-8/CXCL8 in Endothelial Cells during Angiogenesis

Osteopontin deficiency protects joints against destruction in anti-type II collagen antibody-induced arthritis in mice

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