Up‐regulation of stromal cell–derived factor 1 (CXCL12) production in rheumatoid synovial fibroblasts through interactions with T lymphocytes: Role of interleukin‐17 and CD40L–CD40 interaction

Kim, Kyoung-Woon; Cho, Mi‐La; Kim, Hae-Rim; Ju, Ji-hyun; Park, Mi-Kyung; Oh, Hye-Jwa; Kim, Joon‐Seok; Park, Sung-Hwan; Lee, Sang‐Heon; Kim, Ho-Youn

doi:10.1002/art.22439

Cited by 121 publications

(98 citation statements)

References 40 publications

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“…However, the current knowledge on how SDF-1 may be regulated, especially in tumors, is very limited. It is reported that IL-17 induces the production of SDF-1, as well as the expression of SDF-1 mRNA, in cultured Rheumatoid synovial fibroblasts in a dose-dependent manner (32). Interestingly, in a murine bone stromal cell line, SDF-1 expression is found to be down-regulated by TGFh-1, both at the mRNA level and at the protein level (33).…”

Section: Discussionmentioning

confidence: 98%

A Novel Bone Morphogenetic Protein Signaling in Heterotypic Cell Interactions in Prostate Cancer

et al. 2008

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We examined the effect of the extracellular bone morphogenetic protein (BMP) 2 and 7, which are up-regulated in the prostate adenocarcinomas of the conditional Pten deletion mouse model, on primary cultures of cancer-associated fibroblasts (CAF) derived from these tumors. In the CAF, we show that BMP2 or BMP7, but not transforming growth factor B-1, can strikingly stimulate secretion of stromal cell-derived factor-1 (SDF-1), also known as CXCL12. The CAF cells express type I and type II BMP receptors as well as the receptor for SDF-1, CXCR4. SDF-1 activation is associated with BMP-induced Smad phosphorylation, and the stimulatory effect is blocked by BMP antagonist, noggin. The findings that BMP treatment can increase SDF-1 pre-mRNA levels in a time-dependent manner and actinomycin D treatment can abolish stimulatory effect of BMP suggest a transcriptional modulation of SDF-1 by BMP signaling. Using a human microvascular endothelial cell line, we show that SDF-1 present in the conditioned medium from the stimulated CAF can significantly induce tube formation, an effect relating to angiogenic function. Furthermore, we found that BMP2 can also protect the CAF from serum starvationinduced apoptosis independent of SDF-1, implying that BMP may induce other factors to sustain the survival of these cells. In short, this report establishes a novel BMP-SDF-1 axis in the prostate tumor along with a new prosurvival effect of BMP that when considered together with our previously described oncogenic properties of BMP indicate a circuitry for heterotypic cell interactions potentially critical in prostate cancer.

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Section: Discussionmentioning

confidence: 98%

A Novel Bone Morphogenetic Protein Signaling in Heterotypic Cell Interactions in Prostate Cancer

et al. 2008

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“…CXCR4 is reported to be the predominant mechanism for the recruitment of circulating fibrocytes to the lungs (18), and CXCR4 has been shown to be critical for mesenchymal stem cell recruitment to bone in mice (19). The CXCR4 ligand stromal cell-derived factor 1 (CCL12) is up-regulated in both RA serum and synovial tissue (20). Additionally, antagonism of CXCR4 reduces inflammation in CIA (21).…”

Section: Discussionmentioning

confidence: 99%

Circulating fibrocytes contribute to the pathogenesis of collagen antibody–induced arthritis

Galligan¹,

Fish²

2012

Arthritis & Rheumatism

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Objective. Rheumatoid arthritis (RA) is a systemic autoimmune disease resulting in joint inflammation. Fibroblast-like synoviocytes in affected joints are responsible for pannus formation and cytokine/ chemokine production, resulting in leukocyte recruitment and bone/cartilage destruction. Previously, we identified a multipotent stem cell population of activated fibrocytes in the blood of patients with RA that may have a role in disease pathogenesis, perhaps as fibroblast-like synoviocyte precursors. The aim of this study was to further characterize the contribution of circulating fibrocytes to the pathogenesis of RA.Methods. Circulating fibrocytes were isolated from mice with collagen-induced arthritis and transferred intravenously into recipient mice with collagen antibody-induced arthritis (CAIA). The activation status of circulating fibrocytes was determined using multidimensional phosphoflow cytometric analysis of the signaling effectors STAT-5, STAT-1, AKT, and JNK. Circulating fibrocyte trafficking and matrix metalloproteinase (MMP) activity were assessed in real time using fluorescence molecular tomography, specifically labeling circulating fibrocytes with CellVue Maroon and measuring MMP activity using MMPSense 680.Results. The numbers of circulating fibrocytes were increased early during the onset of CAIA, concomitant with their activation, as measured by phosphorylation of STAT-5. Adoptive transfer of circulating fibrocytes augmented disease scores and increased class II major histocompatibility complex expression and peripheral blood phosphoactivation profiles in recipient mice with CAIA. Notably, adoptively transferred fluorescence-labeled circulating fibrocytes rapidly migrated into the affected joints of recipient mice with CAIA, and this was associated with augmented neutrophil recruitment into affected joints and MMP activation.Conclusion. Circulating fibrocytes migrate to joints and influence the onset of disease processes in arthritis.

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“…Chemokines also play a key role in the accumulation of inflammatory cells. 34 Their aberrant expression may be responsible for the induction of chronic inflammatory processes such as rheumatoid arthritis (RA), 35 multiple sclerosis (MS), 36 colitis ulcerosa (CU) 37 and allergic diseases. 38 SDF-1 may be a common downstream executor of inflammatory cell accumulation regardless of circumstances upregulating its expression.…”

Section: Cell-based Therapymentioning

confidence: 99%

Functional diversity of SDF-1 splicing variants

Janowski

2009

Cell Adhesion & Migration

115

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SDF-1 is ubiquitously expressed in vertebrate tissues in a constitutive manner. It performs an essential role in cell migration and proliferation as well as participates in tissue-specific physiological processes such as neuromodulation. It is also involved in many pathological processes including: HIV infection, metastatic malignancy, chronic inflammatory disorders and benign proliferative diseases. SDF-1 is mostly regulated at the splicing, and not transcriptional level. Different splicing variants share agonist potency to their cognate receptor, CXCR4, but are characterized by distinct properties. SDF-1α is the predominant isoform found in all organs, but undergoes rapid proteolysis in blood. SDF-1β is more resistant to blood-dependent degradation, stimulates angiogenesis and is present in highly vascularized organs such as: the liver, spleen and kidneys. In contrast, SDF-1γ is located in very active, less vascularized organs susceptible to infarction such as the heart and the brain. The understanding of the functional diversity of the different splicing variants will help in developing therapeutic strategies.

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Up‐regulation of stromal cell–derived factor 1 (CXCL12) production in rheumatoid synovial fibroblasts through interactions with T lymphocytes: Role of interleukin‐17 and CD40L–CD40 interaction

Cited by 121 publications

References 40 publications

A Novel Bone Morphogenetic Protein Signaling in Heterotypic Cell Interactions in Prostate Cancer

A Novel Bone Morphogenetic Protein Signaling in Heterotypic Cell Interactions in Prostate Cancer

Circulating fibrocytes contribute to the pathogenesis of collagen antibody–induced arthritis

Functional diversity of SDF-1 splicing variants

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