Inflammatory Cytokines Induce a Unique Mineralizing Phenotype in Mesenchymal Stem Cells Derived from Human Bone Marrow

Ferreira, Elisabeth; Porter, Ryan M.; Wehling, Nathalie; O'Sullivan, Regina P.; Liu, Fangjun; Boskey, Adele L.; Estok, Daniel M.; Harris, Mitchell B.; Vrahas, Mark; Evans, Christopher H.; Wells, James W.

doi:10.1074/jbc.m113.471268

Cited by 55 publications

(50 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This agrees with the work of Ferreira et al 17 in which low levels of IL-1 β and TNF- α induced mesenchymal stem cells to differentiate into osteoblasts independent from the NF- κ B signaling pathway. Higher levels of IL-1 β and TNF- α can enhance osteoclastogenesis by direct stimulation of macrophages and osteoclasts.…”

Section: Discussionsupporting

confidence: 93%

NF‐κB decoy oligodeoxynucleotide inhibits wear particle‐induced inflammation in a murine calvarial model

Sato

Pajarinen

Lin

et al. 2015

J Biomedical Materials Res

View full text Add to dashboard Cite

Wear particles induce periprosthetic inflammation and osteolysis through activation of nuclear factor kappa B (NF-κB), which up-regulates the downstream target gene expression for proinflammatory cytokines in macrophages. It was hypothesized that direct suppression of NF-κB activity in the early phases of this disorder could be a therapeutic strategy for preventing the inflammatory response to wear particles, potentially mitigating osteolysis. NF-κB activity can be suppressed via competitive binding with double stranded NF-κB decoy oligodeoxynucleotides (ODNs) that blocks this transcription factor from binding to the promoter regions of targeted genes. In this murine calvarial study, clinically relevant polyethylene particles (PEs) with/without ODN were subcutaneously injected over the calvarial bone. In the presence of PE particles, macrophages migrated to the inflammatory site and induced tumor necrosis factor alpha (TNF-α) and receptor activator of nuclear factor kappa B ligand (RANKL) expression, resulting in an increase in the number of osteoclasts. Local injections of ODN mitigated the expression of TNF-α, RANKL, and induced the expression of two anti-inflammatory, antiresorptive cytokines: interleukin-1 receptor antagonist and osteoprotegerin. Local intervention with NF-κB decoy ODN in early cases of particle-induced inflammation in which the prosthesis is still salvageable may potentially preserve periprosthetic bone stock.

show abstract

Section: Discussionsupporting

confidence: 93%

NF‐κB decoy oligodeoxynucleotide inhibits wear particle‐induced inflammation in a murine calvarial model

Sato

Pajarinen

Lin

et al. 2015

J Biomedical Materials Res

View full text Add to dashboard Cite

show abstract

“…Interestingly, analysis of the extracellular vesicles produced by IL-1β treated mesenchymal stem cells showed a clearly altered ratio of ENPP1 to alkaline phosphatase and less PPi in the vesicle fraction. This work supports the hypothesis that inflammatory cytokines can induce mineralization by altering the enzymes regulating the PPi/Pi ratio on extracellular vesicles [21]. …”

Section: Factors Regulating Articular Cartilage Vesicle Mineralizationsupporting

confidence: 89%

“…For example, bone marrow-derived mesenchymal stem cells undergo massive mineralization in response to interleukin-1β (Il-1β). Interesting work exploring the mechanism of this effect demonstrated that mesenchymal stem cells do not undergo osteoblastic differentiation in response to IL-1β [21]. Instead, mineralization correlated with a decrease in cellular levels of ENPP1.…”

Section: Factors Regulating Articular Cartilage Vesicle Mineralizationmentioning

confidence: 99%

Articular cartilage vesicles and calcium crystal deposition diseases

Rosenthal

2016

Current Opinion in Rheumatology

View full text Add to dashboard Cite

Purpose of review Articular cartilage vesicles (ACVs) are small extracellular vesicles that serve as foci of pathologic calcium crystal deposition in articular cartilage matrix. In this review, I have summarized the role of ACVs in calcium crystal formation and discuss recent findings that impact our understanding of the content, behavior, and origin of ACVs in healthy and diseased joints. The burgeoning interest in extracellular vesicles in other fields renders this a timely and relevant topic. Recent findings I have highlighted recent studies demonstrating that some ACVs originate in the autophagic pathway in healthy articular chondrocytes. I have reviewed accumulating evidence that nonmineralizing functions of ACVs contribute to osteoarthritis. I have also discussed new work supporting a role for extracellular vesicles in interleukin-1 β-induced mineralization and in mediating the catabolic effects of synovial inflammation in osteoarthritis. Summary We are making slow and steady progress in understanding the origin and function of ACVs and other relevant extracellular vesicles in arthritis. Further work in this interesting area is warranted.

show abstract

“…These factors are particularly important for regulating stem cell activities such as mobilization, proliferation, and differentiation. 20,21,[25][26][27][28] More importantly, some of these signals are only transiently activated at the early stage of injury and usually diminish by day 10 after injury. 7,20,21,25,29 In the present study, we have demonstrated that there was limited blood chimerism 3 days after parabiotic surgery, and that the crosscirculatory system required 7 to 10 days to be fully established.…”

Section: Discussionmentioning

confidence: 99%

Circulating Cells Contribute to Cardiomyocyte Regeneration After Injury

Hsueh

Chang

et al. 2015

Circulation Research

View full text Add to dashboard Cite

Rationale:The contribution of bone marrow-borne hematopoietic cells to the ischemic myocardium has been documented. However, a pivotal study reported no evidence of myocardial regeneration from hematopoieticderived cells. The study did not take into account the possible effect of early injury-induced signaling as the test mice were parabiotically paired to partners immediately after surgery-induced myocardial injury when crosscirculation has not yet developed. Objective:

show abstract

Inflammatory Cytokines Induce a Unique Mineralizing Phenotype in Mesenchymal Stem Cells Derived from Human Bone Marrow

Cited by 55 publications

References 36 publications

NF‐κB decoy oligodeoxynucleotide inhibits wear particle‐induced inflammation in a murine calvarial model

NF‐κB decoy oligodeoxynucleotide inhibits wear particle‐induced inflammation in a murine calvarial model

Articular cartilage vesicles and calcium crystal deposition diseases

Circulating Cells Contribute to Cardiomyocyte Regeneration After Injury

Contact Info

Product

Resources

About