Paracrine regulation of fat cell formation in bone marrow cultures via adiponectin and prostaglandins

Yokota, Takafumi; Meka, C. S. Reddy; Medina, Kay L.; Igarashi, Hideya; Takahashi, Masahiko; Nishida, Makoto; Oritani, Kenji; Miyagawa, Jun Ichiro; Funahashi, Tohru; Tomiyama, Yoshiaki; Matsuzawa, Yūji; Kincade, Paul W.

doi:10.1172/jci14506

Cited by 85 publications

(77 citation statements)

References 54 publications

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“…Also, lymphoid cell populations must eventually become PG insensitive in LTBMCs. PGE 2 concentrations in stromal culture supernatants increased from 0.5 ϫ 10 Ϫ9 to 1.2 ϫ 10 Ϫ9 M after 24 h of adiponectin treatment (28). The level was much lower than the PGE 2 concentrations tested in previous studies, and it was unclear whether changes of this magnitude would be physiologically significant and whether the action of PGs would be sufficiently restricted to lymphoid progenitors.…”

Section: A Potential Role For Pgs In Adiponectin-mediated Responsesmentioning

confidence: 65%

“…In an earlier study, we showed that human stromal cells contained adiponectin protein (28). RT-PCR analysis revealed that the adherent layers of cultures established from murine bone marrow also contained transcripts for adiponectin (data not shown).…”

Section: Adiponectin Inhibits B Lymphopoiesis In Ltbmcsmentioning

confidence: 82%

“…We recently found that adiponectin directly blocks the differentiation of preadipocytes through induction of COX-2 and synthesis of prostanoids (28). PGs are known to induce apoptosis in immature lymphocytes (6,39,40) and it seemed possible that they participate in the inhibitory responses previously discussed.…”

Section: A Potential Role For Pgs In Adiponectin-mediated Responsesmentioning

confidence: 95%

“…Synthesis of recombinant adiponectin was induced by isopropyl-␤-D-thiogalactoside. Bacterial extracts were prepared using standard methods and recombinant human adiponectin was purified by DEAE-5PW ion-exchange HPLC (Toso, Japan) as previously described (28). Effect of adiponectin was evaluated at 10 g/ml throughout this report.…”

Section: Reagentsmentioning

confidence: 99%

“…We recently determined that adiponectin is made by fat cells within human bone marrow and blocks differentiation of marrow preadipocytes through a paracrine mechanism (28). Furthermore, the protein suppresses myelomonocytic progenitor growth and macrophage functions in culture (29).…”

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confidence: 99%

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Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Yokota

Meka

Kouro

et al. 2003

The Journal of Immunology

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128

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Adiponectin, an adipocyte-derived hormone, is attracting considerable interest as a potential drug for diabetes and obesity. Originally cloned from human s.c. fat, the protein is also found in bone marrow fat cells and has an inhibitory effect on adipocyte differentiation. The aim of the present study is to explore possible influences on lymphohematopoiesis. Recombinant adiponectin strongly inhibited B lymphopoiesis in long-term bone marrow cultures, but only when stromal cells were present and only when cultures were initiated with the earliest category of lymphocyte precursors. Cyclooxygenase inhibitors abrogated the response of early lymphoid progenitors to adiponectin in stromal cell-containing cultures. Furthermore, PGE2, a major product of cyclooxygenase-2 activity, had a direct inhibitory influence on purified hematopoietic cells, suggesting a possible mechanism of adiponectin action in culture. In contrast to lymphopoiesis, myelopoiesis was slightly enhanced in adiponectin-treated bone marrow cultures, and even when cultures were initiated with single lymphomyeloid progenitors. Finally, human B lymphopoiesis was also sensitive to adiponectin in stromal cell cocultures. These results suggest that adiponectin can negatively and selectively influence lymphopoiesis through induction of PG synthesis. They also indicate ways that adipocytes in bone marrow can contribute to regulation of blood cell formation.

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Section: A Potential Role For Pgs In Adiponectin-mediated Responsesmentioning

confidence: 65%

Section: Adiponectin Inhibits B Lymphopoiesis In Ltbmcsmentioning

confidence: 82%

Section: A Potential Role For Pgs In Adiponectin-mediated Responsesmentioning

confidence: 95%

Section: Reagentsmentioning

confidence: 99%

mentioning

confidence: 99%

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Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Yokota

Meka

Kouro

et al. 2003

The Journal of Immunology

Self Cite

128

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Adiponectin stimulates prostaglandin E₂ production in rheumatoid arthritis synovial fibroblasts

Kusunoki¹,

Kitahara²,

Kojima³

et al. 2010

Arthritis & Rheumatism

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Objective. Adipokines may influence inflammatory and/or immune responses. This study was undertaken to examine whether adiponectin affects the production of prostaglandin E 2 (PGE 2 ) by rheumatoid arthritis synovial fibroblasts (RASFs).Methods. Synovial tissue was obtained from patients with RA who were undergoing joint replacement surgery. Fibroblast-like cells from the third or fourth passage were used as RASFs. Expression of adiponectin receptor messenger RNA (mRNA) and protein was detected. PGE 2 (converted from arachidonic acid) was measured by enzyme-linked immunosorbent assay (ELISA). Expression of mRNA and protein for cyclooxygenase 2 (COX-2) and membrane-associated PGE synthase 1 (mPGES-1), key enzymes involved in PGE 2 synthesis, was detected in RASFs. The effects of RNA interference (RNAi) targeting the adiponectin receptor genes and the receptor signal inhibitors were examined. The influence of adiponectin on NF-B activation in RASFs was measured with an ELISA kit.Results. Adiponectin receptors were detected in RASFs. Adiponectin increased both COX-2 and mPGES-1 mRNA and protein expression by RASFs in a time-and concentration-dependent manner. PGE 2 production by RASFs was also increased by the addition of adiponectin, and this increase was inhibited by RNAi for the adiponectin receptor gene, or coincubation with the receptor signal inhibitors. Enhancement of NF-B activation by adiponectin as well as by interleukin-1␤ was observed in RASFs.Conclusion. Our findings indicate that adiponectin induces COX-2 and mPGES-1 expression, resulting in the enhancement of PGE 2 production by RASFs. Thus, adiponectin may play a role in the pathogenesis of synovitis in RA patients.

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Skeletal involvement in patients with diabetes mellitus

Carnevale

Romagnoli

D'Erasmo

2004

Diabetes Metabolism Res

141

145

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Studies on skeletal involvement in patients with diabetes mellitus have generated conflicting results, largely because of the pathogenetic complexity of the condition. Several mechanisms may contribute to skeletal damage, including the increased urinary excretion coupled with the lower intestinal absorption of calcium, the inappropriate homeostatic response in terms of parathyroid hormone secretion, and also the complex alteration of vitamin D regulation. Decreased or increased insulin and IGF-1 concentrations and the effects of the accumulation of glycation endproducts on the bone tissue could also play a role. A possible genetic predisposition is also currently under investigation. Finally, the role of fat tissue in type 1 and type 2 diabetes and that of diabetic complications also deserve note. As far as bone mass is concerned, in adult patients with type 1 diabetes a moderately reduced bone mineral density has been shown in both axial and appendicular skeleton. On the contrary, patients with type 2 diabetes seem to have higher bone mineral density in respect to healthy control subjects, especially when overweight women are considered. No clear relationship between bone mass measurements and biochemical parameters of mineral metabolism has been shown in the different types of diabetes. Cohort studies recently carried out on large samples indicate that diabetic patients (with both type 1 and type 2 disease) have a higher risk for fracture, in particular for hip fracture, the most dangerous osteoporotic complication. This seems to be dependent both on qualitative and quantitative alterations of the bone, as well as on extra-skeletal factors due to the neuropathic and microangiopathic complications of the disease.

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Paracrine regulation of fat cell formation in bone marrow cultures via adiponectin and prostaglandins

Cited by 85 publications

References 54 publications

Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Adiponectin stimulates prostaglandin E₂ production in rheumatoid arthritis synovial fibroblasts

Skeletal involvement in patients with diabetes mellitus

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Paracrine regulation of fat cell formation in bone marrow cultures via adiponectin and prostaglandins

Cited by 85 publications

References 54 publications

Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Adiponectin, a Fat Cell Product, Influences the Earliest Lymphocyte Precursors in Bone Marrow Cultures by Activation of the Cyclooxygenase-Prostaglandin Pathway in Stromal Cells

Adiponectin stimulates prostaglandin E2 production in rheumatoid arthritis synovial fibroblasts

Skeletal involvement in patients with diabetes mellitus

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Product

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Adiponectin stimulates prostaglandin E₂ production in rheumatoid arthritis synovial fibroblasts