Selective Inhibition of Dexamethasone-Induced Apoptosis in Rat Thymocytes by Herbimycin A

Lee, Eibai; Miura, Masahiko; Yoshinari, Miyako; Iwai, Hideyuki; Kariya, Kimio

doi:10.1006/bbrc.1994.1902

Cited by 24 publications

(24 citation statements)

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“…6B). In the primary spongiosa, c-Fos was expressed strongly in osteoblasts, cells known to up-regulate their expression of c-Fos in response to factors such as parathyroid hormone (48,49), indicating that the lower intensity of the signal for c-Fos in osteoclasts inside the bones was not due to suboptimal specimen fixation or processing.…”

Section: Tnf But Not Il-1 Increases C-fos Expression In Osteoclast mentioning

confidence: 97%

Osteoclast Precursor Interaction with Bone Matrix Induces Osteoclast Formation Directly by an Interleukin-1-mediated Autocrine Mechanism

Yao

Xing

Qin

et al. 2008

Journal of Biological Chemistry

100

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Interleukin-1 (IL-1) and tumor necrosis factor (TNF) mediate bone resorption in a variety of diseases affecting bone. Like TNF, IL-1 is secreted by osteoclast precursors (OCPs), but unlike TNF, it does not induce osteoclast formation directly from OCPs in vitro. TNF induces IL-1 expression and activates c-Fos, a transcription factor required in OCPs for osteoclast formation. Here, we examined whether IL-1 can induce osteoclast formation directly from OCPs overexpressing c-Fos and whether interaction with bone matrix affects OCP cytokine expression. We infected OCPs with c-Fos or green fluorescent protein retrovirus, cultured them with macrophage colony-stimulating factor and IL-1 on bone slices or plastic dishes, and assessed osteoclast and resorption pit formation and expression of IL-1 by OCPs. We used a Transwell assay to determine whether OCPs secrete IL-1 when they interact with bone matrix. IL-1 induced osteoclast formation directly from c-Fos-expressing OCPs on plastic. c-Fos-expressing OCPs formed osteoclasts spontaneously on bone slices without addition of cytokines. OCPs on bone secreted IL-1, which induced osteoclast formation from c-Fos-expressing OCPs in the lower Transwell dishes. The bone matrix proteins dentin sialoprotein and osteopontin, but not transforming growth factor-␤, stimulated OCP expression of IL-1 and induced c-Fos-expressing OCP differentiation into osteoclasts. Osteoclasts eroding inflamed joints have higher c-Fos expression compared with osteoclasts inside bone. We conclude that OCPs expressing c-Fos may induce their differentiation directly into osteoclasts by an autocrine mechanism in which they produce IL-1 through interaction with bone matrix. TNF could induce c-Fos expression in OCPs at sites of inflammation in bone to promote this autocrine mechanism and thus amplify bone loss.

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Section: Tnf But Not Il-1 Increases C-fos Expression In Osteoclast mentioning

confidence: 97%

Osteoclast Precursor Interaction with Bone Matrix Induces Osteoclast Formation Directly by an Interleukin-1-mediated Autocrine Mechanism

Yao

Xing

Qin

et al. 2008

Journal of Biological Chemistry

100

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“…Tyrosine protein kinase inhibitors have been shown to induce apoptosis in HL-60 cells within 18 h [11], and our results show that they can inhibit apoptosis in HL-60 cells in a much shorter period of treatment. Herbimycin A, another tyrosine kinase inhibitor, has been shown to inhibit TNF-and dexamethasone-induced apoptosis in U937 cells and rat thymocytes respectively [12,16]. However, tyrosine phosphorylation regulates TNF-and didemnin B-induced apoptosis differently.…”

Section: Resultsmentioning

confidence: 99%

Protein tyrosine kinase inhibitors prevent didemnin B‐induced apoptosis in HL‐60 cells

1996

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“…The cells were immediately incubated with RPMI 1640 medium supplemented with 10% fetal calf serum at a density of 10 × 10 6 cells / ml under 5% CO 2 in air (25).…”

Section: Cell Culturementioning

confidence: 99%

“…The intact and fragmented DNA was assayed by the diphenylamine method. DNA fragmentation was expressed as the percentage of fragmented DNA in total DNA (intact DNA ± fragmented DNA) (25).…”

Section: Dna Fragmentationmentioning

confidence: 99%

Wogonin Prevents Glucocorticoid-Induced Thymocyte Apoptosis Without Diminishing Its Anti-inflammatory Action

et al. 2007

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Abstract. The effect of wogonin, a flavone highly purified from the roots of Scutellaria baicalensis, on apoptotic cell death was re-evaluated in rat thymocytes. This flavone inhibited glucocorticoid-induced apoptotic changes such as DNA fragmentation, phosphatidylserine translocation, and nuclear condensation in rat thymocytes. Similar inhibition was also observed in apoptosis induced by other inducers such as etoposide. No significant changes of these apoptotic features were observed in rat thymocytes treated with wogonin alone, suggesting that this flavone protects against glucocorticoid-mediated immunosuppression caused by thymocyte apoptosis. Wogonin was reported to possess anti-inflammatory action in some previous studies, but this flavone had no effect on carrageenan-induced paw edema in this study. The simultaneous treatment of wogonin and glucocorticoid neither enhanced nor reduced the anti-inflammatory effect of glucocorticoid. These results indicate that wogonin is likely to prevent the immunosuppression of glucocorticoid without diminishing its drug efficacy as an anti-inflammatory agent.

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Selective Inhibition of Dexamethasone-Induced Apoptosis in Rat Thymocytes by Herbimycin A

Cited by 24 publications

References 0 publications

Osteoclast Precursor Interaction with Bone Matrix Induces Osteoclast Formation Directly by an Interleukin-1-mediated Autocrine Mechanism

Osteoclast Precursor Interaction with Bone Matrix Induces Osteoclast Formation Directly by an Interleukin-1-mediated Autocrine Mechanism

Protein tyrosine kinase inhibitors prevent didemnin B‐induced apoptosis in HL‐60 cells

Wogonin Prevents Glucocorticoid-Induced Thymocyte Apoptosis Without Diminishing Its Anti-inflammatory Action

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