IL-12-Mediated and IL-18-Mediated Nitric Oxide-Induced Apoptosis of Adherent Bone Marrow Cells in TNF-α-Induced Osteoclast Formation

Author(s):  
Hideki Kitaura ◽  
Tomo Aonuma ◽  
Emiko Fukumoto ◽  
Keisuke Kimura ◽  
Toshiya Fujii ◽  
...  
2011 ◽  
Vol 89 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Hideki Kitaura ◽  
Yuji Fujimura ◽  
Masako Yoshimatsu ◽  
Haruka Kohara ◽  
Yukiko Morita ◽  
...  

2006 ◽  
Vol 107 (1) ◽  
pp. 22-31 ◽  
Author(s):  
Hideki Kitaura ◽  
Mutsuhito Tatamiya ◽  
Noriko Nagata ◽  
Yuji Fujimura ◽  
Toshiko Eguchi ◽  
...  

2002 ◽  
Vol 169 (9) ◽  
pp. 4732-4738 ◽  
Author(s):  
Hideki Kitaura ◽  
Noriko Nagata ◽  
Yuji Fujimura ◽  
Hitoshi Hotokezaka ◽  
Noriaki Yoshida ◽  
...  

2013 ◽  
Vol 83 (1) ◽  
pp. 26-35 ◽  
Author(s):  
Luciana Simão Carmo ◽  
Marcelo Macedo Rogero ◽  
Mayara Cortez ◽  
Monica Yamada ◽  
Patrícia Silva Jacob ◽  
...  

An excessive consumption of a high-fat diet (HFD) results in becoming overweight or obese, which triggers a chronic inflammatory condition that is associated with a high white blood cell count. Because of the potential for yerba maté (Ilex paraguariensis) (YM) to impact obesity, this study aimed to investigate the effects of YM consumption on the hematological response and on the production of interleukin (IL)-1α, IL-6, tumor necrosis factor (TNF)-α, and IL-10 by bone marrow cells from Wistar rats fed a HFD. Male Wistar rats were fed a control (CON) or HFD diet for twelve weeks. At the end of this period, the rats received YM (1 g/kg/day body weight) for 4 weeks. After euthanasia, hemograms and myelograms were evaluated, while the bone marrow cells were cultured in the presence or absence of lipopolysaccharide (LPS) to evaluate the production of IL-1α, IL-6, TNF-α, and IL-10. The consumption of YM reduced the body weight, the body adiposity, and the cholesterol levels in HFD-fed rats. Bone marrow cells from the HFD group produced more IL-1α, IL-6, and TNF-α, and less IL-10, when compared to cells from the control group, and YM consumption reduced the IL-1α, IL-6, and TNF-α production by the cells. However, cells from the HFD rats that were stimulated with LPS increased their IL-1α, IL-6, and TNF-α production, but YM consumption did not change this result. In summary, the consumption of YM affects the production of IL-1α, IL-6, and TNF-α by bone marrow cells, promotes weight loss, decreases the number of white blood cells, and significantly improves serum cholesterol level in HFD-fed rats. However, the bone marrow cells from the HFD+YM-fed rats challenged with LPS did not show improvement in the inflammatory response compared to the cells from animals fed only a HFD that were also challenged with LPS.


2003 ◽  
Vol 197 (8) ◽  
pp. 1029-1035 ◽  
Author(s):  
Reimi Kawaida ◽  
Toshiaki Ohtsuka ◽  
Junichi Okutsu ◽  
Tohru Takahashi ◽  
Yuho Kadono ◽  
...  

Osteoclasts are multinucleated cells that resorb bones, and are derived from hematopoietic cells of the monocyte/macrophage lineage. The receptor activator of NF-κB ligand (RANKL, also called ODF/TRANCE/OPGL) stimulates both osteoclast differentiation from osteoclast progenitors and activation of mature osteoclasts. To identify genes responsible for osteoclast differentiation, we used a molecular indexing technique. Here, we report a clone of one of these genes whose transcription is induced by soluble RANKL (sRANKL) in both the RAW264.7 cells of the mouse macrophage cell line and the mouse primary bone marrow cells. The predicted protein was found to be a mouse homologue of Jun dimerization protein 2 (JDP2), a member of the AP-1 family of transcription factors, containing a basic region-leucine zipper motif. Transient transfection experiments revealed that overexpression of JDP2 leads to activation of both tartrate-resistant acid phosphatase (TRAP) and cathepsin K gene promoters in RAW264.7 cells. Infection of mouse primary bone marrow cells with retroviruses expressing JDP2-facilitated sRANKL-mediated formation of TRAP-positive multinuclear osteoclasts. Importantly, antisense oligonucleotide to JDP2 strongly suppressed sRANKL-induced osteoclast formation of RAW264.7 cells. Our findings suggest that JDP2 may play an important role in the RANK-mediated signal transduction system, especially in osteoclast differentiation.


2004 ◽  
Vol 89-90 ◽  
pp. 331-334 ◽  
Author(s):  
Seiichi Ishizuka ◽  
Noriyoshi Kurihara ◽  
Daishiro Miura ◽  
Kazuya Takenouchi ◽  
Jillian Cornish ◽  
...  

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4239-4239
Author(s):  
Mamta Gupta ◽  
Shiv K. Gupta ◽  
Arthur G. Balliet ◽  
Barbara Hoffman ◽  
Dan A. Lieberman

Abstract GADD45 (Growth arrest and DNA damge) regulates cell growth following exposure to diverse stimuli. It has been shown that, mice lacking the gadd45a gene exhibit genomic instability and increased carcinogenesis, but the exact role of the gadd45 family genes still remains unclear. In this study we have aimed at determining the effect of gadd45a or gadd45b deficiency on the response of bone marrow derived myeloid cells to genotoxic stress agents by using gadd45a or gadd45b null mice. We have found that myeloid progenitor cells from gadd45a or gadd45b-null mice are more sensitive to ultraviolet-radiation (UV), VP-16 or daunorubicin induced apoptosis. Introduction of wild-type gadd45 into gadd45-deficient bone marrow cells restored the wild-type apoptotic phenotype. In-vitro colony formation following stress responses has shown that bone marrow cells from gadd45a or gadd45b-deficient mice have a decreased ability to form haematopoetic colonies. Gadd45a or gadd45b-deficient bone marrow cells also displayed defective G2/M cell cycle checkpoint following exposure to either UV and V-16 but were still able to undergo G2/M arrest following exposure to daunorubicin, indicating the existence of different G2/M checkpoints in response to these anticancer agents. Taken together these findings identify gadd45a or gadd45b as anti-apoptotic gene(s), and suggests that the absence of gadd45a or gadd45b results in higher susceptibility of haematopoetic cells to UV radiation and certain anticancer drugs.


Sign in / Sign up

Export Citation Format

Share Document