Tumor necrosis factor alpha is associated with disease activity and the degree of anemia in patients with rheumatoid arthritis

Vreugdenhil, Gerard; Löwenberg, Bob; Eijk, H.G. Van; Swaak, A. J. G.

doi:10.1111/j.1365-2362.1992.tb01495.x

Cited by 75 publications

(56 citation statements)

References 36 publications

(20 reference statements)

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“…Opposing effects of TNF-␣ at different concentrations have been observed previously in skeletal (Alvarez et al, 2001) and cardiac muscle (Mann, 2003). The 10-20 ng/ml of TNF-␣ used in the above referenced studies exceed even the pathological levels seen in severe inflammatory diseases (Vreugdenhil et al, 1992;Nakashima et al, 1995). Effect of TNF-␣ at these levels cannot be considered physiological.…”

Section: Journal Of Cell Science 120 (4)mentioning

confidence: 74%

“…We have observed that the addition of 0.05 ng/ml of recombinant TNF-␣ to differentiation medium, which simulates the raised TNF-␣ level in injured muscle, stimulates myogenesis in myoblasts. However, at 0.5 or 5 ng/ml [levels seen in inflammatory diseases (Vreugdenhil et al, 1992;Nakashima et al, 1995)] TNF-␣ inhibits myogenesis (Chen et al, 2007). As a pleiotropic cytokine, TNF-␣ is known to exert divergent actions depending on concentration.…”

Section: Journal Of Cell Science 120 (4)mentioning

confidence: 99%

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TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Zhan

Jin

Chen

et al. 2007

Journal of Cell Science

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manner. Stretch stimulated the cleavage activity of TACE. Conversely, TACE inhibitor TAPI or TACE siRNA abolished stretch activation of p38. In addition, conditioned medium from stretched myoblast cultures activated p38 in unstretched myoblasts, which required TACE activity in the donor myoblasts, and TNF-␣ receptors in the recipient myoblasts. These results indicate that posttranscriptional activation of TACE mediates the mechanotransduction that activates p38-dependent myogenesis via the release of TNF-␣.

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Section: Journal Of Cell Science 120 (4)mentioning

confidence: 74%

Section: Journal Of Cell Science 120 (4)mentioning

confidence: 99%

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Zhan

Jin

Chen

et al. 2007

Journal of Cell Science

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“…That is, the lowserum-differentiation media were supplemented with TNF-␣ each day it was replaced. This is approximately the concentration of TNF-␣ seen in different pathological conditions (Vreugdenhil et al, 1992;Chen et al, 2004). For clarity, data are expressed as a ratio of the fusion index of the stressed cell group to the unstressed cell group, termed fusion index (FI) ratio.…”

mentioning

confidence: 99%

Antioxidant Levels Represent a Major Determinant in the Regenerative Capacity of Muscle Stem Cells

Urish

Vella

Okada³

et al. 2009

MBoC

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Stem cells are classically defined by their multipotent, long-term proliferation, and self-renewal capabilities. Here, we show that increased antioxidant capacity represents an additional functional characteristic of muscle-derived stem cells (MDSCs). Seeking to understand the superior regenerative capacity of MDSCs compared with myoblasts in cardiac and skeletal muscle transplantation, our group hypothesized that survival of the oxidative and inflammatory stress inherent to transplantation may play an important role. Evidence of increased enzymatic and nonenzymatic antioxidant capacity of MDSCs were observed in terms of higher levels of superoxide dismutase and glutathione, which appears to confer a differentiation and survival advantage. Further when glutathione levels of the MDSCs are lowered to that of myoblasts, the transplantation advantage of MDSCs over myoblasts is lost when transplanted into both skeletal and cardiac muscles. These findings elucidate an important cause for the superior regenerative capacity of MDSCs, and provide functional evidence for the emerging role of antioxidant capacity as a critical property for MDSC survival post-transplantation. INTRODUCTIONMyogenic cell transplantation has been proposed as a promising therapeutic approach in the treatment of skeletal and cardiac muscle injury. Early studies of myoblast transplantation into dystrophic skeletal muscle yielded limited regeneration of dystrophin-expressing muscle fibers (Beauchamp et al., 1994;Gussoni et al., 1997;Qu-Petersen et al., 2002). Similarly, given the limited regenerative ability of cardiac muscle, cell transplantation has been proposed as an alternative to heart transplantation (Assmus et al., 2006;Lunde et al., 2006;Schachinger et al., 2006).A major obstacle in both cardiac and skeletal myogenic therapies is the poor rate of engraftment of myogenic cells after transplantation (Taylor et al., 1998;Oshima et al., 2005). In skeletal muscle, numerous groups have observed a rapid inflammatory response that appears to contribute to rapid cell loss and limit therapeutic success (Beauchamp et al., 1994;Gussoni et al., 1997;Beauchamp et al., 1999). Multiple groups have postulated that the small number of injected cells that survive transplantation in both cardiac and skeletal muscle may represent a special subpopulation of stem-like cells (Qu et al., 1998;Beauchamp et al., 1999;Qu-Petersen et al., 2002).For these reasons, our group attempted to isolate this putative subpopulation of cells using a modified preplate technique. This procedure was initially developed to purify myoblasts from nonmyogenic cells, including fibroblasts, of whole tissue preparations based on the differential adhesion characteristics of the cells to a collagen coated flask (Rando and Blau, 1994). Our group modified this technique to isolate various populations of myogenic cells, including a population of early adhering preplate (EP) cells and a late adhering preplate (LP) cell population from which a subpopulation of long-term proliferating (LTP) cells,...

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“…Adenoviruses can sometimes cause a severe multisystem or septic shock-like disease and it was found that increased IL-6, IL-8, and TNF-a levels were associated with decreased perfusion, febrile peaks, tonic clonic seizures, and septic shock in children with adenoviral infection [6]. TNF-a has also been found to be elevated in the plasma of active rheumatoid arthritis pediatric patients [7], and the highest levels were found in correlation with anemia in rheumatoid arthritis [8].…”

mentioning

confidence: 96%

Tumor Necrosis Factor-α in Children with Human Immunodeficiency Virus Infection

Levy¹,

Danon²

1995

Pediatric Hematology and Oncology

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Tumor necrosis factor alpha is associated with disease activity and the degree of anemia in patients with rheumatoid arthritis

Cited by 75 publications

References 36 publications

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

TACE release of TNF-α mediates mechanotransduction-induced activation of p38 MAPK and myogenesis

Antioxidant Levels Represent a Major Determinant in the Regenerative Capacity of Muscle Stem Cells

Tumor Necrosis Factor-α in Children with Human Immunodeficiency Virus Infection

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