Inhibition of myoblast differentiation by Sfrp1 and Sfrp2

Descamps, Simon; Arzouk, Hayat; Bacou, Francis; Bernardi, Henri; Fédon, Yann; Gay, Stéphanie; Reyne, Yves; Rossano, Bernadette; Levin, Jonathan M.

doi:10.1007/s00441-008-0574-z

Cited by 47 publications

(32 citation statements)

References 27 publications

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“…Although we found that PDZRN3 inhibits Wnt–β-catenin signaling during osteoblast differentiation, it might not inhibit such signaling during myogenic differentiation, given that our previous study showed that depletion of PDZRN3 inhibited myogenic differentiation without affecting the expression of myogenin (Ko et al , 2006). Wnt–β-catenin signaling is thought to promote the differentiation of myoblasts into myotubes in part by increasing the expression of myogenin (Rochat et al , 2004; Descamps et al , 2008). PDZRN3 might thus contribute to different signaling pathways during osteoblast and myogenic differentiation.…”

Section: Discussionmentioning

confidence: 99%

PDZRN3 Negatively Regulates BMP-2–induced Osteoblast Differentiation through Inhibition of Wnt Signaling

Honda

Yamamoto

Ishii

et al. 2010

MBoC

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Section: Discussionmentioning

confidence: 99%

PDZRN3 Negatively Regulates BMP-2–induced Osteoblast Differentiation through Inhibition of Wnt Signaling

Honda

Yamamoto

Ishii

et al. 2010

MBoC

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“…After 50 μM PQ was treated for 48 h, cell viability was measured using a troponin T (a muscle differentiation marker, clone JLT-12; Sigma), as described previously (38).…”

Section: Methodsmentioning

confidence: 99%

DDS, 4,4′-diaminodiphenylsulfone, extends organismic lifespan

Cho

Park

Keam

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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DDS, 4,4′-diaminodiphenylsulfone, is the most common drug prescribed to treat Hansen disease patients. In addition to its antibacterial activity, DDS has been reported to be involved in other cellular processes that occur in eukaryotic cells. Because DDS treatment significantly enhances the antioxidant activity in humans, we examined its effect on lifespan extension. Here we show that DDS extends organismic lifespan using Caenorhabditis elegans as a model system. DDS treatment caused a delay in aging and decreased the levels of a mitochondrial complex. The oxygen consumption rate was also significantly lowered. Consistent with these data, paraquat treatment evoked less reactive oxygen species in DDS-treated worms, and these worms were less sensitive to paraquat. Interestingly enough, all of the molecular events caused by DDS treatment were consistently reproduced in mice treated with DDS for 3 mo and in the C2C12 muscle cell line. Structural prediction identified pyruvate kinase (PK) as a protein target of DDS. Indeed, DDS bound and inhibited PK in vitro and inhibited it in vivo, and a PK mutation conferred extended lifespan of C. elegans. Supplement of pyruvate to the media protected C2C12 cells from apoptosis caused by paraquat. Our findings establish the significance of DDS in lowering reactive oxygen species generation and extending the lifespan, which renders the rationale to examining the possible effect of DDS on human lifespan extension.F irst synthesized a century ago, 4,4′-diaminodiphenylsulfone (DDS) is a drug still used to treat many skin diseases. Specifically, DDS is a principal drug in a multidrug regimen recommended by the World Health Organization for the treatment of leprosy (1-4). DDS acts as an antibiotic in a manner similar to sulphonamides by inhibiting bacterial synthesis of dihydrofolic acid through competition with para-aminobenzoic acid (PABA) for the active site of dihydropteroate synthetase (DHPS) (5). In addition to its antibacterial activity, DDS has been reported to be involved in other cellular processes that occur in eukaryotic cells, such as inflammation, migration, and apoptosis (6). However, there has been controversy over the issue of whether DDS acts as a pro-oxidant (especially when a higher dose of DDS is used rather than a standard dose) or antioxidant (7-9). Most studies on the pro-oxidant effects of DDS have been based on its use at high concentrations. For example, in human dermal fibroblasts, a high dose of DDS (1.5 mM) induced oxidative stress and glutathione depletion (10), but in rat livers, DDS administration at a dose of 30 mg/kg body weight resulted in oxidative stress (11). Therefore, the debate regarding the nature of DDS as a pro-oxidant or antioxidant appears to reflect the dosage effect. Another interesting observation is that Hansen disease patients in Korea, who usually have taken DDS for several decades, had a longer lifespan in spite of their socioeconomical disadvantages (12). This finding prompted us to examine whether and how DDS treatment extends an...

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“…Moreover, exposure of adipose cells to increasing 4-HNE concentrations causes biological events associated with the development of IR. In this context, 4-HNE may cause a selective impairment of insulin signaling in adipocytes by the downregulation of IRS-1 and upregulation of p38 MAPK activity, thereby leading to increased production of lactate and impaired adiponectin secretion [132][133][134]. Nonetheless, in differentiating (pre)adipocytes, oxidative stress can induce intracellular 4-HNE production, which in turn activates p38 MAPK [135].…”

Section: -Hydroxynonenalmentioning

confidence: 99%