Exogenous Pleiotrophin Applied to Lesioned Nerve Impairs Muscle Reinnervation

Blondet, Brigitte; Carpentier, Gilles; Ferry, Arnaud; Courty, José

doi:10.1007/s11064-006-9095-x

Cited by 22 publications

(14 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Gastrocnemius and soleus muscles were evaluated by the measurement of in situ isometric muscle contraction in response to nerve stimulation, as described previously (4). Mice were anesthetized using a pentobarbital solution (60 mg/kg ip), and supplemental doses were given as required to maintain deep anesthesia during experiments.…”

Section: Muscle Contractile Propertiesmentioning

confidence: 99%

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

Britto

Begue

Rossano

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

Self Cite

103

View full text Add to dashboard Cite

Ferry A, Bonnieu A, Ollendorff V, Favier FB. REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy. Am J Physiol Endocrinol Metab 307: E983-E993, 2014. First published October 14, 2014 doi:10.1152/ajpendo.00234.2014.-REDD1 (regulated in development and DNA damage response 1) has been proposed to inhibit the mechanistic target of rapamycin complex 1 (mTORC1) during in vitro hypoxia. REDD1 expression is low under basal conditions but is highly increased in response to several catabolic stresses, like hypoxia and glucocorticoids. However, REDD1 function seems to be tissue and stress dependent, and its role in skeletal muscle in vivo has been poorly characterized. Here, we investigated the effect of REDD1 deletion on skeletal muscle mass, protein synthesis, proteolysis, and mTORC1 signaling pathway under basal conditions and after glucocorticoid administration. Whereas skeletal muscle mass and typology were unchanged between wildtype (WT) and REDD1-null mice, oral gavage with dexamethasone (DEX) for 7 days reduced tibialis anterior and gastrocnemius muscle weights as well as tibialis anterior fiber size only in WT. Similarly, REDD1 deletion prevented the inhibition of protein synthesis and mTORC1 activity (assessed by S6, 4E-BP1, and ULK1 phosphorylation) observed in gastrocnemius muscle of WT mice following single DEX administration for 5 h. However, our results suggest that REDD1-mediated inhibition of mTORC1 in skeletal muscle is not related to the modulation of the binding between TSC2 and 14-3-3. In contrast, our data highlight a new mechanism involved in mTORC1 inhibition linking REDD1, Akt, and PRAS40. Altogether, these results demonstrated in vivo that REDD1 is required for glucocorticoidinduced inhibition of protein synthesis via mTORC1 downregulation. Inhibition of REDD1 may thus be a strategy to limit muscle loss in glucocorticoid-mediated atrophy. regulated in development and DNA damage response 1; protein synthesis; mechanistic target of rapamycin; autophagy; glucocorticoids; proline-rich Akt substrate of 40 kDa

show abstract

Section: Muscle Contractile Propertiesmentioning

confidence: 99%

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

Britto

Begue

Rossano

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

Self Cite

103

View full text Add to dashboard Cite

show abstract

“…Positive terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) cells were automatically counted by a program detecting the maximum of Sobel's gradients, as previously described (25).…”

Section: Tissue Preparation and Apoptosis Assaymentioning

confidence: 99%

A Simple Approach to Cancer Therapy Afforded by Multivalent Pseudopeptides That Target Cell-Surface Nucleoproteins

et al. 2011

Self Cite

View full text Add to dashboard Cite

Recent studies have implicated the involvement of cell surface forms of nucleolin in tumor growth. In this study, we investigated whether a synthetic ligand of cell-surface nucleolin known as N6L could exert antitumor activity. We found that N6L inhibits the anchorage-dependent and independent growth of tumor cell lines and that it also hampers angiogenesis. Additionally, we found that N6L is a proapoptotic molecule that increases Annexin V staining and caspase-3/7 activity in vitro and DNA fragmentation in vivo. Through affinity isolation experiments and mass-spectrometry analysis, we also identified nucleophosmin as a new N6L target. Notably, in mouse xenograft models, N6L administration inhibited human tumor growth. Biodistribution studies carried out in tumor-bearing mice indicated that following administration N6L rapidly localizes to tumor tissue, consistent with its observed antitumor effects. Our findings define N6L as a novel anticancer drug candidate warranting further investigation. Cancer Res; 71(9); 3296-305. Ó2011 AACR.

show abstract

“…Image processing and analysis were done using the ImageJ software (National Institutes of Health) (17). Nuclei labeling was quantified as described previously using ImageJ (18).…”

Section: Matrigel Plug Assay and Vegfr-2-expressing Cell Staining-liquidmentioning

confidence: 99%

Age-related Changes in Rat Myocardium Involve Altered Capacities of Glycosaminoglycans to Potentiate Growth Factor Functions and Heparan Sulfate-altered Sulfation

Huynh

Morin

Carpentier

et al. 2012

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

Background: Heparan sulfates (HS) are important cell behavior regulators. Results: With age, HS structural changes affect myocardial growth factor functionalities. Conclusion: This reveals the importance of HS on the control of essential tissue repair effectors during aging. Significance: Changes in cardiac HS may alter tissue homeostasis and impair heart function. This might also limit the success of protein therapies and implantation of therapeutic cells.

show abstract

Exogenous Pleiotrophin Applied to Lesioned Nerve Impairs Muscle Reinnervation

Cited by 22 publications

References 25 publications

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

REDD1 deletion prevents dexamethasone-induced skeletal muscle atrophy

A Simple Approach to Cancer Therapy Afforded by Multivalent Pseudopeptides That Target Cell-Surface Nucleoproteins

Age-related Changes in Rat Myocardium Involve Altered Capacities of Glycosaminoglycans to Potentiate Growth Factor Functions and Heparan Sulfate-altered Sulfation

Contact Info

Product

Resources

About