Share This Author
Connective tissue cells expressing fibro/adipogenic progenitor markers increase under chronic damage: relevance in fibroblast-myofibroblast differentiation and skeletal muscle fibrosis
- Osvaldo Contreras, D. Rebolledo, J. E. Oyarzún, H. Olguín, E. Brandan
- Biology, MedicineCell and Tissue Research
- 7 January 2016
It is shown that cells positive for Tcf4 and PDGFR-α are expressed in skeletal muscle under normal conditions and are increased in various skeletal muscles of mdx mice, a murine model for DMD, wild type muscle after sciatic denervation and muscle subjected to chronic damage.
ALS skeletal muscle shows enhanced TGF-β signaling, fibrosis and induction of fibro/adipogenic progenitor markers
- D. Gonzalez, Osvaldo Contreras, D. Rebolledo, J. Espinoza, B. van Zundert, E. Brandan
- BiologyPloS one
- 16 May 2017
Evidence is presented that fibrosis observed in skeletal muscle of symptomatic hSOD1G93A mice is accompanied with an induction of TGF-β signaling, and also that FAPs might be involved in triggering a fibrotic response and the targeting of pro-fibrotic factors might be a suitable therapeutic approach to improve muscle function in several degenerative diseases.
Copper Reduces Aβ Oligomeric Species and Ameliorates Neuromuscular Synaptic Defects in a C. elegans Model of Inclusion Body Myositis
- D. Rebolledo, R. Aldunate, R. Kohn, I. Neira, A. Minniti, N. Inestrosa
- BiologyThe Journal of Neuroscience
- 13 July 2011
The results indicate that copper modulates Aβ-induced pathology and suggest that Aβ oligomers are triggering neuromuscular dysfunction, and the relevance of modulating the amyloidogenic component as an alternative therapeutic approach for this debilitating disease is emphasized.
The inhibition of CTGF/CCN2 activity improves muscle and locomotor function in a murine ALS model
Results reveal that CTGF/CCN2 might be a novel therapeutic target to ameliorate symptoms and improve the quality of life of ALS patients.
ACE2 Is Augmented in Dystrophic Skeletal Muscle and Plays a Role in Decreasing Associated Fibrosis
First evidence supporting ACE2 as an important therapeutic target to improve the dystrophic skeletal muscle phenotype is found, in wild type and mdx skeletal muscle and in a model of induced chronic damage in wt mice.
Intracellular amyloid formation in muscle cells of Aβ-transgenic Caenorhabditis elegans: determinants and physiological role in copper detoxification
It is found that intracellular Aβ aggregation in muscle cells of Caenorhabditis elegans overexpressing Aβ peptide is affected by two single amino acid substitutions, E22G (Arctic) and V18A (NIC).
Sarcolemmal targeting of nNOSμ improves contractile function of mdx muscle.
The expression of NOS-M in skeletal muscle may be therapeutically beneficial in DMD and other muscle diseases characterized by the loss of nNOSμ from the sarcolemma, and significantly attenuates force loss owing to damaging eccentric contractions and repetitive isometric contractions, while also improving force recovery after fatigue.
Denervation-induced skeletal muscle fibrosis is mediated by CTGF/CCN2 independently of TGF-β.
Role of hypoxia in skeletal muscle fibrosis: Synergism between hypoxia and TGF-β signaling upregulates CCN2/CTGF expression specifically in muscle fibers.
Inclusion Body Myositis: A View from the Caenorhabditis elegans Muscle
- D. Rebolledo, A. Minniti, P. Grez, R. Fadić, R. Kohn, N. Inestrosa
- BiologyMolecular Neurobiology
- 5 September 2008
Evidence that supports the use of Caenorhabditis elegans as a biological model for IBM is reviewed, which hypothesize that the great degree of similarity between nematode and human genes known to be involved in IBM as well as the considerable conservation of biological mechanisms across species is an important feature that must be taken into consideration when deciding on theUse of this nematodes as a model.