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3 edition of Senescence in normal and DMD myoblasts found in the catalog.

Senescence in normal and DMD myoblasts

Mark Ashford Mahabir

Senescence in normal and DMD myoblasts

by Mark Ashford Mahabir

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Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

Thesis (M.Sc.) -- University of Toronto, 2001.

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative. --
ID Numbers
Open LibraryOL19082207M
ISBN 100612588351

  However, the encouraging results obtained by grafting mouse myoblasts into the mdx mouse model, 5 translated into several clinical trial failures with DMD patients. These clinical failures are ultimately due to intrinsic differences between mouse and human myoblasts in their proliferative capacities, 10 and thus the scalability of human. 6% of DMD myoblasts had a liCe-span of 50 doublings in tissue culture, and by age 7 DMD myoblasts capable of 10 doublings were rare. Our results suggest that the myoblast:~ (satellite cells) of even the youngest DMD patients have undergone extensive division in .

samples comprising primary myoblasts and their corre-sponding immortalized clones in both differentiated and undifferentiated states (average of 4 cell culture repli-cates each) from 5 human subjects (Table 1; 2 healthy and 3 with Duchenne muscular dystrophy—DMD), to-gether with primary populations of non-myogenic. However, transplantation of autologous myoblasts with genetic manipulations may be potentially limited due to gradual senescence of myogenic cells in ageing patients. Interestingly, a decline in replicative capacity was observed with increasing donor age, and was accelerated in DMD myoblasts as compared to control myoblasts [32].

Normal cells in culture display a limited capacity to divide and reach a non-proliferative state called cellular senescence. Spontaneous escape from senescence resulting in an indefinite life span is an exceptionally rare event for normal human cells and viral oncoproteins have been shown to extend the replicative life span but not to immortalize them.   Transplantation of Myoblasts to Duchenne Muscular Dystrophy (DMD) Patients The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government.


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Senescence in normal and DMD myoblasts by Mark Ashford Mahabir Download PDF EPUB FB2

Senescence in Normal Senescence in normal and DMD myoblasts book DMD Myoblasts Master of Science 1 Mark -4shford Mahabir Graduate Department of Mrdical Biophysics University of Toronto Abstract Progressive muscle wasting in Duchennr muscular dystrophy (DMD) may be due to repeated cycles of muscle damage and regeneration leading to senescence of satellite cells in patient muscle.

Myoblasts from muscle biopsy of Duchenne muscular dystrophy patients (DMD) when cultured in vitro generally exhibit a strictly limited proliferative life span and enter rapidly into senescence Cited by:   It is known that primary DM myoblasts do not show evident morphological abnormalities and are capable of normally differentiating; 43,51,52 however, we have recently observed that DM2 myoblasts are characterized by senescence related features mainly consisting in the early appearance of cytological alterations and impairment of the pre-mRNA Cited by:   Experimental Cell Research () Myoblast Senescence in Muscular Dystrophy WOODRING E.

WRIGHT Department of Cell Biology and Internal Medicine, University of Texas Health Science Center at Dallas, Dallas, TXUSA The limited proliferative capacity of normal diploid cells predicts that the utilization of cell divisions in vivo should reduce the lifespan of Cited by:   Analysis of transduced DMD myoblasts by RT-PCR revealed an apparent higher level of skipping for some exons compared to the level observed in normal myoblasts (Figure 3b), which has been previously described.

13 Exons 52 and 53 skipping could be detected on a DMD background, and exon 47 skipping levels appeared a little bit higher, although 47 Cited by: Desmin expression of (a) DMD-Tag-hTERT myoblasts and (c) DMD-Tag myoblasts.

Antigen expression of (b) DMD-Tag-hTERT and (d) DMD-Tag myoblasts (original magnification ´).For each marker, cells. the effects of replicative senescence on the myogenic programme of human myoblasts.

Human satellite cells have been aged in vitro in order to dissociate the effects of the proliferative aging from those due to the environment.

We demonstrate that senescent myoblasts are still able to differentiate and form. CiteSeerX - Document Details (Isaac Councill, Lee Giles, Pradeep Teregowda): paper or electronic formats.

The author retains ownership of the copyright in this thesis. Neither the thesis nor substantial extracts fiom it may be printed or othemise reproduced without the author's permission.

L'auteur a accordé une Licence non exclusive permettant à la Bibliothèque nationale du Canada de. In Duchenne muscular dystrophy (DMD) patients, absence of dystrophin causes muscle wasting by impacting both the myofiber integrity and the properties of muscle stem cells (MuSCs).

Investigation of DMD encompasses the use of MuSCs issued from human skeletal muscle. However, DMD-derived MuSC usage is restricted by the limited number of divisions that human MuSCs can undertake in vitro. Analysis of transduced DMD myoblasts by RT-PCR revealed an apparent higher level of skipping for some exons compared to the level observed in normal myoblasts, which has been previously described.

13 Exons 52 and 53 skipping could be detected on a DMD background, and exon 47 skipping levels appeared a little bit higher, although 47 is an in. Gene delivery by transplantation of normal myoblasts has been proposed as a treatment of the primary defect, lack of the muscle protein dystrophin, that causes Duchenne muscular dystrophy (DMD), a.

Dahlqvist et al. previously demonstrated in immortalized mouse myoblasts (C2C12) that BMP4 has an inhibitory effect on muscle differentiation (Dahlqvist et al., ).To determine if this also holds true in primary human myoblast cultures and to study if systematic differences between healthy and DMD cells are present, we added recombinant BMP4 to the cell cultures.

University lecture book in Hungarian. 1st edition2nd, revised edition dystrophin-negative muscle cell line established from the mdx mouse model of DMD but not in normal myoblasts. The maintenance of proteome integrity is of primary importance in post-mitotic tissues such as muscle cells; thus, protein quality control mechanisms must be carefully regulated to ensure their optimal efficiency, a failure of these processes being associated with various muscular disorders.

Duchenne muscular dystrophy (DMD) is one of the most common and severe forms of muscular dystrophies. Five billion normal myoblasts were injected into each of 21 Duchenne muscular dystrophy (DMD) boys aged yr to assess the feasibility, safety, and efficacy of the Phase II myoblast transfer.

Defective myoblasts identified in Duchenne muscular dystrophy. Proceedings of the National Academy of Sciences of the United States of America.

; – [PMC free article] Bockhold KJ, Rosenblatt JD, Partridge TA. Aging normal and dystrophic mouse muscle: analysis of myogenicity in cultures of living single fibers. Muscle & nerve. Myoblast transfer therapy (MTT) was proposed in the 70's as a potential treatment for muscular dystrophies, based upon the early results obtained in mdx mice: dystrophin expression was restored in this model by intramuscular injections of normal myoblasts.

These results were quickly followed by clin. Journals & Books; Help 7 JunePages Regular Article. Transplantation of Normal and DMD Myoblasts Expressing the Telomerase Gene in SCID Mice.

H.M. BlauAccelerated age-related decline in replicative life-span of Duchenne muscular dystrophy myoblasts: Implications for cell and gene therapy. Somat. Cell Mol. Genet., 16 ( As a consequence of cellular senescence induced by hyperphosphatemia, cultured myoblasts lose their proliferative capacity and this phenomenon has been related to the development of sarcopenia.

In this regard, it has been described that myostatin and activin, which are linked to sarcopenia, are also inhibitors of the myoblasts proliferation [ 58 ]. Overview of Research in DMD II: Experimental Studies. Abstracts from 10th International Congress of World Muscle Society - 28 September to 1 October/ Foz do Iguassu Brazil.

T.P A new original compound, which inhibits calpain and reactive oxygen species, reduces the dystrophic progression of. Duchenne muscular dystrophy (DMD) is the most common, affect‐ Unlike primary rodent myoblasts, primary human myoblasts rapidly show senescence in vitro.

This limitation is manifested as progressively compromised differentiation and proliferation po‐ while maintaining a normal karyotype,15 However. Unlike normal, non-cancerous cells, inducing senescence in cancer cells is advantageous to limiting growth. Although, limiting the proliferative potential, promoting senescence, and/or reducing metabolic flexibility of skeletal muscle cells can be detrimental to adaptation and growth (Machida and Booth,Nehlin et al.,Rathbone et.Gussoni E, Pavlath G, Lanctot AM, et al.

Normal dystrophin transcripts detected in Duchenne muscular dystrophy patients after myoblast transplantation. Nature ; - Crossref.