Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Basma F. Benabdallah is active.

Publication


Featured researches published by Basma F. Benabdallah.


Cell Transplantation | 2008

Inhibiting myostatin with follistatin improves the success of myoblast transplantation in dystrophic mice.

Basma F. Benabdallah; Manaf Bouchentouf; Pascal Bigey; Annick Michaud; Pierre Chapdelaine; Daniel Scherman; Jacques P. Tremblay

Duchenne muscular dystrophy is a recessive disease due to a mutation in the dystrophin gene. Myoblast transplantation permits to introduce the dystrophin gene in dystrophic muscle fibers. However, the success of this approach is reduced by the short duration of the regeneration following the transplantation, which reduces the number of hybrid fibers. Our aim was to verify whether the success of the myoblast transplantation is enhanced by blocking the myostatin signal with an antagonist, follistatin. Three different approaches were studied to overexpress follistatin in the muscles of mdx mice transplanted with myoblasts. First, transgenic follistatin/mdx mice were generated; second, a follistatin plasmid was electroporated in mdx muscles, and finally, follistatin was induced in mdx mice muscles by a treatment with a histone deacetylase inhibitor. The three approaches improved the success of the myoblast transplantation. Moreover, fiber hypertrophy was also observed in all muscles, demonstrating that myostatin inhibition by follistatin is a good method to improve myoblast transplantation and muscle function. Myostatin inhibition by follistatin in combination with myoblast transplantation is thus a promising novel therapeutic approach for the treatment of muscle wasting in diseases such as Duchenne muscular dystrophy.


Cell Transplantation | 2009

Overexpression of Follistatin in Human Myoblasts Increases Their Proliferation and Differentiation, and Improves the Graft Success in SCID Mice:

Basma F. Benabdallah; Manaf Bouchentouf; Jacques P. Tremblay

Duchenne muscular dystrophy is caused by the absence of functional dystrophin, leading to the myofiber membrane instability and progressive muscle atrophy. Myoblast transplantation in dystrophic muscles is a potential therapy, as it permits the long-term restoration of dystrophin expression in transplanted muscles. However, the success of this approach is limited by the short period of muscle repair following myoblast transplantation. Myostatin, a powerful inhibitor of muscle growth, is involved in terminating the period of muscle repair following injury by reducing myoblast proliferation and differentiation. Follistatin forms a complex with myostatin, preventing its interaction with its receptor and thus blocking the myostatin signal. Here, we used a lentivirus to overexpress the follistatin protein in normal myoblasts to block the myostatin signaling. We measured the potential of transduced myoblasts to proliferate and to form multinucleated myotubes in vitro. And finally, we considered the engraftment success of those transduced myoblasts in comparison with control cells in vivo within SCID mice TA muscle. Our results first confirmed the overexpression of follistatin into lentivirus transduced myoblasts, and second showed that the overexpression of the follistatin in normal human myoblasts improved in vitro their proliferation rate by about 1.5-fold after 96 h and also their differentiation rate by about 1.6- and 1.8-fold, respectively, in the absence and in the presence of recombinant myostatin. Finally, our data demonstrated that the engraftment of human normal myoblasts overexpressing the follistatin protein into SCID mouse muscles was enhanced by twofold.


Molecular therapy. Nucleic acids | 2013

Targeted Gene Addition of Microdystrophin in Mice Skeletal Muscle via Human Myoblast Transplantation

Basma F. Benabdallah; Arnaud Duval; Pierre Chapdelaine; Michael C. Holmes; Eli Haddad; Jacques P. Tremblay; Christian M. Beauséjour

Zinc finger nucleases (ZFN) can facilitate targeted gene addition to the genome while minimizing the risks of insertional mutagenesis. Here, we used a previously characterized ZFN pair targeting the chemokine (C-C motif) receptor 5 (CCR5) locus to introduce, as a proof of concept, the enhanced green fluorescent protein (eGFP) or the microdystrophin genes into human myoblasts. Using integrase-defective lentiviral vectors (IDLVs) and chimeric adenoviral vectors to transiently deliver template DNA and ZFN respectively, we achieved up to 40% targeted gene addition in human myoblasts. When the O6-methylguanine-DNA methyltransferaseP140K gene was co-introduced with eGFP, the frequency of cells with targeted integration could be increased to over 90% after drug selection. Importantly, gene-targeted myoblasts retained their mitogenic activity and potential to form myotubes both in vitro and in vivo when injected into the tibialis anterior of immune-deficient mice. Altogether, our results could lead to the development of improved cell therapy transplantation protocols for muscular diseases.


Stem Cells and Development | 2013

A soluble granulocyte colony stimulating factor decoy receptor as a novel tool to increase hematopoietic cell homing and reconstitution in mice.

Audrey Fortin; Basma F. Benabdallah; Lina Palacio; Cynthia L. Carbonneau; Oanh Nl Le; Elie Haddad; Christian M. Beauséjour

The relative ineffectiveness of hematopoietic stem cells in reaching the bone marrow upon transplantation combined with the limited number of these cells available is a major reason for graft failure and delayed hematopoietic recovery. Hence, the development of strategies that could enhance homing is of high interest. Here, we provide evidence that homing is severely impaired postexposure to ionizing radiation (IR) in mice, an effect we found was time dependent and could be partially rescued using mesenchymal stromal cell (MSC) therapy. In an attempt to further increase homing, we took advantage of our observation that the granulocyte colony stimulating factor (G-CSF), a cytokine known to induce cell mobilization, is increased in the marrow of mice shortly after their exposure to IR. As such, we developed a truncated, yet functional, soluble G-CSF receptor (solG-CSFR), which we hypothesized could act as a decoy and foster homing. Using MSCs or conditioned media as delivery vehicles, we show that an engineered solG-CSFR has the potential to increase homing and hematopoietic reconstitution in mice. Altogether, our results provide novel findings at the interplay of IR and stromal cell therapy and present the regulation of endogenous G-CSF as an innovative proof-of-concept strategy to manipulate hematopoietic cell homing.


Cytotherapy | 2014

Heterotopic bone formation derived from multipotent stromal cells is not inhibited in aged mice

Cynthia L. Carbonneau; Geneviève Despars; Gaël Moquin Beaudry; Basma F. Benabdallah; Saadallah Bouhanik; Josée Dépôt; Alain Moreau; Christian M. Beauséjour

BACKGROUND AIMS Decreased bone formation with age is believed to arise, at least in part, because of the influence of the senescent microenvironment. In this context, it is unclear whether multipotent stromal cell (MSC)-based therapies would be effective for the treatment of bone diseases. METHODS With the use of a heterotopic bone formation model, we investigated whether MSC-derived osteogenesis is impaired in aged mice compared with young mice. RESULTS We found that bone formation derived from MSCs is not reduced in aged mice. These results are supported by the unexpected finding that conditioned media collected from ionizing radiation-induced senescent MSCs can stimulate mineralization and delay osteoclastogenesis in vitro. CONCLUSIONS Overall, our results suggest that impaired bone formation with age is mainly cell-autonomous and provide a rationale for the use of MSC-based therapies for the treatment of bone diseases in the elderly.


Experimental Cell Research | 2007

A new pro-migratory activity on human myogenic precursor cells for a synthetic peptide within the E domain of the mechano growth factor

Philippe Mills; J.F. Lafreniere; Basma F. Benabdallah; E. El Fahime; Jacques-P. Tremblay


Cytotherapy | 2010

Targeted gene addition to human mesenchymal stromal cells as a cell-based plasma-soluble protein delivery platform

Basma F. Benabdallah; Emilie Allard; Shuyuan Yao; Geoffrey Friedman; Philip D. Gregory; Nicoletta Eliopoulos; Julie Fradette; Jeffrey L. Spees; Elie Haddad; Michael C. Holmes; Christian M. Beauséjour


Transplantation | 2004

Myoblast survival enhancement and transplantation success improvement by heat-shock treatment in mdx mice.

Manaf Bouchentouf; Basma F. Benabdallah; Jacques P. Tremblay


Transplantation | 2005

Improved success of myoblast transplantation in mdx mice by blocking the myostatin signal.

Basma F. Benabdallah; Manaf Bouchentouf; Jacques P. Tremblay


Biochemistry and Cell Biology | 2003

Tubulyzine , a novel tri-substituted triazine, prevents the early cell death of transplanted myogenic cells and improves transplantation success

E. El Fahime; M. Bouchentouf; Basma F. Benabdallah; D. Skuk; J.F. Lafreniere; Y.T. Chang; Jacques P. Tremblay

Collaboration


Dive into the Basma F. Benabdallah's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Elie Haddad

Université de Montréal

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Alain Moreau

Université de Montréal

View shared research outputs
Top Co-Authors

Avatar
Researchain Logo
Decentralizing Knowledge