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Article ; Online: Novel TGF-beta antagonist inhibits tumor growth and angiogenesis by inducing IL-2 receptor-driven STAT1 activation.

Penafuerte, Claudia / Bautista-Lopez, Norma / Bouchentouf, Manaf / Birman, Elena / Forner, Kathy / Galipeau, Jacques

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 12, Page(s) 6933–6944

Abstract: Carcinoma derived TGF-β acts as a potent pro-oncogenic factor and suppresses antitumor immunity. To antagonize TGF-β-mediated effects in tandem with a proinflammatory immune stimulus, we generated a chimeric protein borne of the fusion of IL-2 and the ... ...

Abstract	Carcinoma derived TGF-β acts as a potent pro-oncogenic factor and suppresses antitumor immunity. To antagonize TGF-β-mediated effects in tandem with a proinflammatory immune stimulus, we generated a chimeric protein borne of the fusion of IL-2 and the soluble extracellular domain of TGF-βR II (FIST). FIST acts as a decoy receptor trapping active TGF-β in solution and interacts with IL-2-responsive lymphoid cells, inducing a distinctive hyperactivation of STAT1 downstream of IL-2R, which in turn promotes SMAD7 overexpression. Consequently, FIST-stimulated lymphoid cells are resistant to TGF-β-mediated suppression and produce significant amounts of proinflammatory cytokines. STAT1 hyperactivation further induces significant secretion of angiostatic CXCL10. Moreover, FIST upregulates T-bet expression in NK cells promoting a potent Th1-mediated antitumor response. As a result, FIST stimulation completely inhibits pancreatic cancer (PANC02) and melanoma (B16) tumor growth in immunocompetent C57BL/6 mice. In addition, melanoma cells expressing FIST fail to form tumors in CD8(-/-), CD4(-/-), B cell-deficient (μMT), and beige mice, but not in NOD-SCID and Rag2/γc knockout mice, consistent with the pivotal role of FIST-responsive, cancer-killing NK cells in vivo. In summary, FIST constitutes a novel strategy of treating cancer that targets both the host's angiogenic and innate immune response to malignant cells.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Cell Proliferation/drug effects ; Interleukin-2 Receptor beta Subunit ; Killer Cells, Natural/immunology ; Mice ; Neoplasms/drug therapy ; Neoplasms/immunology ; Neoplasms/pathology ; Neovascularization, Pathologic/drug therapy ; Receptors, Interleukin-2/metabolism ; Recombinant Fusion Proteins/pharmacology ; Recombinant Fusion Proteins/therapeutic use ; STAT1 Transcription Factor/metabolism ; Transforming Growth Factor beta/antagonists & inhibitors ; Tumor Burden/drug effects
Chemical Substances	Antineoplastic Agents ; Interleukin-2 Receptor beta Subunit ; Receptors, Interleukin-2 ; Recombinant Fusion Proteins ; STAT1 Transcription Factor ; Stat1 protein, mouse ; Transforming Growth Factor beta
Language	English
Publishing date	2011-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1003816
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

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Article ; Online: Erythropoietin gene-enhanced marrow mesenchymal stromal cells decrease cisplatin-induced kidney injury and improve survival of allogeneic mice.

Eliopoulos, Nicoletta / Zhao, Jing / Forner, Kathy / Birman, Elena / Young, Yoon Kow / Bouchentouf, Manaf

Molecular therapy : the journal of the American Society of Gene Therapy

2011 Volume 19, Issue 11, Page(s) 2072–2083

Abstract: Bone marrow-derived mesenchymal stromal cells (MSCs) are promising for regenerative medicine applications, such as for renoprotection and repair in acute kidney injury (AKI). Erythropoietin (Epo) can also exert cytoprotective effects on various tissues ... ...

Abstract	Bone marrow-derived mesenchymal stromal cells (MSCs) are promising for regenerative medicine applications, such as for renoprotection and repair in acute kidney injury (AKI). Erythropoietin (Epo) can also exert cytoprotective effects on various tissues including the kidney. We hypothesized that MSCs gene-enhanced to secrete Epo may produce a significant beneficial effect in AKI. Mouse Epo-secreting MSCs were generated, tested in vitro, and then implanted by intraperitoneal injection in allogeneic mice previously administered cisplatin to induce AKI. Epo-MSCs significantly improved survival of implanted mice as compared to controls (67% survival versus 33% with Vehicle only). Also, Epo-MSCs led to significantly better kidney function as shown by lower levels of blood urea nitrogen (72 ± 9.5 mg/dl versus 131 ± 9.20 mg/dl) and creatinine (74 ± 17 µmol/l versus 148±19.4 µmol/l). Recipient mice also showed significantly decreased amylase and alanine aminotransferase blood concentrations. Kidney sections revealed significantly less apoptotic cells and more proliferating cells. Furthermore, PCR revealed the presence of implanted cells in recipient kidneys, with Epo-MSCs leading to significantly increased expression of Epo and of phosphorylated-Akt (Ser473) (P-Akt) in these kidneys. In conclusion, our study demonstrates that Epo gene-enhanced MSCs exert significant tissue protective effects in allogeneic mice with AKI, and supports the potential use of gene-enhanced cells as universal donors in acute injury.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/therapy ; Animals ; Bone Marrow Cells/cytology ; Cell Survival/drug effects ; Cisplatin ; Culture Media, Conditioned/pharmacology ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Erythropoietin/genetics ; Kidney/drug effects ; Kidney/metabolism ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stem Cells/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Survival Analysis ; Transduction, Genetic ; Transplantation, Homologous
Chemical Substances	Culture Media, Conditioned ; Erythropoietin (11096-26-7) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2011-08-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1038/mt.2011.162
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Zs.A 5640: Show issues

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Article ; Online: Bone marrow mesenchymal stromal cell therapy for external urethral sphincter restoration in a rat model of stress urinary incontinence.

Corcos, Jacques / Loutochin, Oleg / Campeau, Lysanne / Eliopoulos, Nicoletta / Bouchentouf, Manaf / Blok, Bertil / Galipeau, Jacques

Neurourology and urodynamics

2011 Volume 30, Issue 3, Page(s) 447–455

Abstract: Objective: To assess the effect of intra-sphincteric injections of bone marrow mesenchymal stromal cells (MSCs) on Valsalva leak point pressure (VLPP) changes in an animal model of stress urinary incontinence (SUI).: Materials and methods: Twenty- ... ...

Abstract	Objective: To assess the effect of intra-sphincteric injections of bone marrow mesenchymal stromal cells (MSCs) on Valsalva leak point pressure (VLPP) changes in an animal model of stress urinary incontinence (SUI). Materials and methods: Twenty-four female Sprague-Dawley rats underwent bilateral pudendal nerve section to induce SUI. Six rats were SUI controls, 6 received periurethral injection of Plasma-Lyte (SUI placebo control) and 12 were given periurethral injection of PKH26-labeled MSCs. Four weeks after injection, conscious cystometry was undertaken in animals and VLPP recorded. All groups were sacrificed, and frozen urethra sections were submitted to pathology and immunohistochemistry assessment. Results: Rat MSCs were positive for the cell surface antigens CD44, CD73, CD90, and RT1A, and negative for CD31, CD45, and RT1B, confirming their stem cell phenotype. In vitro, differentiated MSCs expressed α-smooth muscle actin (SMA) and desmin, markers of smooth and striated muscles in vivo. Immunohistochemistry of rat urethras revealed PKH26-labeled MSCs in situ and at the injection site. LPP was significantly improved in animals injected with MSCs. Mean LPP was 24.28 ± 1.47 cmH(2) O in rats implanted with MSCs and 16.21 ± 1.26 cmH(2) O in SUI controls (P<0.001). Atrophic urethras with implanted MSCs were positively stained for myosin heavy chain and desmin. Conclusion: Rat MSCs have the ability to differentiate and skew their phenotype towards smooth and striated muscles, as demonstrated by SMA up-regulation and desmin expression. Periurethral injection of MSCs in an animal model of SUI restored the damaged external urethral sphincter and significantly improved VLPP.
MeSH term(s)	Analysis of Variance ; Animals ; Atrophy ; Biomarkers/metabolism ; Bone Marrow Transplantation ; Cell Differentiation ; Cells, Cultured ; Disease Models, Animal ; Female ; Immunohistochemistry ; Injections ; Mesenchymal Stem Cell Transplantation ; Phenotype ; Pressure ; Rats ; Rats, Sprague-Dawley ; Regeneration ; Time Factors ; Urethra/metabolism ; Urethra/pathology ; Urethra/physiopathology ; Urethra/surgery ; Urinary Incontinence, Stress/metabolism ; Urinary Incontinence, Stress/pathology ; Urinary Incontinence, Stress/physiopathology ; Urinary Incontinence, Stress/surgery ; Urodynamics
Chemical Substances	Biomarkers
Language	English
Publishing date	2011-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604904-7
ISSN	1520-6777 ; 0733-2467
ISSN (online)	1520-6777
ISSN	0733-2467
DOI	10.1002/nau.20998
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Zs.A 1828: Show issues

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

Benabdallah, Basma F / Bouchentouf, Manaf / Tremblay, Jacques P

Transplantation

2005 Volume 79, Issue 12, Page(s) 1696–1702

Abstract: Background: : Duchenne muscular dystrophy (DMD) is caused by a dystrophin gene mutation. Transplantation of normal myoblasts results in long-term restoration of dystrophin. However, the success of this approach is compromised by the limited time of ... ...

Abstract	Background: : Duchenne muscular dystrophy (DMD) is caused by a dystrophin gene mutation. Transplantation of normal myoblasts results in long-term restoration of dystrophin. However, the success of this approach is compromised by the limited time of regeneration following muscle damage. Myostatin is known to be responsible for limiting skeletal muscle regeneration. Our purpose is to verify whether blocking the myostatin signal in mdx host mice or in normal myoblasts transplanted in mdx host mice would increase the extent of muscle repair and thus allow the formation of more dystrophin-positive fibers. Methods: : Transgenic mdx mice carrying a dominant negative form of myostatin receptor (dnActRIIB) were used to test the fiber resistance to damage and to act as a host for normal myoblast transplantation. Myoblasts obtained from nondystrophic transgenic mice carrying the dominant negative myostatin receptor were also transplanted in nontransgenic mdx mice. Results: : Transgenic mdx mice carrying the dnActRIIB gene have bigger muscles than mdx mice with the normal gene of ActRIIB. Their fiber resistance to exercise-induced damage was also greatly improved. Moreover, the success of normal myoblast transplantation was significantly enhanced in mdx/dnActRIIB mice. Finally, nondystrophic dnActRIIB myoblasts formed more abundant and bigger dystrophin positive fibers when transplanted in mdx mice. Conclusions: : Blocking the myostatin signal in mdx mice allowed the size of muscle fibers to increase, the fiber resistance to damage induced by exercise to increase, and the success of normal myoblast transplantation to improve. The transplantation in mdx mice of dnActRIIB myoblasts formed more abundant and larger dystrophin positive fibers.
MeSH term(s)	Animals ; Animals, Newborn ; Desmin ; Dystrophin/genetics ; Male ; Mice ; Mice, Inbred mdx ; Mice, Transgenic ; Muscle Fibers, Skeletal/pathology ; Muscle, Skeletal/pathology ; Muscular Dystrophy, Animal/genetics ; Muscular Dystrophy, Animal/pathology ; Mutation ; Myoblasts/transplantation ; Myostatin ; Signal Transduction ; Transforming Growth Factor beta/physiology
Chemical Substances	Desmin ; Dystrophin ; Mstn protein, mouse ; Myostatin ; Transforming Growth Factor beta
Language	English
Publishing date	2005-05-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/01.tp.0000167379.27872.2b
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Myoblast survival enhancement and transplantation success improvement by heat-shock treatment in mdx mice.

Bouchentouf, Manaf / Benabdallah, Basma F / Tremblay, Jacques P

Transplantation

2004 Volume 77, Issue 9, Page(s) 1349–1356

Abstract: Background: Duchenne muscular dystrophy is a disease caused by the incapacity to synthesize dystrophin, which is implicated in the maintenance of the sarcolemma integrity. Myoblast transplantation is a potential treatment of this disease. However, most ... ...

Abstract	Background: Duchenne muscular dystrophy is a disease caused by the incapacity to synthesize dystrophin, which is implicated in the maintenance of the sarcolemma integrity. Myoblast transplantation is a potential treatment of this disease. However, most of the transplanted cells die very rapidly after their injection. Heat-shock proteins (HSPs) are over-expressed when cells undergo various types of stresses. Our goal was thus to investigate whether the expression of HSPs (HSP70 in particular) could protect myoblasts from death after intramuscular injection. Methods: HSP70 expression was induced by warming the cells at 42 degrees C for 60 minutes. HSP70 over-expression was quantified by Western blot analysis. The in vitro effect of HSPs on cell survival was evaluated by fluorescence-activated cell sorter analysis using the Hoescht/propidium iodide-labeling technique, and their in vivo effects were investigated by transplanting TnI-LacZ myoblasts labeled with [methyl-14C] thymidine. Results: Western blots indicated a sevenfold over-expression of the HSP70 after the heat-shock treatment. In vitro, the heat-shock treatment protected 18% of the cells from staurosporine- (1 microM) induced apoptosis. HSPs also protected 10% of the cells from death induced by either tumor necrosis factor-alpha (30 ng/mL) or glucose oxydase (0.1 U/mL). In vivo, the treatment improved the cell survival by twofold 5 days after the graft and increased by fourfold the long-term graft success. Conclusions: The heat-shock treatment is a practical approach for improving the success of myoblast transplantation; in fact, using this kind of treatment, there is no need to genetically modify the cells before their transplantation.
MeSH term(s)	Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Survival ; Enzyme Inhibitors/pharmacology ; Graft Survival ; HSP70 Heat-Shock Proteins/metabolism ; Heat-Shock Response ; Mice ; Mice, Inbred C57BL ; Mice, Inbred mdx ; Muscular Dystrophy, Animal/therapy ; Muscular Dystrophy, Duchenne/therapy ; Myoblasts, Skeletal/cytology ; Myoblasts, Skeletal/metabolism ; Myoblasts, Skeletal/transplantation ; Reactive Oxygen Species/metabolism ; Staurosporine/pharmacology ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Antineoplastic Agents ; Enzyme Inhibitors ; HSP70 Heat-Shock Proteins ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha ; Staurosporine (H88EPA0A3N)
Language	English
Publishing date	2004-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208424-7
ISSN	1534-6080 ; 0041-1337
ISSN (online)	1534-6080
ISSN	0041-1337
DOI	10.1097/01.tp.0000121503.01535.f5
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Zs.A 488: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Exercise improves the success of myoblast transplantation in mdx mice.

Bouchentouf, Manaf / Benabdallah, Basma F / Mills, Philippe / Tremblay, Jacques P

Neuromuscular disorders : NMD

2006 Volume 16, Issue 8, Page(s) 518–529

Abstract: Transplantation of normal muscle precursor cells is a potential approach to restore dystrophin expression within dystrophin [deficient] mdx mice, a model of Duchenne Muscular Dystrophy. This study aims to evaluate whether exercise could improve graft ... ...

Abstract	Transplantation of normal muscle precursor cells is a potential approach to restore dystrophin expression within dystrophin [deficient] mdx mice, a model of Duchenne Muscular Dystrophy. This study aims to evaluate whether exercise could improve graft success and hybrid fiber distribution within mdx muscle. eGFP(+) Muscle precursor cells were transplanted into tibialis anterior muscles of mdx mice using a single injection trajectory. During the following weeks, muscle fiber breaks were induced by making mdx mice swim. To evaluate fiber damage, Evans blue solution was injected intraperitoneally to mice 16h before their sacrifice. Tibialis anterior muscles were then harvested and eGFP, dystrophin and Evans blue labeling were analyzed by fluorescent microscopy. Twenty minutes of exercise (i.e., swimming) were used to induce damage in about 30% of TA muscle fibers. Graft success, evaluated as the percentage of hybrid fibers which are eGFP(+), was improved by 1.9-fold after swimming 3 times per week during 4 weeks and by 1.8-fold after daily swimming. Hybrid muscle fiber transversal and longitudinal distribution were also increased after repeated physical efforts. Exercise induced fiber breaks, which improved MPC recruitment and fusion and increased long-term graft success and also transverse and longitudinal distribution of hybrid fibers.
MeSH term(s)	Animals ; Animals, Newborn ; Cell Differentiation/physiology ; Cells, Cultured ; Disease Models, Animal ; Dystrophin/metabolism ; Elapid Venoms/pharmacology ; Evans Blue ; Graft Survival/physiology ; Green Fluorescent Proteins ; Male ; Mice ; Mice, Inbred mdx ; Muscle Fibers, Skeletal/cytology ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/cytology ; Muscle, Skeletal/physiology ; Muscle, Skeletal/surgery ; Muscular Dystrophy, Duchenne/therapy ; Myoblasts/cytology ; Myoblasts/physiology ; Myoblasts/transplantation ; Physical Conditioning, Animal/physiology ; Tissue Transplantation/methods ; Treatment Outcome
Chemical Substances	Dystrophin ; Elapid Venoms ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9) ; notexin (37223-96-4) ; Evans Blue (45PG892GO1)
Language	English
Publishing date	2006-08
Publishing country	England
Document type	Journal Article
ZDB-ID	1077681-3
ISSN	1873-2364 ; 0960-8966
ISSN (online)	1873-2364
ISSN	0960-8966
DOI	10.1016/j.nmd.2006.06.003
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Zs.A 3258: Show issues

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Article ; Online: Cytokine modulation of TLR expression and activation in mesenchymal stromal cells leads to a proinflammatory phenotype.

Romieu-Mourez, Raphaëlle / François, Moïra / Boivin, Marie-Noëlle / Bouchentouf, Manaf / Spaner, David E / Galipeau, Jacques

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 182, Issue 12, Page(s) 7963–7973

Abstract: Bone marrow-derived mesenchymal stromal cells (MSC) possess an immune plasticity manifested by either an immunosuppressive or, when activated with IFN-gamma, an APC phenotype. Herein, TLR expression by MSC and their immune regulatory role were ... ...

Abstract	Bone marrow-derived mesenchymal stromal cells (MSC) possess an immune plasticity manifested by either an immunosuppressive or, when activated with IFN-gamma, an APC phenotype. Herein, TLR expression by MSC and their immune regulatory role were investigated. We observed that human MSC and macrophages expressed TLR3 and TLR4 at comparable levels and TLR-mediated activation of MSC resulted in the production of inflammatory mediators such as IL-1beta, IL-6, IL-8/CXCL8, and CCL5. IFN-alpha or IFN-gamma priming up-regulated production of these inflammatory mediators and expression of IFNB, inducible NO synthase (iNOS), and TRAIL upon TLR activation in MSC and macrophages, but failed to induce IL-12 and TNF-alpha production in MSC. Nonetheless, TLR activation in MSC resulted in the formation of an inflammatory site attracting innate immune cells, as evaluated by human neutrophil chemotaxis assays and by the analysis of immune effectors retrieved from Matrigel-embedded MSC injected into mice after in vitro preactivation with cytokines and/or TLR ligands. Hence, TLR-activated MSC are capable of recruiting immune inflammatory cells. In addition, IFN priming combined with TLR activation may increase immune responses induced by Ag-presenting MSC through presentation of Ag in an inflammatory context, a mechanism that could be applied in a cell-based vaccine.
MeSH term(s)	Adult ; Animals ; Cells, Cultured ; Cytokines/immunology ; Cytokines/metabolism ; Female ; Gene Expression Regulation ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Interferon Regulatory Factor-1/metabolism ; Ligands ; Ligases/metabolism ; Male ; Mice ; Phenotype ; Proto-Oncogene Proteins c-rel/metabolism ; Stromal Cells/immunology ; Stromal Cells/metabolism ; Toll-Like Receptor 3/genetics ; Toll-Like Receptor 3/metabolism ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
Chemical Substances	Cytokines ; Interferon Regulatory Factor-1 ; Ligands ; Proto-Oncogene Proteins c-rel ; Toll-Like Receptor 3 ; Toll-Like Receptor 4 ; Ligases (EC 6.-) ; guanosine 3',5'-polyphosphate synthetases (EC 6.-)
Language	English
Publishing date	2009-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.0803864
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Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

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Article: 1,25-dihydroxyvitamin D3 increases the transplantation success of human muscle precursor cells in SCID mice.

Stephan, Lionel / Bouchentouf, Manaf / Mills, Philippe / Lafreniere, Jean-François / Tremblay, Jacques P

Cell transplantation

2007 Volume 16, Issue 4, Page(s) 391–402

Abstract: Human muscle precursor cell (hMPC) transplantation is a potential therapy for severe muscle trauma or myopathies. Some previous studies demonstrated that 1,25-dihydroxyvitamin-D3 (1,25-D3) acted directly on myoblasts, regulating their proliferation and ... ...

Abstract	Human muscle precursor cell (hMPC) transplantation is a potential therapy for severe muscle trauma or myopathies. Some previous studies demonstrated that 1,25-dihydroxyvitamin-D3 (1,25-D3) acted directly on myoblasts, regulating their proliferation and fusion. 1,25-D3 is also involved in apoptosis modulation of other cell types and may thus contribute to protect the transplanted hMPCs. We have therefore investigated whether 1,25-D3 could improve the hMPC graft success. The 1,25-D3 effects on hMPC proliferation, fusion, and survival were initially monitored in vitro. hMPCs were also grafted in the tibialis anterior of SCID mice treated or not with 1,25-D3 to determine its in vivo effect. Graft success, proliferation, and viability of transplanted hMPCs were evaluated. 1,25-D3 enhanced proliferation and fusion of hMPCs in vitro and in vivo. However, 1,25-D3 did not protect hMPCs from various proapoptotic factors (in vitro) or during the early posttransplantation period. 1,25-D3 enhanced hMPC graft success because the number of muscle fibers expressing human dystrophin was significantly increased in the TA sections of 1,25-D3-treated mice (166.75 +/- 20.64) compared to the control mice (97.5 +/- 16.58). This result could be partly attributed to the improvement of the proliferation and differentiation of hMPCs in the presence of 1,25-D3. Thus, 1,25-D3 administration could improve the clinical potential of hMPC transplantation currently developed for muscle trauma or myopathies.
MeSH term(s)	Animals ; Apoptosis ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Dystrophin/metabolism ; Female ; Graft Survival ; Humans ; Infant ; Male ; Mesenchymal Stem Cell Transplantation ; Mice ; Mice, SCID ; Muscle Cells/transplantation ; Survival Rate ; Vitamin D/analogs & derivatives ; Vitamin D/therapeutic use
Chemical Substances	Dystrophin ; dihydroxy-vitamin D3 ; Vitamin D (1406-16-2)
Language	English
Publishing date	2007-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1135816-6
ISSN	0963-6897
ISSN	0963-6897
DOI	10.3727/000000007783464876
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Zs.A 3556: Show issues

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Article ; Online: Human marrow-derived mesenchymal stromal cells decrease cisplatin renotoxicity in vitro and in vivo and enhance survival of mice post-intraperitoneal injection.

Eliopoulos, Nicoletta / Zhao, Jing / Bouchentouf, Manaf / Forner, Kathy / Birman, Elena / Yuan, Shala / Boivin, Marie-Noelle / Martineau, Daniel

American journal of physiology. Renal physiology

2010 Volume 299, Issue 6, Page(s) F1288–98

Abstract: Acute kidney injury (AKI) can occur from the toxic side-effects of chemotherapeutic agents such as cisplatin. Bone marrow-derived mesenchymal stromal cells (MSCs) have demonstrated wide therapeutic potential often due to beneficial factors they secrete. ... ...

Abstract	Acute kidney injury (AKI) can occur from the toxic side-effects of chemotherapeutic agents such as cisplatin. Bone marrow-derived mesenchymal stromal cells (MSCs) have demonstrated wide therapeutic potential often due to beneficial factors they secrete. The goal of this investigation was to evaluate in vitro the effect of human MSCs (hMSCs) secretome on cisplatin-treated human kidney cells, and in vivo the consequence of hMSCs intraperitoneal (ip) implantation in mice with AKI. Our results revealed that hMSCs-conditioned media improved survival of HK-2 human proximal tubular cells exposed to cisplatin in vitro. This enhanced survival was linked to increased expression of phosphorylated Akt (Ser473) and was reduced by a VEGF-neutralizing antibody. In vivo testing of these hMSCs established that ip administration in NOD-SCID mice decreased cisplatin-induced kidney function impairment, as demonstrated by lower blood urea nitrogen levels and higher survival. In addition, blood phosphorous and amylase levels were also significantly decreased. Moreover, hMSCs reduced the plasma levels of several inflammatory cytokines/chemokines. Immunohistochemical examination of kidneys showed less apoptotic and more proliferating cells. Furthermore, PCR indicated the presence of hMSCs in mouse kidneys, which also showed enhanced expression of phosphorylated Akt. In conclusion, our study reveals that hMSCs can exert prosurvival effects on renal cells in vitro and in vivo, suggests a paracrine contribution for kidney protective abilities of hMSCs delivered ip, and supports their clinical potential in AKI.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/pathology ; Acute Kidney Injury/therapy ; Animals ; Cell Proliferation/drug effects ; Cells, Cultured ; Cisplatin/adverse effects ; Culture Media, Conditioned/pharmacology ; Cytokines/blood ; Humans ; Male ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells/physiology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Middle Aged ; Proto-Oncogene Proteins c-akt/metabolism ; Stromal Cells/physiology
Chemical Substances	Culture Media, Conditioned ; Cytokines ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2010-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00671.2009
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Article ; Online: Induction of cardiac angiogenesis requires killer cell lectin-like receptor 1 and α4β7 integrin expression by NK cells.

Bouchentouf, Manaf / Forner, Kathy-Ann / Cuerquis, Jessica / Michaud, Véronique / Zheng, Jiamin / Paradis, Pierre / Schiffrin, Ernesto L / Galipeau, Jacques

Journal of immunology (Baltimore, Md. : 1950)

2010 Volume 185, Issue 11, Page(s) 7014–7025

Abstract: Recent findings indicate that NK cells are involved in cardiac repair following myocardial infarction. The aim of this study is to investigate the role NK cells in infarct angiogenesis and cardiac remodeling. In normal C57BL/6 mice, myelomonocytic ... ...

Abstract	Recent findings indicate that NK cells are involved in cardiac repair following myocardial infarction. The aim of this study is to investigate the role NK cells in infarct angiogenesis and cardiac remodeling. In normal C57BL/6 mice, myelomonocytic inflammatory cells invaded infarcted heart within 24 h followed by a lymphoid/NK cell infiltrate by day 6, accompanied by substantial expression of IL-2, TNF-α, and CCL2. In contrast, NOD SCID mice had virtually no lymphoid cells infiltrating the heart and did not upregulate IL-2 levels. In vitro and in vivo, IL-2-activated NK cells promoted TNF-α-stimulated endothelial cell proliferation, enhanced angiogenesis and reduced fibrosis within the infarcted myocardium. Adoptive transfer of IL-2-activated NK cells to NOD SCID mice improved post-myocardial infarction angiogenesis. RNA silencing technology and neutralizing Abs demonstrated that this process involved α4β7 integrin/VCAM-1 and killer cell lectin-like receptor 1/N-cadherin-specific binding. In this study, we show that IL-2-activated NK cells reduce myocardial collagen deposition along with an increase in neovascularization following acute cardiac ischemia through specific interaction with endothelial cells. These data define a potential role of activated NK cells in cardiac angiogenesis and open new perspectives for the treatment of ischemic diseases.
MeSH term(s)	Animals ; Cell Communication/immunology ; Cell Proliferation ; Cells, Cultured ; Chemotaxis, Leukocyte/immunology ; Cytotoxicity Tests, Immunologic ; Endothelium, Vascular/cytology ; Endothelium, Vascular/immunology ; Endothelium, Vascular/metabolism ; Integrins/biosynthesis ; Integrins/physiology ; Interleukin-2/physiology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Lymphocyte Activation/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, SCID ; Neovascularization, Physiologic/immunology ; Receptors, Immunologic/biosynthesis ; Receptors, Immunologic/physiology ; Tumor Necrosis Factor-alpha/physiology
Chemical Substances	Integrins ; Interleukin-2 ; Klrg1 protein, mouse ; Receptors, Immunologic ; Tumor Necrosis Factor-alpha ; integrin alpha4beta7
Language	English
Publishing date	2010-12-01
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1001888
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