Prevention of experimental autoimmune encephalomyelitis in DA rats by grafting primary skin fibroblasts engineered to express transforming growth factor-<i>β</i>1

Zargarova, T. A.; Кулакова, О. Г.; Prassolov, Vladimir; Жармухамедова, Т. Ю.; Tsyganova, V. G.; Turobov, V. I.; Ivanov, Dmitry; Parfenov, M; Судомоина, М. А.; Chernajovsky, Yuti; Фаворова, О. О.

doi:10.1111/j.1365-2249.2004.02539.x

Cited by 10 publications

(4 citation statements)

References 49 publications

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“…Fibroblasts were cultured as previously described [18]. Briefly, cells were incubated in a humidified atmosphere of 5% CO 2 and grown in Dulbecco's minimum essential medium (DMEM, Hyclone) supplemented with 10% foetal bovine serum (FBS, Hyclone), 50 units/ml penicillin and 50 µg/ml streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Genetic Variations of Heat Shock Protein 84 in Mice Mediate Cellular Glucocorticoid Response

Zhao

Shen

Chen

et al. 2010

Cell Physiol Biochem

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Heat shock protein 90 (Hsp90), encoded by hsp84 and hsp86 in mice, has been confirmed to modulate glucocorticoid receptor (GR) function; however, the contribution of Hsp90 in glucocorticoid (GC) sensibility/resistance has received less attention. Previously, we found that genetic variations of Hsp84 are related to differences in the in vivo GC-GR responses between BALB/c and C57BL/6 mice suffering from traumatic injury. To evaluate the modulation of Hsp84 polymorphisms on the GC response, we used a cellular heat-stress injury (HSI) model combined with a transgene-plasmid infection approach and assessed HSI-induced cellular damage and GR nuclear translocation, with or without dexamethasone pretreatment. We demonstrated that after HSI, fibroblasts from the C57BL/6 line exhibit higher cellular survival, higher nuclear GR levels and lower lactate dehydrogenase activity compared to those from the BALB/c line. We showed that dexamethasone-rescued HSI-induced damage is accompanied by increasing nuclear GR levels in both lines. Importantly, this protection against HSI was greater in C57BL/6 fibroblasts and was resistant to geldanamycin, a selective inhibitor of Hsp90. Importantly, transfection of the hsp84-transgene from C57BL/6 mice increased the nuclear GR levels and lessened HSI-induced damage in BALB/c fibroblasts. Our data thereby demonstrate that Hsp84 from C57BL/6 mice modulates higher cellular GC-GR responsiveness.

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Section: Methodsmentioning

confidence: 99%

Genetic Variations of Heat Shock Protein 84 in Mice Mediate Cellular Glucocorticoid Response

Zhao

Shen

Chen

et al. 2010

Cell Physiol Biochem

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“…Fibroblast culture was established as described previously [11,25]. Briefly, fibroblasts were incubated at 5% CO 2 in a humidified 37°C incubator, cultured with Dulbecco's minimum essential medium (DMEM) supplemented with 10% heat-inactivated fetal bovine serum (FBS) three times a week.…”

Section: Primary Fibroblasts Culture and Treatmentsmentioning

confidence: 99%

Upregulation of Ski in Fibroblast is Implicated in the Peroxisome Proliferator- Activated Receptor d-Mediated Wound Healing

Zhang

et al. 2012

Cell Physiol Biochem

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Background/Aim: Both peroxisome proliferator-activated receptor (PPAR) δ and Ski are investigate the interaction of PPARδ and Ski and this interaction-associated effect in wound healing. Methods: Effect of PPARδ activation on Ski expression was detected in rat skin fibroblasts by real-time PCR and western blot. Luciferase assay, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay were performed to identify the binding site of PPARδ in the promoter region of rat Ski gene. And the functional activity of PPARδ regulation to Ski was detected in fibroblast proliferation and rat skin wound healing model. Results: PPARδ agonist GW501516 upregulated Ski expression in a dose-dependent manner. Direct repeat-1 (DR1) response element locating at -865∼-853 in Ski promoter region was identified to mediate PPARδ binding to Ski and associated induction of Ski. Furthermore, PPARδ upregulated Ski to promote fibroblasts proliferation and rat skin wound repair, which could be largely blocked by pre-treated with Ski RNA interference. Conclusion: This study demonstrates that Ski is a novel target gene for PPARδ and upregulation of Ski to promote fibroblast proliferation is implicated in the PPARδ-mediated wound healing.

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“…In a different study, TGF-β1 has been used to downregulate EAE: Zargarova et al retrovirally transduced primary skin fibroblasts ex vivo with TGF-β1 and then intraperitoneally administered the transduced cells during the priming phase of EAE. They observed a significant reduction in mortality versus control EAE mice treated with non-transduced fibroblasts [24].…”

Section: Th17-treg Cytokines Familymentioning

confidence: 97%

Gene therapy of multiple sclerosis

Furlan¹,

Maiorino²,

Gatta³

et al. 2010

Gene Therapy for Autoimmune and Inflammatory Diseases

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Multiple sclerosis (MS) constitutes a difficult challenge for the design of innovative therapies: the aetiology is unknown, the pathogenesis only partially understood, and the whole process is multi-focal, chronic, and occurring beyond anatomical barriers, making the delivery of potentially therapeutic molecules difficult. Gene therapy, thus, constitutes a realistic alternative to ensure prolonged, and site-specific delivery of therapies. Recent advancements in the comprehension of the immunopathological processes leading to central nervous system inflammation, and the development of new gene therapy tools, such as RNA-interference, are rapidly leading to a large array of possibilities of intervention, documented in the present review in its animal model, experimental autoimmune encephalomyelitis (EAE). Since progressive forms of MS remain orphan of efficient therapies, the field is open for less conventional interventions such as gene therapy.

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Prevention of experimental autoimmune encephalomyelitis in DA rats by grafting primary skin fibroblasts engineered to express transforming growth factor-β1

Cited by 10 publications

References 49 publications

Genetic Variations of Heat Shock Protein 84 in Mice Mediate Cellular Glucocorticoid Response

Genetic Variations of Heat Shock Protein 84 in Mice Mediate Cellular Glucocorticoid Response

Upregulation of Ski in Fibroblast is Implicated in the Peroxisome Proliferator- Activated Receptor d-Mediated Wound Healing

Gene therapy of multiple sclerosis

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