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GROUP | CONDITION | SAMPLES |
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Islets |
GSM680277 GSM680278 GSM680279 GSM680280 GSM680281 GSM680282
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GSM680266 GSM680267 GSM680268 GSM680269 GSM680270
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GSM680271 GSM680272 GSM680273 GSM680274 GSM680275 GSM680276
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Submission Date: Feb 27, 2011
Summary: TGFbi (transforming growth factor-beta-induced) is a secreted protein and is capable of binding to both extracellular matrix (ECM) and cells. It thus acts as a bifunctional molecule enhancing ECM and cell interactions, a lack of which results in dysfunction of many cell types. In this study, we investigated the role of TGFbi in the function and survival of islets. Based on DNA microarray analysis followed by qPCR confirmation, the TGFbi gene showed drastic increases in expression in islets after culture. We demonstrated that recombinant TGFbi could preserve the integrity and enhance the function of cultured islets. Such a beneficial effect was mediated via signalling through FAK. Exogenous TGFbi was capable of sustaining high-level FAK phosphorylation in isolated islets, and FAK knockdown by siRNA in islets resulted in compromised islet function. TGFbi Tg islets showed better integrity and insulin release after in vitro culture. In vivo, b-cell proliferation was detectable in Tg but not wild type pancreata. At age above 12 months, Tg pancreata contained giant islets. Tg mice displayed better glucose tolerance than the controls. Tg islets were more potent in lowering blood glucose when transplanted into syngeneic mice with streptozotocin-induced diabetes, and these transplanted islets also underwent regeneration. Our results indicate that TGFbi is a vital trophic factor promoting islet survival, function and regeneration. At least some of its beneficial effect was mediated by signalling through FAK.
GEO Accession ID: GSE27547
PMID: 21471441
Submission Date: Feb 27, 2011
Summary: TGFbi (transforming growth factor-beta-induced) is a secreted protein and is capable of binding to both extracellular matrix (ECM) and cells. It thus acts as a bifunctional molecule enhancing ECM and cell interactions, a lack of which results in dysfunction of many cell types. In this study, we investigated the role of TGFbi in the function and survival of islets. Based on DNA microarray analysis followed by qPCR confirmation, the TGFbi gene showed drastic increases in expression in islets after culture. We demonstrated that recombinant TGFbi could preserve the integrity and enhance the function of cultured islets. Such a beneficial effect was mediated via signalling through FAK. Exogenous TGFbi was capable of sustaining high-level FAK phosphorylation in isolated islets, and FAK knockdown by siRNA in islets resulted in compromised islet function. TGFbi Tg islets showed better integrity and insulin release after in vitro culture. In vivo, b-cell proliferation was detectable in Tg but not wild type pancreata. At age above 12 months, Tg pancreata contained giant islets. Tg mice displayed better glucose tolerance than the controls. Tg islets were more potent in lowering blood glucose when transplanted into syngeneic mice with streptozotocin-induced diabetes, and these transplanted islets also underwent regeneration. Our results indicate that TGFbi is a vital trophic factor promoting islet survival, function and regeneration. At least some of its beneficial effect was mediated by signalling through FAK.
GEO Accession ID: GSE27547
PMID: 21471441
Signatures:
Control Condition
Perturbation Condition
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