The Experts below are selected from a list of 14439 Experts worldwide ranked by ideXlab platform
Fan Yang - One of the best experts on this subject based on the ideXlab platform.
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winner of the young investigator award of the society for biomaterials at the 10th world biomaterials congress may 17 22 2016 montreal qc canada microribbon based hydrogels accelerate stem cell based bone regeneration in a mouse critical size cranial defect model
Journal of Biomedical Materials Research Part A, 2016Co-Authors: Lihsin Han, Bogdan Conrad, Michael T Chung, Lorenzo Deveza, Xinyi Jiang, Andrew Wang, Manish J Butte, Michael T Longaker, Derrick C Wan, Fan YangAbstract:Stem cell-based therapies hold great promise for enhancing tissue regeneration. However, the majority of cells die shortly after transplantation, which greatly diminishes the efficacy of stem cell-based therapies. Poor cell engraftment and survival remain a major bottleneck to fully exploiting the power of stem cells for regenerative medicine. Biomaterials such as hydrogels can serve as artificial matrices to protect cells during delivery and guide desirable cell fates. However, conventional hydrogels often lack macroporosity, which restricts cell proliferation and delays matrix deposition. Here we report the use of injectable, macroporous microribbon (μRB) hydrogels as stem cell carriers for bone repair, which supports direct cell encapsulation into a macroporous scaffold with rapid spreading. When transplanted in a critical-sized, mouse cranial defect model, μRB-based hydrogels significantly enhanced the survival of transplanted adipose-derived stromal cells (ADSCs) (81%) and enabled up to three-fold cell proliferation after 7 days. In contrast, conventional hydrogels only led to 27% cell survival, which continued to decrease over time. MicroCT imaging showed μRBs enhanced and accelerated mineralized bone repair compared to hydrogels (61% vs. 34% by week 6), and stem cells were required for bone repair to occur. These results suggest that Paracrine Signaling of transplanted stem cells are responsible for the observed bone repair, and enhancing cell survival and proliferation using μRBs further promoted the Paracrine-Signaling effects of ADSCs for stimulating endogenous bone repair. We envision μRB-based scaffolds can be broadly useful as a novel scaffold for enhancing stem cell survival and regeneration of other tissue types. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 1321-1331, 2016.
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microribbon based hydrogels accelerate stem cell based bone regeneration in a mouse critical size cranial defect model
Journal of Biomedical Materials Research Part A, 2016Co-Authors: Lihsin Han, Bogdan Conrad, Michael T Chung, Lorenzo Deveza, Xinyi Jiang, Andrew Wang, Manish J Butte, Michael T Longaker, Derrick C Wan, Fan YangAbstract:Stem cell-based therapies hold great promise for enhancing tissue regeneration. However, the majority of cells die shortly after transplantation, which greatly diminishes the efficacy of stem cell-based therapies. Poor cell engraftment and survival remain a major bottleneck to fully exploiting the power of stem cells for regenerative medicine. Biomaterials such as hydrogels can serve as artificial matrices to protect cells during delivery and guide desirable cell fates. However, conventional hydrogels often lack macroporosity, which restricts cell proliferation and delays matrix deposition. Here we report the use of injectable, macroporous microribbon (µRB) hydrogels as stem cell carriers for bone repair, which supports direct cell encapsulation into a macroporous scaffold with rapid spreading. When transplanted in a criticalsized, mouse cranial defect model, µRB-based hydrogels significantly enhanced the survival of transplanted adipose-derived stromal cells (ADSCs) (81%) and enabled up to three-fold cell proliferation after 7 days. In contrast, conventional hydrogels only led to 27% cell survival, which continued to decrease over time. MicroCT imaging showed µRBs enhanced and accelerated mineralized bone repair compared to hydrogels (61% vs. 34% by week 6), and stem cells were required for bone repair to occur. These results suggest that Paracrine Signaling of transplanted stem cells are responsible for the observed bone repair, and enhancing cell survival and proliferation using µRBs further promoted the Paracrine-Signaling effects of ADSCs for stimulating endogenous bone repair. We envision µRB-based scaffolds can be broadly useful as a novel scaffold for enhancing stem cell survival and regeneration of other tissue types.
Katsuhiko Mikoshiba - One of the best experts on this subject based on the ideXlab platform.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Abstract Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca 2+ ) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca 2+ ] i oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca 2+ ] i oscillations in hMSCs and found that IP 3 -induced Ca 2+ release is essential for spontaneous [Ca 2+ ] i oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap–junction channel; it stimulates the P 2 Y 1 receptors, resulting in the activation of PLC-β to produce IP 3 . We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca 2+ ] i oscillations. Furthermore, we found that [Ca 2+ ] i oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca 2+ ] i oscillations. As the hMSCs differentiated to adipocytes, the [Ca 2+ ] i oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca 2+ ] i oscillations in undifferentiated hMSCs.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca(2+)) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca(2+)](i) oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca(2+)](i) oscillations in hMSCs and found that IP(3)-induced Ca(2+) release is essential for spontaneous [Ca(2+)](i) oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap-junction channel; it stimulates the P(2)Y(1) receptors, resulting in the activation of PLC-beta to produce IP(3). We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca(2+)](i) oscillations. Furthermore, we found that [Ca(2+)](i) oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca(2+)](i) oscillations. As the hMSCs differentiated to adipocytes, the [Ca(2+)](i) oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca(2+)](i) oscillations in undifferentiated hMSCs.
Yoshiyuki Hirayama - One of the best experts on this subject based on the ideXlab platform.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Abstract Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca 2+ ) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca 2+ ] i oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca 2+ ] i oscillations in hMSCs and found that IP 3 -induced Ca 2+ release is essential for spontaneous [Ca 2+ ] i oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap–junction channel; it stimulates the P 2 Y 1 receptors, resulting in the activation of PLC-β to produce IP 3 . We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca 2+ ] i oscillations. Furthermore, we found that [Ca 2+ ] i oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca 2+ ] i oscillations. As the hMSCs differentiated to adipocytes, the [Ca 2+ ] i oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca 2+ ] i oscillations in undifferentiated hMSCs.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca(2+)) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca(2+)](i) oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca(2+)](i) oscillations in hMSCs and found that IP(3)-induced Ca(2+) release is essential for spontaneous [Ca(2+)](i) oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap-junction channel; it stimulates the P(2)Y(1) receptors, resulting in the activation of PLC-beta to produce IP(3). We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca(2+)](i) oscillations. Furthermore, we found that [Ca(2+)](i) oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca(2+)](i) oscillations. As the hMSCs differentiated to adipocytes, the [Ca(2+)](i) oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca(2+)](i) oscillations in undifferentiated hMSCs.
Lihsin Han - One of the best experts on this subject based on the ideXlab platform.
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winner of the young investigator award of the society for biomaterials at the 10th world biomaterials congress may 17 22 2016 montreal qc canada microribbon based hydrogels accelerate stem cell based bone regeneration in a mouse critical size cranial defect model
Journal of Biomedical Materials Research Part A, 2016Co-Authors: Lihsin Han, Bogdan Conrad, Michael T Chung, Lorenzo Deveza, Xinyi Jiang, Andrew Wang, Manish J Butte, Michael T Longaker, Derrick C Wan, Fan YangAbstract:Stem cell-based therapies hold great promise for enhancing tissue regeneration. However, the majority of cells die shortly after transplantation, which greatly diminishes the efficacy of stem cell-based therapies. Poor cell engraftment and survival remain a major bottleneck to fully exploiting the power of stem cells for regenerative medicine. Biomaterials such as hydrogels can serve as artificial matrices to protect cells during delivery and guide desirable cell fates. However, conventional hydrogels often lack macroporosity, which restricts cell proliferation and delays matrix deposition. Here we report the use of injectable, macroporous microribbon (μRB) hydrogels as stem cell carriers for bone repair, which supports direct cell encapsulation into a macroporous scaffold with rapid spreading. When transplanted in a critical-sized, mouse cranial defect model, μRB-based hydrogels significantly enhanced the survival of transplanted adipose-derived stromal cells (ADSCs) (81%) and enabled up to three-fold cell proliferation after 7 days. In contrast, conventional hydrogels only led to 27% cell survival, which continued to decrease over time. MicroCT imaging showed μRBs enhanced and accelerated mineralized bone repair compared to hydrogels (61% vs. 34% by week 6), and stem cells were required for bone repair to occur. These results suggest that Paracrine Signaling of transplanted stem cells are responsible for the observed bone repair, and enhancing cell survival and proliferation using μRBs further promoted the Paracrine-Signaling effects of ADSCs for stimulating endogenous bone repair. We envision μRB-based scaffolds can be broadly useful as a novel scaffold for enhancing stem cell survival and regeneration of other tissue types. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 104A: 1321-1331, 2016.
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microribbon based hydrogels accelerate stem cell based bone regeneration in a mouse critical size cranial defect model
Journal of Biomedical Materials Research Part A, 2016Co-Authors: Lihsin Han, Bogdan Conrad, Michael T Chung, Lorenzo Deveza, Xinyi Jiang, Andrew Wang, Manish J Butte, Michael T Longaker, Derrick C Wan, Fan YangAbstract:Stem cell-based therapies hold great promise for enhancing tissue regeneration. However, the majority of cells die shortly after transplantation, which greatly diminishes the efficacy of stem cell-based therapies. Poor cell engraftment and survival remain a major bottleneck to fully exploiting the power of stem cells for regenerative medicine. Biomaterials such as hydrogels can serve as artificial matrices to protect cells during delivery and guide desirable cell fates. However, conventional hydrogels often lack macroporosity, which restricts cell proliferation and delays matrix deposition. Here we report the use of injectable, macroporous microribbon (µRB) hydrogels as stem cell carriers for bone repair, which supports direct cell encapsulation into a macroporous scaffold with rapid spreading. When transplanted in a criticalsized, mouse cranial defect model, µRB-based hydrogels significantly enhanced the survival of transplanted adipose-derived stromal cells (ADSCs) (81%) and enabled up to three-fold cell proliferation after 7 days. In contrast, conventional hydrogels only led to 27% cell survival, which continued to decrease over time. MicroCT imaging showed µRBs enhanced and accelerated mineralized bone repair compared to hydrogels (61% vs. 34% by week 6), and stem cells were required for bone repair to occur. These results suggest that Paracrine Signaling of transplanted stem cells are responsible for the observed bone repair, and enhancing cell survival and proliferation using µRBs further promoted the Paracrine-Signaling effects of ADSCs for stimulating endogenous bone repair. We envision µRB-based scaffolds can be broadly useful as a novel scaffold for enhancing stem cell survival and regeneration of other tissue types.
Seiko Kawano - One of the best experts on this subject based on the ideXlab platform.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Abstract Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca 2+ ) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca 2+ ] i oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca 2+ ] i oscillations in hMSCs and found that IP 3 -induced Ca 2+ release is essential for spontaneous [Ca 2+ ] i oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap–junction channel; it stimulates the P 2 Y 1 receptors, resulting in the activation of PLC-β to produce IP 3 . We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca 2+ ] i oscillations. Furthermore, we found that [Ca 2+ ] i oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca 2+ ] i oscillations. As the hMSCs differentiated to adipocytes, the [Ca 2+ ] i oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca 2+ ] i oscillations in undifferentiated hMSCs.
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atp autocrine Paracrine Signaling induces calcium oscillations and nfat activation in human mesenchymal stem cells
Cell Calcium, 2006Co-Authors: Seiko Kawano, Keishi Otsu, Akinori Kuruma, Satoshi Shoji, Eri Yanagida, Yuko Muto, Fumio Yoshikawa, Yoshiyuki Hirayama, Katsuhiko MikoshibaAbstract:Human bone marrow-derived mesenchymal stem cells (hMSCs) have the potential to differentiate into several types of cells. Calcium ions (Ca(2+)) play an important role in the differentiation and proliferation of hMSCs. We have demonstrated that spontaneous [Ca(2+)](i) oscillations occur without agonist stimulation in hMSCs. However, the precise mechanism of its generation remains unclear. In this study, we investigated the mechanism and role of spontaneous [Ca(2+)](i) oscillations in hMSCs and found that IP(3)-induced Ca(2+) release is essential for spontaneous [Ca(2+)](i) oscillations. We also found that an ATP autocrine/Paracrine Signaling pathway is involved in the oscillations. In this pathway, an ATP is secreted via a hemi-gap-junction channel; it stimulates the P(2)Y(1) receptors, resulting in the activation of PLC-beta to produce IP(3). We were able to pharmacologically block this pathway, and thereby to completely halt the [Ca(2+)](i) oscillations. Furthermore, we found that [Ca(2+)](i) oscillations were associated with NFAT translocation into the nucleus in undifferentiated hMSCs. Once the ATP autocrine/Paracrine Signaling pathway was blocked, it was not possible to detect the nuclear translocation of NFAT, indicating that the activation of NFAT is closely linked to [Ca(2+)](i) oscillations. As the hMSCs differentiated to adipocytes, the [Ca(2+)](i) oscillations disappeared and the translocation of NFAT ceased. These results provide new insight into the molecular and physiological mechanism of [Ca(2+)](i) oscillations in undifferentiated hMSCs.
