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Hisako Ohgawara - One of the best experts on this subject based on the ideXlab platform.

  • biocompatibility of two different types of extracellular matrix in bioartificial Endocrine Pancreas in dogs a preliminary report
    Journal of Artificial Organs, 2001
    Co-Authors: Kazuya Edamura, Hisako Ohgawara, Koko Nasu, Yukiko Iwami, Ayako Sato, Shiho Ishikawa, Naoaki Matsuki, Kenichiro Ono, Hiroyuki Ogawa, Nobuo Sasaki
    Abstract:

    The biocompatibility of synthetic extracellular matrix (ECM) in the diffusion chamber of a bioartificial Endocrine Pancreas (Bio-AEP) was investigated in normal beagle dogs. Two different types of ECM were used in this study, type I collagen treated with pepsin to ensure lower antigenicity (type I LA) and reconstituted basement membrane matrix (Matrigel derived from Englbreth-Holm-Swarm mouse sarcoma. Bio-AEPs with type I LA or Matrigel without pancreatic Endocrine cells were implanted into the abdominal cavities of beagle dogs (n=4). At 1 month after implantation, laparoscopy revealed no abnormalities in the Bio-AEPs with type I LA, whereas it revealed encapsulation of one of the Bio-AEPs with Matrigel with fibrous tissue, and in that case the Bio-AEP was removed. At 3 months after implantation, the remaining Bio-AEP with Matrigel was completely destroyed, whereas the Bio-AEPs with type I LA showed no abnormal findings. Microscopically, an invasion of red blood cells and macrophages into the chamber was observed in the Bio-AEPs with Matrigel. A proliferation of fibroblasts around the Matrigel was observed in one case. In contrast, light microscopic findings revealed no abnormal findings in the Bio-AEP with type I LA. These results suggest that the cell growth and differentiation factors and adhesion molecules in Matrigel may play an important role in fibrous encapsulation and may be incompatible with dogs, and that type I LA is more suitable for Bio-AEP.

  • bioartificial Endocrine Pancreas bio aep for treatment of diabetes effect of implantation of bio aep on the Pancreas
    Cell Transplantation, 1999
    Co-Authors: Sachiko Hirotani, Reiko Eda, Takako Kawabata, Shohei Fuchinoue, Satoshi Teraoka, Tetsuzo Agishi, Hisako Ohgawara
    Abstract:

    Recently, we described a diffusion chamber for a bioartificial Endocrine Pancreas (Bio-AEP). Pancreatic islet cells in the Bio-AEP device were isolated from the immune system of the host by an artificial barrier, while nutrients, electrolytes, oxygen, and bioactive secretory products were exchanged across this barrier. This experiment was designed to evaluate whether the diffusion chamber could be useful as a Bio-AEP in the treatment of diabetes. Six streptozotocin (STZ)-induced diabetic rats each received a diffusion chamber containing 8 x 10(6) MIN6 cells as a xenograft Bio-AEP. In the STZ diabetic rats with Bio-AEPs, a return to normoglycemia was observed up to 30 weeks after implantation, without the use of any immunosuppressant. A gradual increase in the body weight of the rats was also observed. In three STZ diabetic rats, diffusion chambers without MIN6 cells were implanted as a sham operation. The fasting blood glucose levels in these three rats remained higher than 600 mg/dl, after implantation, and they lost weight. Thirty-five weeks after implantation, the pancreata were removed from the rats that underwent xenoimplantation, those that had the sham operation, and the normal control rats. In the sham-operated animals, the exocrine tissues of the pancreata were vacuolated and pancreatic B cells were not seen in the islets. In contrast, in the pancreata from the xenoimplantation, the exocrine tissues were normal, and a few pancreatic B cells were seen in the islets. These results indicated that xenoimplantation using the Bio-AEP might retard the progress of diabetes.

  • Xenoimplantation using a diffusion chamber with a B-cell line (MIN6) as a bioartificial Endocrine Pancreas (BIO-AEP)
    Cell Transplantation, 1996
    Co-Authors: Hisako Ohgawara, Yoshihiko Nakagawa, Sachiyo Karibe, Jun-ichi Miyazaki, S. Sato, Toshihiro Akaike
    Abstract:

    Abstract This experiment was designed to investigate whether MIN6-cells, which are derived from transgenic mouse insulinoma cells, could be a useful tool for transplantation. An implantable diffusion chamber for a bioartificial Endocrine Pancreas (Bio-AEP) was constructed by placing a pancreatic B-cell line (MIN6) in a mixed matrix in the center of a ring holder sandwiched between two nuclepore membranes (pore size 0.2 μm), which were held in place by a silicone seal. Nine streptozotocin (STZ)-induced diabetic rats were each implanted with the diffusion chamber containing mouse insulinoma cells (xenograft-implantation) as a Bio-AEP, but without any immunosuppressant. In three of the STZ-diabetic rats with a Bio-AEP, a return to normoglycemia was observed up to 20 wk after implantation (good control). Four of the nine STZ-diabetic rats, which had received diffusion chambers with MIN6, also showed a return to normoglycemia for up to 10 wk (fair control). In two of the rats, blood glucose levels showed poor control. The results indicate that MIN6 cells should be useful for the implantation of xenographic cells in diabetic animals.

Leif Jansson - One of the best experts on this subject based on the ideXlab platform.

Toshihiro Akaike - One of the best experts on this subject based on the ideXlab platform.

  • Xenoimplantation using a diffusion chamber with a B-cell line (MIN6) as a bioartificial Endocrine Pancreas (BIO-AEP)
    Cell Transplantation, 1996
    Co-Authors: Hisako Ohgawara, Yoshihiko Nakagawa, Sachiyo Karibe, Jun-ichi Miyazaki, S. Sato, Toshihiro Akaike
    Abstract:

    Abstract This experiment was designed to investigate whether MIN6-cells, which are derived from transgenic mouse insulinoma cells, could be a useful tool for transplantation. An implantable diffusion chamber for a bioartificial Endocrine Pancreas (Bio-AEP) was constructed by placing a pancreatic B-cell line (MIN6) in a mixed matrix in the center of a ring holder sandwiched between two nuclepore membranes (pore size 0.2 μm), which were held in place by a silicone seal. Nine streptozotocin (STZ)-induced diabetic rats were each implanted with the diffusion chamber containing mouse insulinoma cells (xenograft-implantation) as a Bio-AEP, but without any immunosuppressant. In three of the STZ-diabetic rats with a Bio-AEP, a return to normoglycemia was observed up to 20 wk after implantation (good control). Four of the nine STZ-diabetic rats, which had received diffusion chambers with MIN6, also showed a return to normoglycemia for up to 10 wk (fair control). In two of the rats, blood glucose levels showed poor control. The results indicate that MIN6 cells should be useful for the implantation of xenographic cells in diabetic animals.

Olle Korsgren - One of the best experts on this subject based on the ideXlab platform.

  • the transplanted fetal Endocrine Pancreas undergoes an inherent sequential differentiation similar to that in the native Pancreas an ultrastructural study in the pig to mouse model
    Diabetes, 2001
    Co-Authors: Agneta Lukinius, Olle Korsgren
    Abstract:

    This study examines, at the ultrastructural level, whether the fetal porcine Endocrine Pancreas (insulin, glucagon, somatostatin, and pancreatic polypeptide [PP]- and islet amyloid polypeptide [IAPP]-containing cells) develops normally after transplantation under the kidney capsule in athymic mice. We have thus used an in vivo pig-to-mouse model for the differentiation of the Endocrine Pancreas removed from its normal milieu. Islet-like cell clusters (ICCs) were prepared from the fetal porcine Pancreas as previously described and transplanted under the renal capsule of athymic mice. At various times after transplantation, the Endocrine Pancreas was removed and the level of differentiation was compared with the native Pancreas of the same biological age. At the ultrastructural level, several sequential steps could be identified based on the morphology and hormone content of the secretory granules of the Endocrine cell examined. Applying this approach, we could demonstrate that the ontogeny of the transplanted fetal pig Pancreas follows the same sequential differentiation as the native Pancreas. The process seems to be under stringent control, apparently directly related to the biological age of the tissue, and independent not only of the new environment under the kidney capsule but also of the adult and xenogeneic milieu provided after transplantation to the athymic nude mouse. Therefore, all four major hormone-producing cells seem to develop normally after transplantation when compared with the development in the native Pancreas. IAPP was produced by the pluripotent fetal Endocrine cells as well as the adult alpha-, beta-, and delta-cell granules in the native Pancreas; however, in the transplanted Pancreas, IAPP expression was demonstrated only in beta-cells, delta-cells, and PP cells. No IAPP was found in granules of the alpha-cell lineage. The results suggest a sequential differentiation of all four major types of islet cells from a common pluripotent progenitor cell, which seems to be located in the pancreatic ducts. Therefore, the results presented strongly suggest that the ontogeny of the four major Endocrine islet cells is determined by genetic information carried by the progenitor cells and not by the systemic or local environment.

  • blood flow regulation in the transplanted fetal Endocrine Pancreas acquisition of a nitric oxide dependent glucose induced increase in blood flow
    Transplantation, 1996
    Co-Authors: Olle Korsgren, Rolf Karlsten, F Sundler, Leif Jansson
    Abstract:

    Blood flow regulation in the transplanted fetal Endocrine Pancreas: Acquisition of a nitric oxide-dependent glucose-induced increase in blood flow.

Suad Efendic - One of the best experts on this subject based on the ideXlab platform.

  • diazepam binding inhibitor and the Endocrine Pancreas
    Neuropharmacology, 1991
    Co-Authors: Claes-göran Östenson, Marita Hilliges, Olle Johansson, S Karlsson, Bo Ahrén, Suad Efendic
    Abstract:

    Summary Regulation of blood glucose homeostasis is complex. Its major hormonal regulators include insulin, glucagon and somatostatin from the Endocrine Pancreas. Secretion of these hormones is controlled predominantly by the supply of nutrients in the circulation but also by nerve signals and other peptides. Thus, it is likely that peptides, released from cells of the gut or Endocrine Pancreas or from peptidergic nerves, affect glucose homeostasis by modulating the secretion of insulin, glucagon and somatostatin. When searching for novel gut peptides with such effects, diazepam binding inhibitor (DBI) was isolated from the porcine small intestine. By immunocytochemistry, DBI has been demonstrated to occur not only in the gut but also in Endocrine cells of the pancreatic islets, namely in the somatostatin-producing D-cells in pig and man, and in the glucagon-producing A-cells in rat. Porcine DBI (pDBI; 10 −8 –10 −7 M) has been shown to suppress glucose-stimulated release of insulin from both isolated islets and perfused Pancreas of the rat. Furthermore, secretion of insulin stimulated by either the sulfonylurea glibenclamide or the phosphodiesterase inhibitor 3-isobutyl-I-methylxanthine (IBMX), was inhibited by the peptide. In contrast, arginine-induced release of insulin was unaffected by pDBI. Moreover, pDBI decreased arginine-induced release of glucagon from the perfused rat Pancreas, whereas release of somatostatin was unchanged. Notably, rat DBI, structurally identical with rat acyl-CoA-binding protein, has also been demonstrated to inhibit glucose-stimulated release of insulin in the rat, both in vivo and in vitro . Long-term exposure of cultured fetal rat islets to pDBI (10 −8 M) significantly decreased the synthesis of DNA in islet cells. In conclusion, DBI moderately suppresses the secretion of insulin from the B-cells, when stimulated by agents closing ATP-sensitive K + -channels (glucose, glibenclamide) or enhancing the formation of cAMP (IBMX). The mechanism of such an effect is not likely to involve binding of DBI to benzodiazepine-recognition sites of GABA-receptors, since B-cells are reportedly lacking this type of receptor. It cannot be ruled out that the peptide exerts its effect indirectly by binding factors important in regulation of secretion of insulin, due to its ability to bind amphiphilic compounds. The occurrence of DBI immunoreactivity in non-B-cells of the islets suggests that the peptide may modulate secretion of insulin locally through paracrine interaction.