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2. Concomitant differentiation of a population of mouse embryonic stem cells into neuron-like cells and Schwann cell-like cells in a slow-flow microfluidic device

Author

Ramamurthy, Poornapriya, White, Joshua B., Park, Joong Yull, Hume, Richard I., Ebisu, Fumi, Mendez, Flor, Takayama, Shuichi, and Barald, Kate F

Subjects
Neurons, Cell Differentiation, Mouse Embryonic Stem Cells, Article, Intramolecular Oxidoreductases, Mice, Cochlear Implants, Lab-On-A-Chip Devices, Animals, Schwann Cells, Hearing Loss, Spiral Ganglion, Macrophage Migration-Inhibitory Factors, Myelin Sheath
Abstract

To send meaningful information to the brain, an inner ear cochlear implant (CI) must become closely coupled to as large and healthy a population of remaining spiral ganglion neurons (SGN) as possible. Inner ear gangliogenesis depends on macrophage migration inhibitory factor (MIF), a directionally attractant neurotrophic cytokine made by both Schwann and supporting cells (Bank et al., 2012). MIF-induced mouse embryonic stem cell (mESC)-derived "neurons" could potentially substitute for lost or damaged SGN. mESC-derived "Schwann cells" produce MIF, as do all Schwann cells (Huang et al., a; Roth et al., 2007; Roth et al., 2008) and could attract SGN to a "cell-coated" implant.Neuron- and Schwann cell-like cells were produced from a common population of mESCs in an ultra-slow-flow microfluidic device. As the populations interacted, "neurons" grew over the "Schwann cell" lawn, and early events in myelination were documented. Blocking MIF on the Schwann cell side greatly reduced directional neurite outgrowth. MIF-expressing "Schwann cells" were used to coat a CI: Mouse SGN and MIF-induced "neurons" grew directionally to the CI and to a wild-type but not MIF-knockout organ of Corti explant.Two novel stem cell-based approaches for treating the problem of sensorineural hearing loss are described. Developmental Dynamics 246:7-27, 2017. © 2016 Wiley Periodicals, Inc.

Published
2016

4. Concomitant differentiation of a population of mouse embryonic stem cells into neuron-like cells and schwann cell-like cells in a slow-flow microfluidic device.

Author

Ramamurthy, Poornapriya, White, Joshua B., Yull Park, Joong, Hume, Richard I., Ebisu, Fumi, Mendez, Flor, Takayama, Shuichi, and Barald, Kate F.

Abstract

Background: To send meaningful information to the brain, an inner ear cochlear implant (CI) must become closely coupled to as large and healthy a population of remaining spiral ganglion neurons (SGN) as possible. Inner ear gangliogenesis depends on macrophage migration inhibitory factor (MIF), a directionally attractant neurotrophic cytokine made by both Schwann and supporting cells (Bank et al., 2012). MIF-induced mouse embryonic stem cell (mESC)-derived 'neurons' could potentially substitute for lost or damaged SGN. mESC-derived 'Schwann cells' produce MIF, as do all Schwann cells (Huang et al., a; Roth et al., 2007; Roth et al., 2008) and could attract SGN to a 'cell-coated' implant. Results: Neuron- and Schwann cell-like cells were produced from a common population of mESCs in an ultra-slow-flow microfluidic device. As the populations interacted, 'neurons' grew over the 'Schwann cell' lawn, and early events in myelination were documented. Blocking MIF on the Schwann cell side greatly reduced directional neurite outgrowth. MIF-expressing 'Schwann cells' were used to coat a CI: Mouse SGN and MIF-induced 'neurons' grew directionally to the CI and to a wild-type but not MIF-knockout organ of Corti explant. Conclusions: Two novel stem cell-based approaches for treating the problem of sensorineural hearing loss are described. Developmental Dynamics 246:7-27, 2017. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Published
2017
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5. Influence of hormones and hormone metabolites on the growth of schwann cells derived from embryonic stem cells and on tumor cell lines expressing variable levels of neurofibromin This article was accepted for inclusion in the Special Focus on Stem Cells??? Developmental Dynamics 236 #12 .

Author

Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Internal Medicine-Molecular Medicine and Genetics, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan Medical School, 3053 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, Department of Pediatrics, Neurology Division, University of Florida College of Medicine, Gainesville, Florida, Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida, Roth, Therese M., Ramamurthy, Poornapriya, Muir, David, Wallace, Margaret R., Zhu, Yuan, Chang, Lou, Barald, Kate F., Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Internal Medicine-Molecular Medicine and Genetics, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan Medical School, 3053 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, Department of Pediatrics, Neurology Division, University of Florida College of Medicine, Gainesville, Florida, Department of Molecular Genetics and Microbiology, University of Florida College of Medicine, Gainesville, Florida, Roth, Therese M., Ramamurthy, Poornapriya, Muir, David, Wallace, Margaret R., Zhu, Yuan, Chang, Lou, and Barald, Kate F.

Abstract

Loss of neurofibromin, the protein product of the tumor suppressor gene neurofibromatosis type 1 (NF1), is associated with neurofibromas, composed largely of Schwann cells. The number and size of neurofibromas in NF1 patients have been shown to increase during pregnancy. A mouse embryonic stem cell (mESC) model was used, in which mESCs with varying levels of neurofibromin were differentiated into Schwann-like cells. NF1 cell lines derived from a malignant and a benign human tumor were used to study proliferation in response to hormones. Estrogen and androgen receptors were not expressed or expressed at very low levels in the NF1+/+ cells, at low levels in NF1+/???cells, and robust levels in NF1???/???cells. A 17??-estradiol (E2) metabolite, 2-methoxy estradiol (2ME2) is cytotoxic to the NF1???/??? malignant tumor cell line, and inhibits proliferation in the other cell lines. 2ME2 or its derivatives could provide new treatment avenues for NF1 hormone-sensitive tumors at times of greatet hormonal influence. Developmental Dynamics 237:513???524, 2008.?? 2008 Wiley-Liss, Inc.

Published
2008

6. Macrophage migration inhibitory factor acts as a neurotrophin in the developing inner ear

Author

Bank, Lisa M., primary, Bianchi, Lynne M., additional, Ebisu, Fumi, additional, Lerman-Sinkoff, Dov, additional, Smiley, Elizabeth C., additional, Shen, Yu-chi, additional, Ramamurthy, Poornapriya, additional, Thompson, Deborah L., additional, Roth, Therese M., additional, Beck, Christine R., additional, Flynn, Matthew, additional, Teller, Ryan S., additional, Feng, Luming, additional, Llewellyn, G. Nicholas, additional, Holmes, Brandon, additional, Sharples, Cyrrene, additional, Coutinho-Budd, Jaeda, additional, Linn, Stephanie A., additional, Chervenak, Andrew P., additional, Dolan, David F., additional, Benson, Jennifer, additional, Kanicki, Ariane, additional, Martin, Catherine A., additional, Altschuler, Richard, additional, Koch, Alisa E., additional, Jewett, Ethan M., additional, Germiller, John A., additional, and Barald, Kate F., additional

Published
2013
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7. A mouse embryonic stem cell model of Schwann cell differentiation for studies of the role of neurofibromatosis type 1 in Schwann cell development and tumor formation

Author

Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; The Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Program in Neuroscience, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; The Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan ; Program in Neuroscience, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan Medical School, 3053 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA, Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, Roth, Therese M., Ramamurthy, Poornapriya, Ebisu, Fumi, Lisak, Robert P., Bealmear, Beverly M., Barald, Kate F., Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; The Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; Program in Neuroscience, University of Michigan, Ann Arbor, Michigan, Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan ; The Department of Biomedical Engineering, College of Engineering, University of Michigan, Ann Arbor, Michigan ; Program in Neuroscience, University of Michigan, Ann Arbor, Michigan ; Department of Cell and Developmental Biology, University of Michigan Medical School, 3053 BSRB, 109 Zina Pitcher Place, Ann Arbor, MI 48109-2200, USA, Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan, Roth, Therese M., Ramamurthy, Poornapriya, Ebisu, Fumi, Lisak, Robert P., Bealmear, Beverly M., and Barald, Kate F.

Abstract

The neurofibromatosis Type 1 (NF1) gene functions as a tumor suppressor gene. One known function of neurofibromin, the NF1 protein product, is to accelerate the slow intrinsic GTPase activity of Ras to increase the production of inactive rasGDP, with wide-ranging effects on p21ras pathways. Loss of neurofibromin in the autosomal dominant disorder NF1 is associated with tumors of the peripheral nervous system, particularly neurofibromas, benign lesions in which the major affected cell type is the Schwann cell (SC). NF1 is the most common cancer predisposition syndrome affecting the nervous system. We have developed an in vitro system for differentiating mouse embryonic stem cells (mESC) that are NF1 wild type (+/+), heterozygous (+/−), or null (−/−) into SC-like cells to study the role of NF1 in SC development and tumor formation. These mES-generated SC-like cells, regardless of their NF1 status, express SC markers correlated with their stage of maturation, including myelin proteins. They also support and preferentially direct neurite outgrowth from primary neurons. NF1 null and heterozygous SC-like cells proliferate at an accelerated rate compared to NF1 wild type; this growth advantage can be reverted to wild type levels using an inhibitor of MAP kinase kinase (Mek). The mESC of all NF1 types can also be differentiated into neuron-like cells. This novel model system provides an ideal paradigm for studies of the role of NF1 in cell growth and differentiation of the different cell types affected by NF1 in cells with differing levels of neurofibromin that are neither transformed nor malignant. © 2007 Wiley-Liss, Inc.

Published
2007

8. Macrophage migration inhibitory factor acts as a neurotrophin in the developing inner ear

Author

Bank, Lisa M., primary, Bianchi, Lynne M., additional, Ebisu, Fumi, additional, Lerman-Sinkoff, Dov, additional, Smiley, Elizabeth C., additional, Shen, Yu-chi, additional, Ramamurthy, Poornapriya, additional, Thompson, Deborah L., additional, Roth, Therese M., additional, Beck, Christine R., additional, Flynn, Matthew, additional, Teller, Ryan S., additional, Feng, Luming, additional, Llewellyn, G. Nicholas, additional, Holmes, Brandon, additional, Sharples, Cyrrene, additional, Coutinho-Budd, Jaeda, additional, Linn, Stephanie A., additional, Chervenak, Andrew P., additional, Dolan, David F., additional, Benson, Jennifer, additional, Kanicki, Ariane, additional, Martin, Catherine A., additional, Altschuler, Richard, additional, Koch, Alicia E., additional, Jewett, Ethan M., additional, Germiller, John A., additional, and Barald, Kate F., additional

Published
2012
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9. A Student Team in a University of Michigan Biomedical Engineering Design Course Constructs a Microfluidic Bioreactor for Studies of Zebrafish Development

Author

Shen, Yu-Chi, primary, Li, David, additional, Al-Shoaibi, Ali, additional, Bersano-Begey, Tom, additional, Chen, Hao, additional, Ali, Shahid, additional, Flak, Betsy, additional, Perrin, Catherine, additional, Winslow, Max, additional, Shah, Harsh, additional, Ramamurthy, Poornapriya, additional, Schmedlen, Rachael H., additional, Takayama, Shuichi, additional, and Barald, Kate F., additional

Published
2009
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14. Mouse Embryonic Stem Cells Differentiated into Neuron-like Cells or Schwann Cell-like Cells for the Development of Strategies to Ameliorate Deafness.

Author

Ramamurthy, Poornapriya

Subjects
ES Cells, Neuron-like Cell, Schwann -Like Cell, Microfluidics, Cochlear Implant, Regenration, Cell Therapy
Abstract

Cochlear prostheses (CI) can restore hearing to patients with extensive sensorineural hearing loss (SNHL) by replacing lost or damaged cochlear mechanosensory hair cells (HC) with an electrode array. For the CI to send meaningful acoustic information to the brain, as large a population of remaining inner ear spiral ganglion neurons (SGN) as possible must become functionally coupled to the CI. SGN-CI coupling would be enhanced by a means of inducing directed neurite extension from the remaining SGN to the CI. Macrophage migration inhibitory factor (MIF) is a neurotrophic cytokine, which is expressed in early embryogenesis in the central and peripheral nervous systems, the eye and inner ear, where it is expressed in the supporting cells that underlie the HC and in all Schwann Cells. We produced a mESC-derived neuron-like population of cells from mESC exposed to recombinant MIF that in many respects resemble SGN. Maturation of these MIF mESC-derived neuron-like cells was enhanced by Docosahexaenoic acid, a fatty acid that helps promote neuronal maturation. Such cells could be used eventually to replace lost of damaged SGN. This laboratory also produced the first embryonic stem cell (ESC) derived model of the Schwann Cell. These Schwann cells produce MIF, which is capable of inducing directional neurite outgrowth and supporting the survival of both early stage statoacoustic ganglion neurons (SAG) and their adult counterparts in the SGN as do all Schwann Cells. We have coated CIs with mESC-MIF-producing “Schwann Cells” and observed directional outgrowth and contact formation between the “Schwann Cell”-coated CI and primary mouse embryonic SAG or adult SGN to bring the neurites closer to the CI for better performance. Thus two different stem cell-based approaches have been used to address two different problems in deafness: improved integration of CI with native SGN and replacement of SGN themselves with a stem cell population molecularly engineered to resemble SGN.

Published
2012

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