scholarly journals Distribution and Afferent Effects of Transplanted mESCs on Cochlea in Acute and Chronic Neural Hearing Loss Models

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
So-Young Chang ◽  
Hee-Won Jeong ◽  
Eunjeong Kim ◽  
Jae Yun Jung ◽  
Min Young Lee
Keyword(s):  
Hearing Loss ◽  
Stem Cell ◽  
Mouse Model ◽  
Hearing Aids ◽  
Sensory Deprivation ◽  
Embryonic Stem ◽  
Sensory Cells ◽  
Secondary Degeneration ◽  
Chronic Model ◽  
Loss Models

Hearing loss is a sensory deprivation that can affect the quality of life. Currently, only rehabilitation devices such as hearing aids and cochlear implants are used, without a definitive cure. However, in chronic hearing-deprived patients, in whom secondary auditory neural degeneration is expected, a relatively poor rehabilitation prognosis is projected. Stem cell therapy for cochlear neural structures would be an easier and feasible strategy compared with cochlear sensory cells. Considering the highly developed cochlear implantation technology, improving cochlear neural health has significant medical and social effects. Stem cell delivery to Rosenthal’s canal in an acutely damaged mouse model has been performed and showed cell survival and the possibility of differentiation. The results of stem cell transplantation in chronic auditory neural hearing loss should be evaluated because neural stem cell replacement therapy for chronic (long-term) sensorineural hearing loss is a major target in clinics. In the present study, we established a mouse model that mimicked chronic auditory neural hearing loss (secondary degeneration of auditory neurons after loss of sensory input). Then, mouse embryonic stem cells (mESCs) were transplanted into the scala tympani and survival and distribution of transplanted cells were compared between the acute and chronic auditory neural hearing loss models induced by ouabain or kanamycin (KM), respectively. The mESC survival was similar to the acute model, and perilymphatic distribution of cell aggregates was more predominant in the chronic model. Lastly, the effects of mESC transplantation on neural signal transduction observed in the cochlear nucleus (CN) were compared and a statistical increase was observed in the chronic model compared with other models. These results indicated that after transplantation, mESCs survived in the cochlea and increased the neural signaling toward the central auditory pathway, even in the chronic (secondary) hearing loss mouse model.

Hepatocyte-Like Cells Can Be Derived from Human Umbilical Cord Blood and Embryonic Stem Cells: Tested in a Novel Mouse Model

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3490-3490
Author(s):  
Ping Zhou ◽  
Ryan Lahey ◽  
Daniel Cortes ◽  
Yetunde Olusanya ◽  
Sarah Hohm ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Mouse Model ◽  
Cord Blood ◽  
Liver Damage ◽  
Embryonic Stem ◽  
Human Cells ◽  
Embryoid Bodies ◽  
Recipient Mouse

Abstract Liver transplantation remains the only therapeutic option for many acute and chronic end-stage liver diseases. However, this approach is limited by a serious shortage of donor organs required for transplantation. Hepatocytes have been reported to be generated from cells not originated from liver, such as hematopoietic stem cells, mesenchymal stem cells and most recently embryonic stem cells. However, the frequency of these stem cell-derived hepatocytes is very low in most studies. Therefore, the significance of stem cell contribution to the repair of liver damage is still controversial. To further explore this potential, we used the beta-glucuronidase (GUSB)-null NOD/SCID/MPSVII mouse model for better identification of engrafted human cells. Enriched cord blood primitive cells (lineage depleted cells with high aldehyde dehydrogenase activity, ALDHhiLin−) were transplanted into irradiated NOD/SCID/MPSVII mice. One month after transplantation, carbon tetrachloride (CCl4) was administrated into the mice twice a week for 4 weeks to induce liver damage. In this model, ALDHhiLin− cells efficiently engrafted in the recipient mouse livers as demonstrated by GUSB positive immunohistological staining and the presence of human Alu DNA using PCR. The percentage of human cells in these livers ranged between 3% and 14.2% using quantitative real-time PCR. These engrafted cells improved recovery of the mice from toxic insult, and significantly increased the numbers of surviving mice. Furthermore, human liver-specific a-1-antitrypsin mRNA and albumin protein were expressed in the recipient livers. Interestingly, human vs. murine centromeric fluorescent in situ hybridization analysis on the liver sections demonstrated that most human cells were not fused to mouse cells. However, mouse nuclei were detected in the majority of the albumin-expressing cells, suggesting that fusion had occurred and was responsible for the appearance of donor derived hepatocyte-like cells. With the goal of achieving higher levels of liver reconstitution than had been possible using the adult stem cells, we began studying engraftment of human embryonic stem cells (hESC), which theoretically have the potential to regenerate any tissue. The H1 cell line was cultured on mouse embryonic fibroblasts then allowed to form embryoid bodies (EBs) in suspension culture for 7 days with or without further expansion and differentiation in attached culture for another month. EBs were dissociated into a single cell suspension and transplanted into NOD/SCID/MPSVII mice or NOD/SCID/IL2Rγ−/− mice via the tail vein after 300 RADs sublethal radiation with or without CCl4 administration. Two months post-transplantation, the human EB-derived cells were found to be well engrafted in the NOD/SCID/MPSVII mouse livers, spleens and kidneys, using the clear-cut enzymatic identification method for cells expressing normal levels of beta-glucuronidase in the mice, which are null for the enzyme. Human DNA was also detected in the recipient mouse liver. Most interestingly, human albumin-expressing cells were also found in the livers of engrafted mice. Our data indicate that the progeny of cord blood stem cells can significantly enhance survival of mice with severe liver damage, and that fusion can occur between transplanted and recipient cells. This could be a normal mechanism of liver repair, since hepatocytes exist normally as multinucleate cells. We also demonstrate that the progeny of hESC can be effectively dissociated and transplanted intravenously, then home to the liver and differentiate to the hepatocyte lineage in an immune deficient mouse model of liver damage.

Anatomical and functional recovery by embryonic stem cell-derived neural tissue of a mouse model of brain damage

2004 ◽  
Vol 219 (1-2) ◽  
pp. 107-117 ◽  
Author(s):  
Shunmei Chiba ◽  
Ritsuko Ikeda ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
Mitsuhiro Takeno ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mouse Model ◽  
Embryonic Stem Cell ◽  
Brain Damage ◽  
Functional Recovery ◽  
Embryonic Stem ◽  
Neural Tissue

scholarly journals Differentiation and Transplantation of Embryonic Stem Cell-Derived Cone Photoreceptors into a Mouse Model of End-Stage Retinal Degeneration

2017 ◽  
Vol 8 (6) ◽  
pp. 1659-1674 ◽  
Author(s):  
Kamil Kruczek ◽  
Anai Gonzalez-Cordero ◽  
Debbie Goh ◽  
Arifa Naeem ◽  
Mindaugas Jonikas ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mouse Model ◽  
Embryonic Stem Cell ◽  
Retinal Degeneration ◽  
Embryonic Stem ◽  
Cone Photoreceptors ◽  
End Stage

scholarly journals Musical hallucination associated with hearing loss

2011 ◽  
Vol 69 (2b) ◽  
pp. 395-400 ◽  
Author(s):  
T G Sanchez ◽  
S C M Rocha ◽  
K A B Knobel ◽  
M A Kii ◽  
R M R Santos ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hearing Aids ◽  
Auditory Hallucination ◽  
Sensory Deprivation ◽  
Auditory Memory ◽  
Association Cortex ◽  
Auditory Information ◽  
Nerve Lesion ◽  
Musical Hallucination ◽  
Auditory Association Cortex

In spite of the fact that musical hallucination have a significant impact on patients' lives, they have received very little attention of experts. Some researchers agree on a combination of peripheral and central dysfunctions as the mechanism that causes hallucination. The most accepted physiopathology of musical hallucination associated to hearing loss (caused by cochlear lesion, cochlear nerve lesion or by interruption of mesencephalon or pontine auditory information) is the disinhibition of auditory memory circuits due to sensory deprivation. Concerning the cortical area involved in musical hallucination, there is evidence that the excitatory mechanism of the superior temporal gyrus, as in epilepsies, is responsible for musical hallucination. In musical release hallucination there is also activation of the auditory association cortex. Finally, considering the laterality, functional studies with musical perception and imagery in normal individuals showed that songs with words cause bilateral temporal activation and melodies activate only the right lobe. The effect of hearing aids on the improvement of musical hallucination as a result of the hearing loss improvement is well documented. It happens because auditory hallucination may be influenced by the external acoustical environment. Neuroleptics, antidepressants and anticonvulsants have been used in the treatment of musical hallucination. Cases of improvement with the administration of carbamazepine, meclobemide and donepezil were reported, but the results obtained were not consistent.

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