دورية أكاديمية
Rapid cell-cycle reentry and cell death after acute inactivation of the retinoblastoma gene product in postnatal cochlear hair cells.
| العنوان: | Rapid cell-cycle reentry and cell death after acute inactivation of the retinoblastoma gene product in postnatal cochlear hair cells. |
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| المؤلفون: | Weber T; Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA., Corbett MK, Chow LM, Valentine MB, Baker SJ, Zuo J |
| المصدر: | Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2008 Jan 15; Vol. 105 (2), pp. 781-5. Date of Electronic Publication: 2008 Jan 04. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Washington, DC : National Academy of Sciences |
| مواضيع طبية MeSH: | Genes, Retinoblastoma*, Hair Cells, Auditory/*physiology , Retinoblastoma Protein/*metabolism, Animals ; Animals, Newborn ; Cell Cycle ; Cell Proliferation ; Chromatin/chemistry ; Hair Cells, Auditory/metabolism ; Humans ; Mice ; Mice, Transgenic ; Microscopy, Fluorescence ; Mitosis ; Molecular Motor Proteins/biosynthesis ; Recombination, Genetic ; Regeneration |
| مستخلص: | Unlike lower vertebrates, mammals are unable to replace damaged mechanosensory hair cells (HCs) in the cochlea. Recently, ablation of the retinoblastoma protein (Rb) in undifferentiated mouse HC precursors was shown to cause cochlear HC proliferation and the generation of new HCs, raising the hope that inactivation of Rb in postmitotic HCs could trigger cell division and regenerate functional HCs postnatally. Here, we acutely inactivated Rb in nearly all cochlear HCs of newborn mice, using a newly developed HC-specific inducible Cre mouse line. Beginning 48 h after Rb deletion, approximately 40% of HCs were in the S and M phases of the cell cycle, demonstrating an overriding role for Rb in maintaining the quiescent state of postnatal HCs. Unlike Rb-null HC precursors, such HCs failed to undergo cell division and died rapidly. HC clusters were restricted to the less differentiated cochlear regions, consistent with differentiation-dependent roles of Rb. Moreover, outer HCs expressed the maturation marker prestin, suggesting an embryonic time window for Rb-dependent HC specification. We conclude that Rb plays essential and age-dependent roles during HC proliferation and differentiation, and, in contrast to previous hypotheses, cell death after forced cell-cycle reentry presents a major challenge for mammalian HC regeneration from residual postnatal HCs. |
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| معلومات مُعتمدة: | R01 DC006471 United States DC NIDCD NIH HHS; DC05168 United States DC NIDCD NIH HHS; R21 DC008800 United States DC NIDCD NIH HHS; R25 CA023944 United States CA NCI NIH HHS; DC06471 United States DC NIDCD NIH HHS; CA21765 United States CA NCI NIH HHS; R01 NS044172 United States NS NINDS NIH HHS; A096832 United States PHS HHS; NS044172 United States NS NINDS NIH HHS; P30 CA021765 United States CA NCI NIH HHS; CA023944 United States CA NCI NIH HHS; DC008800 United States DC NIDCD NIH HHS; R21 DC005168 United States DC NIDCD NIH HHS |
| المشرفين على المادة: | 0 (Chromatin) 0 (Molecular Motor Proteins) 0 (Pres protein, mouse) 0 (Retinoblastoma Protein) |
| تواريخ الأحداث: | Date Created: 20080108 Date Completed: 20080206 Latest Revision: 20220317 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC2206613 |
| DOI: | 10.1073/pnas.0708061105 |
| PMID: | 18178626 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1091-6490 |
|---|---|
| DOI: | 10.1073/pnas.0708061105 |