| Restoration of tubular epithelial cells during repair of the postischemic kidney occurs independently of bone marrow-derived stem cells. | |
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MedLine Citation:
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PMID: 16007251 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Ischemia causes kidney tubular cell damage and abnormal renal function. The kidney is capable of morphological restoration of tubules and recovery of function. Recently, it has been suggested that cells repopulating the ischemically injured tubule derive from bone marrow stem cells. We studied kidney repair in chimeric mice expressing GFP or bacterial beta-gal or harboring the male Y chromosome exclusively in bone marrow-derived cells. In GFP chimeras, some interstitial cells but not tubular cells expressed GFP after ischemic injury. More than 99% of those GFP interstitial cells were leukocytes. In female mice with male bone marrow, occasional tubular cells (0.06%) appeared to be positive for the Y chromosome, but deconvolution microscopy revealed these to be artifactual. In beta-gal chimeras, some tubular cells also appeared to express beta-gal as assessed by X-gal staining, but following suppression of endogenous (mammalian) beta-gal, no tubular cells could be found that stained with X-gal after ischemic injury. Whereas there was an absence of bone marrow-derived tubular cells, many tubular cells expressed proliferating cell nuclear antigen, which is reflective of a high proliferative rate of endogenous surviving tubular cells. Upon i.v. injection of bone marrow mesenchymal stromal cells, postischemic functional renal impairment was reduced, but there was no evidence of differentiation of these cells into tubular cells of the kidney. Thus, our data indicate that bone marrow-derived cells do not make a significant contribution to the restoration of epithelial integrity after an ischemic insult. It is likely that intrinsic tubular cell proliferation accounts for functionally significant replenishment of the tubular epithelium after ischemia. |
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Authors:
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Jeremy S Duffield; Kwon Moo Park; Li-Li Hsiao; Vicki R Kelley; David T Scadden; Takaharu Ichimura; Joseph V Bonventre |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2005-06-02 |
Journal Detail:
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Title: The Journal of clinical investigation Volume: 115 ISSN: 0021-9738 ISO Abbreviation: J. Clin. Invest. Publication Date: 2005 Jul |
Date Detail:
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Created Date: 2005-07-11 Completed Date: 2005-08-31 Revised Date: 2009-11-18 |
Medline Journal Info:
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Nlm Unique ID: 7802877 Medline TA: J Clin Invest Country: United States |
Other Details:
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Languages: eng Pagination: 1743-55 Citation Subset: AIM; IM |
Affiliation:
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Renal Division and Department of Medicine, Brigham & Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Bone Marrow Transplantation Epithelial Cells / pathology, physiology Female Green Fluorescent Proteins / genetics, metabolism Hematopoietic Stem Cells / pathology Ischemia / pathology, physiopathology Kidney / blood supply, injuries*, pathology, physiopathology Kidney Tubules / pathology*, physiopathology Male Mice Mice, Inbred C57BL Mice, Transgenic Radiation Chimera Recombinant Proteins / genetics, metabolism Regeneration Reperfusion Injury / pathology, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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DK 38452/DK/NIDDK NIH HHS; DK 39773/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Recombinant Proteins; 0/enhanced green fluorescent protein; 147336-22-9/Green Fluorescent Proteins |
| Comments/Corrections | |
Comment In:
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J Clin Invest. 2005 Jul;115(7):1705-8
[PMID:
16007248
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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