ArticleCell proliferation2007
The cellular origin and proliferative status of regenerating renal parenchyma after mercuric chloride damage and erythropoietin treatment.
Article in Cell proliferation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Isolation of Mesenchymal Stem Cells from Human Deciduous Teeth Pulp.BioMed research international · 2017Article
- Decellularized scaffold of cryopreserved rat kidney retains its recellularization potential.PloS one · 2017Article
- Epidermal growth factor attenuates tubular necrosis following mercuric chloride damage by regeneration of indigenous, not bone marrow-derived cells.Journal of cellular and molecular medicine · 2015Article
- IKVAV regulates ERK1/2 and Akt signalling pathways in BMMSC population growth and proliferation.Cell proliferation · 2014Article
- Therapeutic potential of mesenchymal stem cells in regenerative medicine.Stem cells international · 2013Article
- Bone marrow cells contribute to tubular epithelium regeneration following acute kidney injury induced by mercuric chloride.The Indian journal of medical research · 2012Article
- Regenerative medicine as applied to general surgery.Annals of surgery · 2012Review
- Mesenchymal stem cells: from experiment to clinic.Fibrogenesis & tissue repair · 2011Article
- Stem cells derived from human amniotic fluid contribute to acute kidney injury recovery.The American journal of pathology · 2010Article
- Proliferation of myofibroblasts in the stroma of renal oncocytoma.Cell proliferation · 2010Article
- The long-term label retaining population of the renal papilla arises through divergent regional growth of the kidney.American journal of physiology. Renal physiology · 2009Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIn this study, we have sought to establish the cellular origin and proliferative status of the renal parenchyma as it regenerates after damage induced by mercuric chloride, with or without erythropoietin treatments, that might alter the response. MATERIALS AND
methodsFemale mice were irradiated and male whole bone marrow was transplanted into them. Six weeks later recipient mice were assigned to one of four groups: control, mercuric chloride treated, erythropoietin treated and treated with mercuric chloride plus erythropoietin.
resultsTubular injury scores were high 3 days after mercuric chloride and had recovered partially after 14 days, in line with serum urea nitrogen levels. Confocal microscopy confirmed the tubular location of bone marrow-derived cells. A 'four-in-one' analytical technique (identifying cell origin, tubular phenotype, tubular basement membranes and S-phase status) revealed that tubular necrosis increased bone marrow derivation of renal tubular epithelium from a baseline of approximately 1.3% to approximately 4.0%. Erythropoietin increased the haematocrit, but no other effects were detected.
conclusionAs 1 in 12 proximal tubular cells in S-phase was derived from bone marrow, we conclude that in the kidney, the presence of bone marrow-derived cells makes a minor but important regenerative contribution after tubular necrosis.
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