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Female mice were irradiated and male whole bone marrow (BM<\/jats:styled-content>) was transplanted into them. Six weeks later recipient mice were assigned to one of eight groups: control, P\u2010GCSF<\/jats:styled-content>+, EGF<\/jats:styled-content>+, P\u2010GCSF<\/jats:styled-content>+EGF<\/jats:styled-content>+, HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content>, HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content>+P\u2010GCSF<\/jats:styled-content>+, HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content>+EGF<\/jats:styled-content>+ and HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content>+P\u2010GCSF<\/jats:styled-content>+EGF<\/jats:styled-content>+. Following HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content>, injection tubular injury scores increased and serum urea nitrogen levels reached uraemia after 3\u00a0days, but EGF<\/jats:styled-content>\u2010treated groups were resistant to this acute kidney injury. A four\u2010in\u2010one analytical technique for identification of cellular origin, tubular phenotype, basement membrane and S\u2010phase status revealed that BM<\/jats:styled-content> contributed 1% of proximal tubular epithelium in undamaged kidneys and 3% after HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content> damage, with no effects of exogenous EGF<\/jats:styled-content> or P\u2010GCSF<\/jats:styled-content>. Only 0.5% proximal tubular cells were seen in S\u2010phase in the undamaged group kidneys; this increased to 7\u20138% after HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content> damage and to 15% after addition of EGF<\/jats:styled-content>. Most of the regenerating tubular epithelium originated from the indigenous pool. BM<\/jats:styled-content> contributed up to 6.6% of the proximal tubular cells in S\u2010phase after HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content> damage, but only to 3.3% after additional EGF<\/jats:styled-content>. EGF<\/jats:styled-content> administration attenuated tubular necrosis following HgCl2<\/jats:sub><\/jats:roman><\/jats:styled-content> damage, and the major cause of this protective effect was division of indigenous cells, whereas BM<\/jats:styled-content>\u2010derived cells were less responsive. P\u2010GCSF<\/jats:styled-content> did not influence damage or regeneration.<\/jats:p>","DOI":"10.1111\/jcmm.12478","type":"journal-article","created":{"date-parts":[[2014,11,11]],"date-time":"2014-11-11T11:21:10Z","timestamp":1415704870000},"page":"463-473","source":"Crossref","is-referenced-by-count":14,"title":["Epidermal growth factor attenuates tubular necrosis following mercuric chloride damage by regeneration of indigenous, not bone marrow\u2010derived cells"],"prefix":"10.1111","volume":"19","author":[{"given":"Tzung\u2010Hai","family":"Yen","sequence":"first","affiliation":[{"name":"Department of Nephrology and Division of Clinical Toxicology Chang Gung Memorial Hospital and College of Medicine Chang Gung University Linkou Taiwan"},{"name":"Histopathology Laboratory Cancer Research UK London Research Institute London UK"},{"name":"Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Malcolm R.","family":"Alison","sequence":"additional","affiliation":[{"name":"Histopathology Laboratory Cancer Research UK London Research Institute London UK"},{"name":"Epithelial Stem Cell Group Centre for Tumour Biology Barts Cancer Institute Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert A.","family":"Goodlad","sequence":"additional","affiliation":[{"name":"Histopathology Laboratory Cancer Research UK London Research Institute London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"William R.","family":"Otto","sequence":"additional","affiliation":[{"name":"Histopathology Laboratory Cancer Research UK London Research Institute London UK"},{"name":"Epithelial Stem Cell Group Centre for Tumour Biology Barts Cancer Institute Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rosemary","family":"Jeffery","sequence":"additional","affiliation":[{"name":"Histopathology Laboratory Cancer Research UK London Research Institute London UK"},{"name":"Epithelial Stem Cell Group Centre for Tumour Biology Barts Cancer Institute Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"},{"name":"Molecular Pathology Facility National Centre for Bowel Research and Surgical Innovation Centre for Digestive Diseases Blizard Institute Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H. 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