{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T02:16:01Z","timestamp":1789179361453,"version":"build-2803163510"},"reference-count":37,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2007,7,19]],"date-time":"2007-07-19T00:00:00Z","timestamp":1184803200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2007,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Bone morphogenic protein (BMP)-7 is expressed in the adult kidney and reverses chronic renal injury when given exogenously. Here, we report that a histone deacetylase inhibitor, trichostatin A (TSA), attenuates chronic renal injury, in part, by augmenting the expression of BMP-7 in kidney side population (SP) cells. We induced accelerated nephrotoxic serum nephritis (NTN) in C57BL\/6 mice and treated them with TSA for 3 weeks. Compared with vehicle-treated NTN mice, treatment with TSA prevented the progression of proteinuria, glomerulosclerosis, interstitial fibrosis, and loss of kidney SP cells. Basal gene expression of renoprotective factors such as BMP-7, vascular endothelial growth factor, and hepatocyte growth factor was significantly higher in kidney SP cells as compared with non-SP cells. Treatment with TSA significantly upregulated the expression of BMP-7 in SP cells but not in non-SP cells. Moreover, initiation of treatment with TSA after 3 weeks of NTN (for 3 weeks, until 6 weeks) partially but significantly reversed renal dysfunction. Our results indicate an important role of SP cells in the kidney as one of the possible generator cells of BMP-7 and TSA as a stimulator of the cells in reversing chronic renal disease.<\/jats:p>\n               <jats:p>Disclosure of potential conflicts of interest is found at the end of this article.<\/jats:p>","DOI":"10.1634\/stemcells.2007-0049","type":"journal-article","created":{"date-parts":[[2007,7,20]],"date-time":"2007-07-20T01:19:03Z","timestamp":1184894343000},"page":"2469-2475","source":"Crossref","is-referenced-by-count":48,"title":["Inhibition of Histone Deacetylase Activates Side Population Cells in Kidney and Partially Reverses Chronic Renal Injury"],"prefix":"10.1093","volume":"25","author":[{"given":"Naohiko","family":"Imai","sequence":"first","affiliation":[{"name":"Department of Clinical Renal Regeneration, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiichi","family":"Hishikawa","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Endocrinology, University of Tokyo, Bunkyo-ku, Tokyo, Japan"},{"name":"Department of Clinical Renal Regeneration, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takeshi","family":"Marumo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and Endocrinology, University of Tokyo, Bunkyo-ku, Tokyo, Japan"},{"name":"Department of Clinical Renal Regeneration, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junichi","family":"Hirahashi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Division of Nephrology and 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