{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T18:45:27Z","timestamp":1790189127342,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,9,21]],"date-time":"2007-09-21T00:00:00Z","timestamp":1190332800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2007,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The transcription factor c\u2010Jun regulates the expression of genes involved in proliferation and inflammation in many cell types but its role in human renal disease is largely unclear. In the current study we investigated whether c\u2010Jun activation is associated with human renal disease and if c\u2010Jun activation regulates pro\u2010inflammatory and pro\u2010fibrotic genes in renal cells. Activation of c\u2010Jun was quantified by scoring renal expression of phosphorylated c\u2010Jun (pc\u2010Jun) in control human renal tissue and in biopsies from patients with various renal diseases (diabetic nephropathy, focal glomerulosclerosis, hypertension, IgA nephropathy, membranous glomerulopathy, minimal change disease, membranoproliferative glomerulonephritis, systemic lupus erythematosus, acute rejection, and Wegener's granulomatosis); this was correlated with parameters of renal damage. Furthermore, we studied the functional role of c\u2010Jun activation in human tubular epithelial cells (HK\u20102) stimulated with TGF\u2010\u03b2. Activated c\u2010Jun was present in nuclei of glomerular and tubular cells in all human renal diseases, but only sporadically in controls. Across the diseases, the extent of pc\u2010Jun expression correlated with the degree of focal glomerulosclerosis, interstitial fibrosis, cell proliferation, kidney injury molecule\u20101 (Kim\u20101) expression, macrophage accumulation, and impairment of renal function. In HK\u20102 cells, TGF\u2010\u03b2 induced c\u2010Jun activation after 1 h (+40%, <jats:italic>p<\/jats:italic> &lt; 0.001) and 24 h (+160%, <jats:italic>p<\/jats:italic> &lt; 0.001). The specific c\u2010Jun N\u2010terminal kinase (JNK) inhibitor SP600125 abolished c\u2010Jun phosphorylation at all time points and blunted TGF\u2010\u03b2\u2010 or BSA\u2010induced procollagen\u20101\u03b1 1 and MCP\u20101 gene expression in HK\u20102 cells. We conclude that in human renal disease, the transcription factor c\u2010Jun is activated in glomerular and tubular cells. Activation of c\u2010Jun may be involved in the regulation of inflammation and\/or fibrosis in human renal disease. Copyright \u00a9 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.2228","type":"journal-article","created":{"date-parts":[[2007,9,21]],"date-time":"2007-09-21T08:46:26Z","timestamp":1190364386000},"page":"219-228","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":98,"title":["Glomerular and tubular induction of the transcription factor c\u2010Jun in human renal disease"],"prefix":"10.1002","volume":"213","author":[{"given":"MH","family":"De Borst","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Prakash","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"WBWH","family":"Melenhorst","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"MC","family":"van den 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