{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T01:49:40Z","timestamp":1790819380454,"version":"4.1.0"},"reference-count":67,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2018,10]]},"abstract":"\n Background<\/jats:title>\n \n Mutation of\n HNF1B<\/jats:italic>\n , the gene encoding transcription factor HNF-1\n \u03b2<\/jats:italic>\n , is one cause of autosomal dominant tubulointerstitial kidney disease, a syndrome characterized by tubular cysts, renal fibrosis, and progressive decline in renal function. HNF-1\n \u03b2<\/jats:italic>\n has also been implicated in epithelial\u2013mesenchymal transition (EMT) pathways, and sustained EMT is associated with tissue fibrosis. The mechanism whereby mutated\n HNF1B<\/jats:italic>\n leads to tubulointerstitial fibrosis is not known.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n To explore the mechanism of fibrosis, we created HNF-1\n \u03b2<\/jats:italic>\n \u2013deficient mIMCD3 renal epithelial cells, used RNA-sequencing analysis to reveal differentially expressed genes in wild-type and HNF-1\n \u03b2<\/jats:italic>\n \u2013deficient mIMCD3 cells, and performed cell lineage analysis in HNF-1\n \u03b2<\/jats:italic>\n mutant mice.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The HNF-1\n \u03b2<\/jats:italic>\n \u2013deficient cells exhibited properties characteristic of mesenchymal cells such as fibroblasts, including spindle-shaped morphology, loss of contact inhibition, and increased cell migration. These cells also showed upregulation of fibrosis and EMT pathways, including upregulation of Twist2, Snail1, Snail2, and Zeb2, which are key EMT transcription factors. Mechanistically, HNF-1\n \u03b2<\/jats:italic>\n directly represses\n Twist2<\/jats:italic>\n , and ablation of\n Twist2<\/jats:italic>\n partially rescued the fibroblastic phenotype of HNF-1\n \u03b2<\/jats:italic>\n mutant cells. Kidneys from HNF-1\n \u03b2<\/jats:italic>\n mutant mice showed increased expression of Twist2 and its downstream target\n Snai2<\/jats:italic>\n . Cell lineage analysis indicated that HNF-1\n \u03b2<\/jats:italic>\n mutant epithelial cells do not transdifferentiate into kidney myofibroblasts. Rather, HNF-1\n \u03b2<\/jats:italic>\n mutant epithelial cells secrete high levels of TGF-\n \u03b2<\/jats:italic>\n ligands that activate downstream Smad transcription factors in renal interstitial cells.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Ablation of HNF-1\n \u03b2<\/jats:italic>\n in renal epithelial cells leads to the activation of a Twist2-dependent transcriptional network that induces EMT and aberrant TGF-\n \u03b2<\/jats:italic>\n signaling, resulting in renal fibrosis through a cell-nonautonomous mechanism.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.2018040437","type":"journal-article","created":{"date-parts":[[2018,8,10]],"date-time":"2018-08-10T09:15:14Z","timestamp":1533892514000},"page":"2493-2509","source":"Crossref","is-referenced-by-count":74,"title":["Mechanism of Fibrosis in HNF1B-Related Autosomal Dominant Tubulointerstitial Kidney Disease"],"prefix":"10.1681","volume":"29","author":[{"given":"Siu Chiu","family":"Chan","sequence":"first","affiliation":[{"name":"Department of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[{"name":"Minnesota Supercomputing Institute, University of Minnesota, Minneapolis, Minnesota; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annie","family":"Shao","sequence":"additional","affiliation":[{"name":"Department of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana","family":"Avdulov","sequence":"additional","affiliation":[{"name":"Department of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeremy","family":"Herrera","sequence":"additional","affiliation":[{"name":"Department of Medicine and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karam","family":"Aboudehen","sequence":"additional","affiliation":[{"name":"Department of Medicine 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