Rannar Airik, PhD
- Assistant Professor of Pediatrics and Developmental Biology
Administrative Assistant: Rebecca L. Ceoffe
Dr. Rannar Airik, PhD, joined the Division of Nephrology in August 2015. He obtained his doctoral degree in the field of developmental biology from the Medical University Hannover, Germany, where he worked on the molecular analysis of the lower urinary tract development to decipher the mechanisms of urogenital abnormalities in human diseases known as congenital anomalies of the kidney and urinary tract (CAKUT). He completed his postdoctoral training in the lab of Dr. Friedhelm Hildebrandt.
Dr. Airik’s work has characterized the molecular function of several genes, which if mutated cause nephronophthisis, a genetic form of childhood chronic kidney disease. His work discovered that the genes encode components of DNA damage response signaling pathways and play important role in DNA repair and cell cycle regulation. Using transgenic mice combined with renal injury models he now investigates the molecular mechanisms of nephronophthisis and how DNA damage affects renal homeostasis and regeneration capacity. Understanding how impaired DNA damage response contributes to renal degeneration and fibrosis, features that determine the progression to renal failure would open up avenues for targeting chronic kidney disease.
Dr. Airik holds faculty positions in the Department of Pediatrics and Developmental Biology at the University of Pittsburgh School of Medicine.
Professional and Scientific Society Memberships
- American Society of Human Genetics, 2014-Present
- American Society of Nephrology, 2014-Present
- International Pediatrics Nephrology Association, 2018-Present
Education & Training
- BS, Zoology, University of Tartu, 2002
- MS, Developmental Biology, University of Tartu, 2004
- PhD, Molecular Biology, Medical University Hannover, 2008
- Postdoctoral Work, Molecular Biology, Medical University Hannover, 2008-2009
- Postdoctoral Work, Human Molecular Genetics, University of Michigan, 2009-2013
- Postdoctoral Work, Human Molecular Genetics, Boston Children's Hospital/Harvard Medical School, 2013-2014
Rudat C, Grieskamp T, Röhr C, Airik R, Wrede C, Hegermann J, Herrmann BG, Schuster-Gossler K, Kispert A. Upk3b is dispensable for development and integrity of urothelium and mesothelium. PLoS One9:e112112, 2014 PMID 25389758
Briot A, Jaroszewicz A, Warren CM, Lu J, Touma M, Rudat C, Hofmann JJ, Airik R, Weinmaster G, Lyons K, Wang Y, Kispert A, Pellegrini M, Iruela-Arispe ML. Repression of sox9 by jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells. Dev Cell 31:707-721, 2014 PMID 25535917
Schueler M, Braun DA, Chandrasekar G, Gee HY, Klasson TD, Halbritter J, Bieder A, Porath JD, Airik R, Zhou W, LoTurco JJ, Che A, Otto EA, Böckenhauer D, Sebire NJ, Honzik T, Harris PC, Koon SJ, Gunay-Aygun M, Saunier S, Zerres K, Bruechle NO, Drenth JP, Pelletier L, Tapia-Páez I, Lifton RP, Giles RH, Kere J, Hildebrandt F. DCDC2 Mutations Cause a Renal-Hepatic Ciliopathy by Disrupting Wnt Signaling. Am J Hum Genet 96:81-92, 2015 PMID 25557784
Braun DA, Schueler M, Halbritter J, Gee HY, Porath JD, Lawson JA, Airik R, Shril S, Allen SJ, Stein D, Al Kindy A, Beck BB, Cengiz N, Moorani KN, Ozaltin F, Hashmi S, Sayer JA, Bockenhauer D, Soliman NA, Otto EA, Lifton RP, Hildebrandt F. Whole exome sequencing identifies causative mutations in the majority of consanguineous or familial cases with childhood-onset increased renal echogenicity. Kidney Int 2015 Oct 21 PMID: 26489029
Gee HY, Sadowski CE, Aggarwal PK, Porath JD, Yakulov TA, Schueler M, Lovric S, Ashraf S, Braun DA, Halbritter J, Fang H, Airik R, Vega-Warner V, Cho KJ, Chan TA, Morris LG, Ffrench-Constant C, Allen N, McNeill H, Büscher R, Kyrieleis H, Wallot M, Gaspert A, Kistler T, Milford DV, Saleem MA, Keng WT, Alexander SI, Valentini RP, Licht C, Teh JC, Bogdanovic R, Koziell A, Bierzynska A, Soliman NA, Otto EA, Lifton RP, Holzman LB, Sibinga NE, Walz G, Tufro A, Hildebrandt F. FAT1 mutations cause a glomerulotubular nephropathy. Nat Commun 7:10822, 2016 PMID: 26905694
Airik R, Schueler M, Airik M, Cho J, Porath JD, Mukherjee E, Sims-Lucas S, Hildebrandt F. A FANCD2/FANCI-Associated Nuclease 1-Knockout Model Develops Karyomegalic Interstitial Nephritis. JASN 2016, 2016 Mar 29. ASN.2015101108. PMID: 27026368 Co-corresponding author
Airik R, Schueler M, Airik M, Cho J, Ulanowicz KA, Porath JD, Hurd TW, Bekker-Jensen S, Schrøder JM, Andersen JS, Hildebrandt F. SDCCAG8 Interacts with RAB Effector Proteins RABEP2 and ERC1 and Is Required for Hedgehog Signaling. PLoS One 2016 11(5):e0156081. PMID: 27224062 Co-corresponding author
Vermeren M, Lyraki R, Wani S, Airik R, Albagha O, Mort R, Hildebrandt F, Hurd T. Osteoclast stimulation factor 1 (Ostf1) KNOCKOUT increases trabecular bone mass in mice. Mamm Genome 28:498-514, 2017 PMID: 28936620
Widmeier E, Airik M, Hugo H, Schapiro D, Wedel J, Ghosh CC, Nakayama M, Schneider R, Awad AM, Nag A, Cho J, Schueler M, Clarke CF, Airik R, Hildebrandt F. Treatment with 2,4-Dihydroxybenzoic Acid Prevents FSGS Progression and Renal Fibrosis in Podocyte-Specific Coq6 Knockout Mice. J Am Soc Nephrol. 2019 Feb 8. PMID: 30737270 Co-corresponding author
Weiss AC, Bohnenpoll T, Kurz J, Blank P, Airik R, Lüdtke TH, Kleppa MJ, Deuper L, Kaiser M, Mamo TM, Costa R, von Hahn T, Trowe MO, Kispert A. Delayed onset of smooth muscle cell differentiation leads to hydroureter formation in mice with conditional loss of the zinc finger transcription factor gene Gata2 in the ureteric mesenchyme. J Pathol. 2019 Mar 27. PMID: 30916783
Airik R, Airik M, Schueler M, Bates CM, Hildebrandt F. Roscovitine blocks collecting duct cyst growth in Cep164-deficient kidneys. Kidney Int. 2019 Aug;96(2):320-326. PMID:31248650 Co-corresponding author
Research Interest Summary
Chronic Kidney Disease
NIH R01DK115403, The role of DNA damage response in chronic kidney disease (PI, 40% effort), 2018-2023, National Institute of Diabetes and Digestive and Kidney Diseases, $1,493,918.
NIH R01DK121493, Role of FGFR2 signaling in bladder injury and regeneration (Co-I, 2% effort), 2019-2022, National Institute of Diabetes and Digestive and Kidney Diseases.