The overall goal of the PKD Biomaterials Research Core is to establish and maintain a repository for human and animal biological materials for.investigators within the Kansas PKD Center. The core will provide resources and expertise for the development of high quality research materials, including primary cultures of epithelial cells, histological specimens, DNA, RNA and cell proteins from ADPKD, ARPKD and normal human kidney tissues. The core will also establish and maintain immortalized cell lines from mice with unique PKD gene mutations. The strength of the core is that it will provide a central laboratory with dedicated research staff experienced in 1) the procurement the human tissues and trained on the proper handling of the human biological samples, 2) methods of aseptic collection of cystic and non-cystic tissue and cyst fluid, 3) histological preparation 4) protein, RNA and DNA extraction, 5) animal husbandry, timed breeding and animal genotyping, and 6) preparation of cell lines from specific cell types for PKD mice.
The specific aims of the Core are:
Aim 1 : Establish and maintain a human PKD biomaterial repository.
Aim 2 : Generate and maintain conditionally immortalized renal epithelial cell cultures from animals with unique gene defects that cause PKD.
Aim 3 : Provide technical support and training for in vitro methods for the investigation of the PKD cellular phenotype. The Core will provide unique PKD biomaterials to members of the Kansas PKD Center and to collaborators at the Kansas University Medical Center and other universities.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Specialized Center (P50)
Project #
5P50DK057301-11
Application #
7923963
Study Section
Special Emphasis Panel (ZDK1)
Project Start
2009-09-01
Project End
2011-08-31
Budget Start
2009-09-01
Budget End
2011-08-31
Support Year
11
Fiscal Year
2009
Total Cost
$124,612
Indirect Cost
Name
University of Kansas
Department
Type
DUNS #
016060860
City
Kansas City
State
KS
Country
United States
Zip Code
66160
Parnell, Stephen C; Magenheimer, Brenda S; Maser, Robin L et al. (2018) A mutation affecting polycystin-1 mediated heterotrimeric G-protein signaling causes PKD. Hum Mol Genet 27:3313-3324
Paul, Binu M; Vanden Heuvel, Gregory B (2014) Kidney: polycystic kidney disease. Wiley Interdiscip Rev Dev Biol 3:465-87
Zhou, Xia; Fan, Lucy X; Li, Keguo et al. (2014) SIRT2 regulates ciliogenesis and contributes to abnormal centrosome amplification caused by loss of polycystin-1. Hum Mol Genet 23:1644-55
Swenson-Fields, Katherine I; Vivian, Carolyn J; Salah, Sally M et al. (2013) Macrophages promote polycystic kidney disease progression. Kidney Int 83:855-64
Fan, Lucy X; Li, Xinjian; Magenheimer, Brenda et al. (2012) Inhibition of histone deacetylases targets the transcription regulator Id2 to attenuate cystic epithelial cell proliferation. Kidney Int 81:76-85
Parnell, Stephen C; Puri, Sanjeev; Wallace, Darren P et al. (2012) Protein phosphatase-1ýý interacts with and dephosphorylates polycystin-1. PLoS One 7:e36798
Qiu, Ni; Xiao, Zhousheng; Cao, Li et al. (2012) Conditional mesenchymal disruption of pkd1 results in osteopenia and polycystic kidney disease. PLoS One 7:e46038
Karihaloo, Anil; Koraishy, Farrukh; Huen, Sarah C et al. (2011) Macrophages promote cyst growth in polycystic kidney disease. J Am Soc Nephrol 22:1809-14
Nims, Nancy M; Vassmer, Dianne; Maser, Robin L (2011) Effect of PKD1 gene missense mutations on polycystin-1 membrane topogenesis. Biochemistry 50:349-55
Reif, Gail A; Yamaguchi, Tamio; Nivens, Emily et al. (2011) Tolvaptan inhibits ERK-dependent cell proliferation, Clýýý secretion, and in vitro cyst growth of human ADPKD cells stimulated by vasopressin. Am J Physiol Renal Physiol 301:F1005-13

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