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BogartThesisFinal.pdf (41.09 MB)
ETD Abstract Container
Abstract Header
STAT5 Knockout Mice Show Increased Susceptibility to Cisplatin-Induced Acute Kidney Injury
Author Info
Bogart, Avery M
ORCID® Identifier
http://orcid.org/0000-0002-3912-3177
Permalink:
http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524841830342307
Abstract Details
Year and Degree
2018, Bachelor of Science (BS), Ohio University, Biological Sciences.
Abstract
Acute kidney injury (AKI) affects roughly 13.3 million people annually worldwide, resulting in around 1.7 million deaths per year (Zuk and Bonventre, 2016). Nephrotoxic injury, or drug-induced damage to the kidney from compounds such as cisplatin, is a common cause of AKI because of the kidney’s involvement in the filtration of toxins from the body (Pannu and Nadim, 2008). One factor that greatly enhances AKI is inflammation, which can be caused by a multitude of factors, including cytokines and chemokines. Signal transducer and activator of transcription 5 (STAT5) proteins respond to various cytokines, resulting in the production of additional molecules such as those involved in proliferation, inflammation, differentiation, and regulation of apoptosis, or programmed cell death (Buitenhuis et al., 2003). Previous outcomes from the Coschigano lab displayed that STAT5 knockout animals were more susceptible to the acute toxic effects of streptozotocin (STZ) on the kidney; however, this treatment is not widely acknowledged to be useful in the study of drug-induced AKI. To expand the role of STAT5 in kidney injury, this project turned to a well-defined model of nephrotoxic AKI using cisplatin. Results from this study demonstrated that cisplatin-treated STAT5 knockout mice showed greater kidney pathology and increased expression of serum creatinine, MCP-1, and F4/80 than their wildtype counterparts, indicating an increased susceptibility of these STAT5 knockout animals to drug-induced inflammation and kidney damage. Moreover, these results indicate that STAT5 may be protective against kidney injury through regulation of inflammatory processes.
Committee
Karen Coschigano, PhD (Advisor)
Pages
73 p.
Subject Headings
Biology
Keywords
Kidney, STAT5, cisplatin, inflammation, nephrotoxicity, mouse, acute kidney injury
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Citations
Bogart, A. M. (2018).
STAT5 Knockout Mice Show Increased Susceptibility to Cisplatin-Induced Acute Kidney Injury
[Undergraduate thesis, Ohio University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524841830342307
APA Style (7th edition)
Bogart, Avery.
STAT5 Knockout Mice Show Increased Susceptibility to Cisplatin-Induced Acute Kidney Injury.
2018. Ohio University, Undergraduate thesis.
OhioLINK Electronic Theses and Dissertations Center
, http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524841830342307.
MLA Style (8th edition)
Bogart, Avery. "STAT5 Knockout Mice Show Increased Susceptibility to Cisplatin-Induced Acute Kidney Injury." Undergraduate thesis, Ohio University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1524841830342307
Chicago Manual of Style (17th edition)
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Document number:
ouhonors1524841830342307
Download Count:
49
Copyright Info
© 2018, all rights reserved.
This open access ETD is published by Ohio University Honors Tutorial College and OhioLINK.