Browsing by Author "Ho, Jacqueline"

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    Developing a Research Mentorship Program: The American Society of Pediatric Nephrology's Experience
    (Frontiers, 2019-04-24) Vasylyeva, Tetyana L.; Díaz-González de Ferris, María E.; Hains, David S.; Ho, Jacqueline; Harshman, Lyndsay A.; Reidy, Kimberly J.; Brady, Tammy M.; Okamura, Daryl M.; Samsonov, Dmitry V.; Wenderfer, Scott E.; Hartung, Erum A.; Pediatrics, School of Medicine
    Background: Most pediatric nephrologists work in academia. Mentor-mentee relationships provide support and guidance for successful research career. Mentorship program implementation is valuable in medical fields for providing research opportunities to young faculty. Methods: The American Society of Pediatric Nephrology (ASPN) established a research mentorship program to (a) assist with matching of appropriate mentor-mentee dyads and (b) establish metrics for desirable mentor-mentee outcomes with two independent components: (1) the grants review workshop, a short-term program providing mentor feedback on grant proposals, and (2) the longitudinal program, establishing long-term mentor-mentee relationships. Regular surveys of both mentors and mentees were reviewed to evaluate and refine the program. Results: Twelve mentees and 17 mentors participated in the grant review workshop and 19 mentees were matched to mentors in the longitudinal program. A review of NIH RePORTER data indicated that since 2014, 13 NIH grants have been awarded. Mentees in the longitudinal program reported that the program helped most with identifying an outside mentor, improving grant research content, and with general career development. Mentors perceived themselves to be most helpful in assisting with overall career plans. Email communications were preferred over phone or face-to-face communications. Mentees endorsed strong interest in staying in touch with their mentors and 100% of mentors expressed their willingness to serve in the future. Conclusion: This mentorship program was initiated and supported by a relatively small medical society and has shown early success in cultivating mentoring relationships for a future generation of clinician-scientists.
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    Muc1 is protective during kidney ischemia-reperfusion injury
    (American Physiological Society, 2015-06-15) Pastor-Soler, Núria M.; Sutton, Timothy A.; Mang, Henry E.; Kinlough, Carol L.; Gendler, Sandra J.; Madsen, Cathy S.; Bastacky, Sheldon I.; Ho, Jacqueline; Al-Bataineh, Mohammad M.; Hallows, Kenneth R.; Singh, Sucha; Monga, Satdarshan P.; Kobayashi, Hanako; Haase, Volker H.; Hughey, Rebecca P.; Department of Medicine, IU School of Medicine
    Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs) orchestrate a protective response in renal endothelial and epithelial cells in AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1 activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1) regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized on the apical surface of the thick ascending limb, distal convoluted tubule, and collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced during IRI, and Muc1 transcripts and protein were also present in recovering proximal tubule cells. Kidney damage was worse and recovery was blocked during IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice had reduced levels of HIF-1α, reduced or aberrant induction of HIF-1 target genes involved in the shift of glucose metabolism to glycolysis, and prolonged activation of AMP-activated protein kinase, indicating metabolic stress. Muc1 clearly plays a significant role in enhancing the HIF protective pathway during ischemic insult and recovery in kidney epithelia, providing a new target for developing therapies to treat AKI. Moreover, our data support a role specifically for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present only in tubule epithelial cells.