Grants per year
Personal profile
Research Interests
Chronic kidney disease (CKD) affects approximately 20% of US population. Primary causes for CKD varies from genetic disorder to metabolic problems, but many are unknown. Regardless of the primary cause, CKD progresses with two essential phases; injury to podocyte, the primary barrier for filtration units of kidney, and progressive scarring of kidney, which would eventually obliterate the filtration units and lead to loss of kidney function. My research goal is to understand the molecular mechanisms underlining these two features of CKD in order for developing novel therapeutic approaches for CKD. To address the first phase podocyte injury, we are currently working on a molecule called p110g. Our data suggest that a specific inhibitor of this molecule may provent podocyte injury. For the second, scarring phase, my previous works revealed several pathways that modulate functions of a scar-promoting cytokine, TGF-beta. Now, we have identified a molecule called SARA is a critical gate keeper to prevent cells from becoming scar forming cells. Since in most cases patients seek to medical care when the initial injury had already occurred, targeting SARA might be beneficial approach treating CKD.
We recently found that a signaling molecule, gamma isoform of PI3K (p110g), is increased in diseased podocytes in patients’ samples with progressive form of CKD, but not in those with minimal change disorder. Inhibiting this molecule either chemically or genetically prevents podocyte injury in animal models. These data suggest that molecule is a novel therapeutic target. An effort seeking a novel, safer compound that block activity of p110g has been launched. We also are interested in deciphering a process by which kidney scarring is initiated and progresses after podocyte injury has occurred, with particular focus on a scar-promoting cytokine, TGF-ß. In searching a regulatory molecule for TGF-beta pathway, we recently identified a Smad Anchor for Receptor Activation (SARA) is a key mediator maintaining epithelial cell type, hence preventing them becoming fibrogenic. By identifying a mechanism how this molecule regulates cellular phenotype will bring new insight in preventing progression of CKD.
Education/Academic qualification
PhD, Keio University Medical School
… → 2004
MD, Keio University Medical School
… → 1988
Research interests
- Cell Biology
- Fibrosis
- Kidney
- Molecular Biology
- Signal Transduction
- Stem Cells
- TGF-beta
- Translational Research
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Grants
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Role of Smad Anchor for Receptor Activation (SARA) in skin fibrosis
Bhattacharyya, S. & Hayashida, T.
Ann & Robert H. Lurie Children's Hospital of Chicago, Scleroderma Foundation
4/1/20 → 3/31/22
Project: Research project
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Antifibrotic Actions of SARA
Hayashida, T. & Quaggin, S. E.
Ann & Robert H. Lurie Children's Hospital of Chicago, National Institute of Diabetes and Digestive and Kidney Diseases
6/2/19 → 6/30/21
Project: Research project
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Antifibrotic Actions of SARA
Hayashida, T., Quaggin, S. E. & Schnaper, H. W.
National Institute of Diabetes and Digestive and Kidney Diseases
8/24/17 → 6/1/19
Project: Research project
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Signaling Pathways in Renal Fibrogenesis
Ann & Robert H. Lurie Children's Hospital of Chicago
4/1/15 → 9/30/16
Project: Research project
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Signaling Pathways in Renal Fibrogenesis
Hayashida, T., Kanwar, Y. S. & Schnaper, H. W.
National Institute of Diabetes and Digestive and Kidney Diseases
7/15/10 → 6/30/15
Project: Research project
Research Output
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Anti-TGF-β antibody, 1D11, ameliorates glomerular fibrosis in mouse models after the onset of proteinuria
Liang, X., Schnaper, H. W., Matsusaka, T., Pastan, I., Ledbetter, S. & Hayashida, T., May 2016, In: PloS one. 11, 5, e0155534.Research output: Contribution to journal › Article › peer-review
11 Scopus citations -
Hypoxia-inducible factor-1alfa promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3
Baumann, B., Hayashida, T., Liang, X. & Schnaper, HW., 2016, In: Kidney international. 90, 4, p. 797-808 12 p.Research output: Contribution to journal › Article
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Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3
Baumann, B., Hayashida, T., Liang, X. & Schnaper, H. W., Oct 2016, In: Kidney international. 90, 4, p. 797-808 12 p.Research output: Contribution to journal › Article › peer-review
26 Scopus citations -
Hypoxia-inducible factor-2α and TGF-β signaling interact to promote normoxic glomerular fibrogenesis
Hanna, C., Hubchak, S. C., Liang, X., Rozen-Zvi, B., Schumacker, P. T., Hayashida, T. & William Schnaper, H., Nov 1 2013, In: American Journal of Physiology - Renal Physiology. 305, 9, p. F1323-F1331Research output: Contribution to journal › Article › peer-review
32 Scopus citations -
Serine-204 in the linker region of Smad3 mediates the collagen-I response to TGF-β in a cell phenotype-specific manner
Browne, J. A., Liu, X., Schnaper, H. W. & Hayashida, T., Nov 15 2013, In: Experimental Cell Research. 319, 19, p. 2928-2937 10 p.Research output: Contribution to journal › Article › peer-review
10 Scopus citations