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High-probability grants
According to our matching algorithm, Jing Yu is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2010 — 2014 |
Yu, Jing |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Molecular and Cellular Regulation of Mammalian Renal Medulla Development
DESCRIPTION (provided by applicant): Molecular and cellular regulation of mammalian renal edulla development The renal medulla plays critical roles in body water and salt homeostasis and the regulation of systemic blood pressure. Disorders in water and salt balance cause hyponatremia, hypernatremia and nephrogenic diabetes insipidus. Renal medulla atrophy is a prominent symptom of hydronephrosis, a common condition occurs in approximately 1 in 100 people and a consequence of acute and chronic urinary tract obstructions and neurological deficits. Elucidation of the molecular mechanisms required for renal medulla formation is important not only for the understanding of normal kidney organogenesis and physiology, but will also guide efforts in the development of new strategies of the repair and regeneration of the renal medulla. In spite of the importance of the renal medulla for kidney functions, little is known of the cellular and molecular mechanisms required for its formation. We recently showed that Wn7b signaling is essential for renal medulla formation, mostly likely through its regulation of the orientation of division of prospective medullary collecting duct cells. We showed that Wnt7b is required for canonical Wnt signaling in the renal interstitium and canonical signaling in the renal interstitium plays essential roles for renal medulla formation. How does Wnt7b and renal interstitial canonical Wnt signaling regulate oriented cell division of the prospective medullary collecting ducts and renal medulla formation? We found that both Wnt7b and renal interstitial canonical Wnt signaling are necessary for the renal interstitial expression of p57Kip2, a Cip/Kip family cyclin-dependent kinase inhibitor (CKI) that functions in both CKI-dependent and CKI-independent fashions. Interestingly, p57Kip2 is implicated in both sporadic and congenital Beckwith-Wiedemann Syndrome, a salient feature of which is renal medullary dysplasia, and ablation of p57Kip2 in mice dramatically reduces renal medulla elongation. These data suggest that p57Kip2 acts downstream of Wnt7b and renal interstitial canonical Wnt signaling in the regulation of renal medulla formation. We will test the hypothesis in this proposal (Aims 1 and 2). Oriented cell division in the epithelium is a planar cell polarity (PCP) phenomenon, in which the Wnt/PCP pathway has been implicated. Aim 3 will address the role of the Wnt/PCP pathway in mediating Wnt7b functions in renal medulla formation. Together these studies will significantly expand our knowledge on the establishment of the cortico-medullary axis of the kidney and the development and repair and regeneration of the renal medulla compartment, which is pivotal for physiology of the kidney and beyond. They will also provide mechanistic understanding of the pathogenesis of the renal medullary defects in diseases such as Beckwith-Wiedemann Syndrome.
|
0.957 |
2012 — 2016 |
Yu, Jing |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Project 3 Canonical Wnt Regulation of Renal Interstitium Fate and Function
The embryonic renal interstitium plays critical regulatory roles in renal development. However, our knowledge of its cellular composition, the functions of its individual cellular constituents, and the full scope of its involvement in renal formation and function is far from complete. We found that in the deeper cortex (excluding the part of the cortex from the surface of the kidney to where S-shaped bodies locate) and medulla, the response of Wnt/p-catenin signaling in the embryonic renal interstitium is confined to about two layers of cells adjacent to ureteric trunks (Wnt/p-catenin target cells), and the expression of certain genes in these cells were disrupted when (3-catenin was ablated specifically from the renal interstitium. The overall objective of this proposal is to test the hypothesis the HDACl/2 inhibit epigenetically Wnt/(3-catenin signaling which regulates the fate of it target renal interstitial cells and their function in regulating kidney development. Specifically, using a combination of mouse genetics, biochemical and molecular biology, we will determine the identity ofthe interstitial cells that do and do not respond to Wnt/p-catenin signaling during normal development and their fates in response to ablation of Wnt/p-catenin signaling (Aimi). Further, we will test the hypothesis that the Wnt/p-catenin signaling target interstitial cells affect the proper formation of loop-of- Henle and microvascular endothelium in the developing kidney (Aim2). HDAC1 and HDAC2, histone deacetylases that remove acetyl groups from either core histones or non-histone proteins, function in either an epigenetic or a non-epigenetic manner. In specific Aim 3, we will test the hypothesis that HDACl/2 inhibits Wnt/p-catenin signaling in the renal interstitium epigenetically. The proposed work will significantly expand our mechanistic understanding ofthe regulation of renal interstitial cell fates, and uncover additional functions of the renal interstitium during kidney development. Further, it will define the cellular composition of the majority ofthe renal interstitium which will facilitate future work of targeted manipulation ofthe renal interstitium to reveal additional functions ofthe renal interstitium. The knowledge and information acquired from the proposed research will also assist diagnosis and treatment of congenital renal diseases in children. RELEVANCE (See instructions): Congenital anomaly in the kidney and urinary tract accounts for about 35% of end-stage renal diseases in children (USRDS, 2011). Our proposed research will extend and enhance the mechanistic understanding of the regulation of renal interstitial cell fates and of their regulatory roles in kidney development. It will facilitate development of strategies for diagnosis and treatment of pediatric renal diseases resulted from renal malformation ' .,
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0.957 |