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2 edition of Regulation of SMAD activity in murine polycystic kidney disease. found in the catalog.

Regulation of SMAD activity in murine polycystic kidney disease.

Devina Marcia Ramsaroop

Regulation of SMAD activity in murine polycystic kidney disease.

by Devina Marcia Ramsaroop

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  • 8 Currently reading

Published .
Written in English


About the Edition

In recessive polycystic kidney disease (PKD), renal collecting duct cystogenesis and bile duct dilation are associated with increased cell proliferation. Pathogenic mechanisms are undefined. Bone morphogenetic proteins signal via intracellular SMAD1 to decrease cell proliferation during normal collecting duct formation. These studies test the hypothesis that SMAD activity is decreased in kidney and liver in murine models of PKD. In the B6 cpk/cpk model of recessive PKD, and Balb bpk/bpk model of recessive PKD and biliary dysgenesis, immunoblot and immunohistochemistry demonstrated decreased renal PSMAD1 at P10 when cysts were fully formed. Balb bpk/bpk mice demonstrated decreased PSMAD1 immunostaining in bile ducts. These abnormalities were absent at P1, despite the presence of pathogenic changes. Unaltered PSMAD1 levels in Balb/B6 cpk/cpk model of recessive PKD and liver dysgenesis suggest that SMAD1 activity is modulated by genetic background. We conclude that decreased PSMAD1 may contribute to the proliferative cystic phenotype in murine PKD.

The Physical Object
Pagination184 leaves.
Number of Pages184
ID Numbers
Open LibraryOL19215336M
ISBN 109780494162064

Autosomal dominant polycystic kidney disease (ADPKD) is the most common inheritable cause of end stage renal disease and, as of today, only a single moderately effective treatment is available for patients. Even though ADPKD research has made huge progress over the last decades, the precise disease mechanisms remain elusive. However, a wide variety of cellular . Insuk So's research works with 4, citations and 4, reads, including: Ca 2+ /calmodulin-dependent regulation of polycystic kidney disease 2-like-1 by binding at C-terminal domain.

  Effects of CG on TGF-β/Smad pathway in obstructed mouse kidney. 4,6,26,27,28 and to reduce cyst formation in polycystic kidney disease 10 Kidney Fibrosis in a Murine Model of Alport. Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of end-stage renal failure in humans and results from germline mutations in PKD1 or PKD2.

autosomal recessive polycystic kidney disease (ARPKD) is one of a number of human genetic and acquired diseases in which renal cysts are a central pathological feature. ARPKD has an incidence of 1 in 10, to 1 in 40,, has a mortality of 40–65% in the newborn period, and accounts for ∼5% of all end-stage renal disease in children ().Although ARPKD has a wide . Renal cyst enlargement is associated with the activation of both the circulating and intrarenal renin-angiotensin systems. Angiotensinogen (AGT) .


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Regulation of SMAD activity in murine polycystic kidney disease by Devina Marcia Ramsaroop Download PDF EPUB FB2

Autophagy in Renal Interstitial Fibrosis and Progressive Kidney Disease. A hallmark of chronic kidney disease (CKD) is a progressive deposition of extracellular matrix proteins, which correlate well with the deterioration of renal function, regardless of the etiology of the primary insult [37,38,39].Cited by: 4.

ADPKD kidneys (N = 5) with end stage renal disease (ESRD) and control kidneys (N = 4) were analyzed immnunohistochemically. We evaluated α-SMA, E-cadherin, vimentin, TGF-β1 and Smad 2/3 expression in ADPKD and compared them with those in control by:   1.

Introduction. Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a genetic ciliopathy disorder caused by mutations in the genes encoding either polycystin 1 or polycystin 2, that is characterized by the formation of fluid-filled cysts in the kidneys, liver, and other organs [1,2].Expansion of these cysts progressively destroys the surrounding normal tissue and causes kidney Cited by: 1.

1. Introduction. Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary diseases, affecting around 1/ ∼ 1/ individuals worldwide [1,2].Mutations in the genes Pkd1 and Pkd2, which encode polycystin 1 (PC1) and polycystin 2 (PC2) respectively, result in profound cystogenesis and are the initial causes of ADPKD [3,4].Author: Jinzhao He, Hong Zhou, Jia Meng, Shun Zhang, Xiaowei Li, Shuyuan Wang, Guangying Shao, William Jin.

Human polycystic kidney disease (PKD) is characterized by relentless development and growth of renal cysts in number and size over time that originates in a minority of nephrons.

The resulting cysts compress adjacent tubules and ultimately replace the neighbouring healthy kidney : Almira Kurbegovic, Marie Trudel. Autosomal Dominant Polycystic Kidney Disease (ADPKD) is an inherited systemic disease with intrarenal cystogenesis as its primary characteristic. A variety of mouse models provided information on the requirement of loss of balanced polycystin levels for initiation of cyst formation, the role of proliferation in cystogenesis and the signaling.

HDAC6 and ADPKD. Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common hereditary disorders in humans, affecting 1/ individuals in the United States (Gabow ).The hallmark of ADPKD is the development of multiple bilateral renal cysts that replace normal renal parenchyma, resulting in end-stage renal disease (ESRD) in.

Targeting dysregulated cell cycle and apoptosis for polycystic kidney disease therapy Cell Cycle 6 – ; Park JY, Schutzer WE, Lindsley JN, Bagby SP, Oyama TT, Anderson S, et al. p21 is decreased in polycystic kidney disease and leads to increased epithelial cell cycle progression: roscovitine augments p21 levels.

BMC Nephrol. Introduction. Autosomal dominant polycystic kidney disease (ADPKD) affects approximately 1 in people (Willey et al., ).Patients will develop renal failure as a result of progressive growth of renal cysts, which interfere with normal kidney function.

GSK3 activity is necessary for full stimulation of the production of several pro-inflammatory cytokines, Autosomal dominant polycystic kidney disease (ADPKD) et en synthase kinase 3α-specific regulation of murine hepatic glycogen metabolism.

Cell Metab., 6 (4) (Oct), pp. Polycystic kidney disease (PKD) Several fibrosis associated signaling pathways, such as TGFβ-SMAD, Wnt, and periostin–integrin-linked kinase are also activated in polycystic kidney tissues. () Regulation of myofibroblast activities: calcium pulls some strings behind the scene.

Exp Cell Res – PubMed CrossRef Google. We tested the hypothesis that post-contrast acute kidney injury (PC-AKI) occurs due to increase in transforming growth factor beta (Tgf-β) and pSMAD3 signaling in a murine model of PC-AKI. Mice. Autosomal dominant polycystic kidney disease (ADPKD) ADPKD is the most common lethal monogenic human disease inherited as a dominant trait.

It is estimated to affect at least 10 million individuals world-wide and to account for up to 10% of all patients with end-stage renal disease (ESRD) requiring renal replacement therapy (RRT) by haemodialysis or transplantation.

The primary cilium is a microtubule-based, antenna-like organelle housing several signaling pathways. It follows a cyclic pattern of assembly and deciliation (disassembly and/or shedding), as cells exit and re-enter the cell cycle, respectively.

In general, primary cilia loss leads to kidney cystogenesis. However, in animal models of autosomal dominant polycystic kidney disease. Contrast-induced acute kidney injury (CI-AKI) is a vexing problem and more than 70 million patients undergo studies utilizing iodinated contrast. The molecular mechanisms responsible for CI-AKI are.

An inhibitor of histone deacetylase 6 activity, ACY, reduces cAMP and cyst growth in polycystic kidney disease. Am J Physiol Renal Physiol. ;F– Yanda MK, Liu Q, Cebotaru V, Guggino WB, Cebotaru L. Histone deacetylase 6 inhibition reduces cysts by decreasing via cAMP and Ca2+ in knockout mouse models of polycystic kidney.

Polycystic kidney diseases (PKDs) are primarily characterized by the growth of fluid-filled cysts in renal tubules leading to end-stage renal disease 1,2,ons in the PKD1 or PKD2 genes lead. Nemo R, Murcia N, and Dell KM. Transforming growth factor alpha (TGF-alpha) and other targets of tumor necrosis factor-alpha converting enzyme (TACE) in murine polycystic kidney disease.

Pediatr Res ;57(5 Pt 1)– PubMed CrossRef Google Scholar. Ken Hiratsuka's 14 research works with 89 citations and reads, including: Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injury.

Abstract. Polycystic kidney disease (PKD) is a commonly inherited disorder characterized by cyst formation and fibrosis (Wilson, N Engl J Med –, ) and is caused by mutations in cilia or cilia-related proteins, such as polycystin 1 or 2 (Oh and Katsanis, Development –, ; Kotsis et al., Nephrol Dial Transplant –, ).

Interestingly however, defects reminiscent of polycystic kidney disease (PKD) were also observed, yet exclusively in mutant mice carrying a deletion of more anterior Hoxd genes like Hoxd9 and Hoxd8.

Finally, the distinct functions of Hoxd genes in kidneys correlate well with their specific expression in the MM or UB, respectively.Gpr48 deletion does not alter the activity of the Smad.

Polycystic kidney disease (PKD) is a common genetic disorder characterized by formations of numerous cysts .SNAIL regulation has been extensively studied in the murine UUO model, where an intense flare-up of inflammation occurs in the obstructed kidney. This AKI model is characterized histologically by a large number of leukocytes infiltrating the renal interstitial space, creating a cytokine-rich environment comparable to the microenvironment of.