Literature DB >> 11044221

Induction of apoptosis during development of hypertensive nephrosclerosis.

W Z Ying1, P X Wang, P W Sanders.   

Abstract

BACKGROUND: As the biology of programmed cell death, or apoptosis, is clarified, a role for this process in the pathophysiology of organ dysfunction and fibrosis has been hypothesized. Hypertensive nephrosclerosis represents an important cause of end-stage renal disease. One model of the progressive, noninflammatory, sclerotic renal lesion of hypertension is the Dahl/Rapp salt-sensitive rat, which was examined in this study.
METHODS: Male, Dahl/Rapp salt-sensitive (SS) and Sprague-Dawley rats were placed on either 0.3 or 8.0% NaCl diets for three weeks. Blood pressure was determined, and the kidneys were harvested for histochemical analysis and to obtain total RNA for RNase protection assays and total protein for Western blotting.
RESULTS: An increase in apoptosis in the glomerular and tubular compartments was observed only in kidneys of SS rats on the high-salt diet. These findings occurred at a time when renal function was markedly impaired and irreversible changes in renal morphology developed. Temporally associated with this increase in apoptosis was augmented expression of pro-apoptotic molecules that included Fas, Bax, and Bcl-XS.
CONCLUSIONS: The inappropriate shift in expression of proteins that facilitate apoptosis in the nephron, along with ongoing cell death that manifested at a time when renal function was deteriorating, supported an important role for this process in development of hypertensive nephrosclerosis.

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Year:  2000        PMID: 11044221     DOI: 10.1111/j.1523-1755.2000.00373.x

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  7 in total

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Authors:  Savithri Balasubramanian; Marcel Jansen; M Todd Valerius; Benjamin D Humphreys; Terry B Strom
Journal:  J Am Soc Nephrol       Date:  2012-02-16       Impact factor: 10.121

Review 2.  TNF superfamily: a growing saga of kidney injury modulators.

Authors:  Maria D Sanchez-Niño; Alberto Benito-Martin; Sara Gonçalves; Ana B Sanz; Alvaro C Ucero; Maria C Izquierdo; Adrian M Ramos; Sergio Berzal; Rafael Selgas; Marta Ruiz-Ortega; Jesus Egido; Alberto Ortiz
Journal:  Mediators Inflamm       Date:  2010-10-04       Impact factor: 4.711

3.  Increased proliferative cells in the medullary thick ascending limb of the loop of Henle in the Dahl salt-sensitive rat.

Authors:  Chun Yang; Francesco C Stingo; Kwang Woo Ahn; Pengyuan Liu; Marina Vannucci; Purushottam W Laud; Meredith Skelton; Paul O'Connor; Terry Kurth; Robert P Ryan; Carol Moreno; Shirng-Wern Tsaih; Giannino Patone; Oliver Hummel; Howard J Jacob; Mingyu Liang; Allen W Cowley
Journal:  Hypertension       Date:  2012-11-26       Impact factor: 10.190

4.  FPR-1 (Formyl Peptide Receptor-1) Activation Promotes Spontaneous, Premature Hypertension in Dahl Salt-Sensitive Rats.

Authors:  Jonnelle M Edwards; Shaunak Roy; Sarah L Galla; Jeremy C Tomcho; Nicole R Bearss; Emily W Waigi; Blair Mell; Xi Cheng; Piu Saha; Matam Vijay-Kumar; Cameron G McCarthy; Bina Joe; Camilla F Wenceslau
Journal:  Hypertension       Date:  2021-03-01       Impact factor: 10.190

5.  Activation of the Fas/Fas ligand pathway in hypertensive renal disease in Dahl/Rapp rats.

Authors:  Paul W Sanders; Pei-Xuan Wang
Journal:  BMC Nephrol       Date:  2002-01-07       Impact factor: 2.388

Review 6.  Role of Podocyte Injury in Glomerulosclerosis.

Authors:  Chen-Chen Lu; Gui-Hua Wang; Jian Lu; Pei-Pei Chen; Yang Zhang; Ze-Bo Hu; Kun-Ling Ma
Journal:  Adv Exp Med Biol       Date:  2019       Impact factor: 2.622

7.  Human podocyte injury in the early course of hypertensive renal injury.

Authors:  Da Sun; Jiao-Jiao Wang; Wei Wang; Juan Wang; Li-Ning Wang; Li Yao; Ying-Hui Sun; Zi-Long Li
Journal:  World J Clin Cases       Date:  2019-11-26       Impact factor: 1.337

  7 in total

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