scholarly journals The intrinsic prostaglandin E2–EP4 system of the renal tubular epithelium limits the development of tubulointerstitial fibrosis in mice

2012 ◽  
Vol 82 (2) ◽  
pp. 158-171 ◽  
Author(s):  
Naoki Nakagawa ◽  
Koh-ichi Yuhki ◽  
Jun-ichi Kawabe ◽  
Takayuki Fujino ◽  
Osamu Takahata ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Tubulointerstitial Fibrosis ◽  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Renal Tubular

Osteopontin expressed by renal tubular epithelium mediates interstitial monocyte infiltration in rats

2000 ◽  
Vol 278 (1) ◽  
pp. F110-F121 ◽  
Author(s):  
Hirokazu Okada ◽  
Kenshi Moriwaki ◽  
Raghuram Kalluri ◽  
Tsuneo Takenaka ◽  
Hiroe Imai ◽  
...  
Keyword(s):  
Target Genes ◽  
Renal Plasma Flow ◽  
Mrna Level ◽  
Antisense Oligodeoxynucleotide ◽  
Tubular Epithelium ◽  
Rt Pcr ◽  
Goodpasture Syndrome ◽  
Renal Tubular Epithelium ◽  
Protein Excretion ◽  
Renal Tubular

In this study, we have shown that intravenously administered antisense oligodeoxynucleotide (ODN) was demonstrated to be taken up by tubular epithelium, after which it blocked mRNA expression of target genes in normal and nephritic rats. Therefore, we injected osteopontin (OPN) antisense ODN to Goodpasture syndrome (GPS) rats every second day between days 27 and 35, the time when renal OPN expression increased and interstitial monocyte infiltration was aggravated. In parallel to blockade of tubular OPN expression, this treatment significantly attenuated monocyte infiltration and preserved renal plasma flow in GPS rats at day 37, compared with sense ODN-treated and untreated GPS rats. No significant changes were observed in OPN mRNA level by RT-PCR and histopathology of the glomeruli after ODN treatment, which was compatible with an absence of differences in the urinary protein excretion rate. In conclusion, OPN expressed by tubular epithelium played a pivotal role in mediating peritubular monocyte infiltration consequent to glomerular disease.

scholarly journals Cystic Renal Neoplasia Following Conditional Inactivation of Apc in Mouse Renal Tubular Epithelium

2004 ◽  
Vol 280 (5) ◽  
pp. 3938-3945 ◽  
Author(s):  
Chao-Nan Qian ◽  
Jared Knol ◽  
Peter Igarashi ◽  
Fangming Lin ◽  
Uko Zylstra ◽  
...  
Keyword(s):  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Conditional Inactivation ◽  
Renal Tubular ◽  
Renal Neoplasia

scholarly journals Transcellular Diffusion of Non-Electrolytes across the Renal Tubular Epithelium

1962 ◽  
Vol 45 (4) ◽  
pp. 643-649 ◽  
Author(s):  
José Carlos Peña ◽  
Richard L. Malvin
Keyword(s):  
Tubular Epithelium ◽  
Permeability Characteristics ◽  
Molecular Weights ◽  
Renal Tubular Epithelium ◽  
Significant Movement ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Proximal Tubular Epithelium ◽  
Stop Flow ◽  
Transcellular Diffusion

The stop flow technique was used to investigate the permeability characteristics of the dog nephron to various C14-labeled non-electrolytes. 12 minutes after clamping the ureter, creatinine, PAH, and C14 compound were injected intravenously. 2 minutes later, urine samples were collected. Urea and glycerol were able to enter the tubular urine along the entire nephron at rates which were commensurate with their molecular weights. No significant movement of larger molecules (D-arabinose, D-glucose, and mannitol) could be detected. However, after administration of twenty units of pitressin, D-arabinose was able to diffuse across the distal and proximal tubular epithelium.

scholarly journals Isolation and characterization of cDNA from renal tubular epithelium encoding murine Rantes

1992 ◽  
Vol 41 (1) ◽  
pp. 220-225 ◽  
Author(s):  
Peter Heeger ◽  
Gunter Wolf ◽  
Catherine Meyers ◽  
Mae Jane Sun ◽  
Susan C. O'Farrell ◽  
...  
Keyword(s):  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Isolation And Characterization ◽  
Renal Tubular

HLA-DR Display by Renal Tubular Epithelium and Phenotype of Infiltrate in Interstitial Nephritis

1989 ◽  
Vol 4 (3) ◽  
pp. 205-215 ◽  
Author(s):  
H.-F. Cheng ◽  
F. Nolasco ◽  
J. S. Cameron ◽  
G. Hildreth ◽  
Gillian Neild ◽  
...  
Keyword(s):  
Interstitial Nephritis ◽  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Hla Dr ◽  
Renal Tubular

Sensitivity of normal and neoplastic human renal tubular epithelium to hyperthermia

1988 ◽  
Vol 43 (1-2) ◽  
pp. 1-8 ◽  
Author(s):  
S. Dessureault ◽  
P. Brown ◽  
T. Ghose ◽  
O.P. Kamra ◽  
P. Belitsky
Keyword(s):  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Renal Tubular

scholarly journals DESOXYCORTICOSTERONE ACETATE

1947 ◽  
Vol 85 (2) ◽  
pp. 187-198 ◽  
Author(s):  
Abbie I. Knowlton ◽  
Emily N. Loeb ◽  
Herbert C. Stoerk ◽  
Beatrice C. Seegal
Keyword(s):  
Drinking Water ◽  
Cardiac Hypertrophy ◽  
Arterial Hypertension ◽  
Rat Kidney ◽  
Sodium Ion ◽  
Tubular Epithelium ◽  
Serum Electrolyte ◽  
Renal Tubular Epithelium ◽  
Desoxycorticosterone Acetate ◽  
Renal Tubular

1. Desoxycorticosterone acetate (DCA) and NaCl, in the dosage employed in normal rats, caused renal and cardiac hypertrophy, characteristic changes in the renal tubular epithelium, atrophic changes in the subcapsular zone of the adrenal cortex, and serum electrolyte changes characterized by a rise in sodium and fall in potassium. 2. In rats rendered nephritic with a rabbit anti-rat-kidney serum, the same regimen caused similar changes. In addition, DCA given concurrently with NaCl greatly intensified the nephritic process and gave rise to striking arterial hypertension. 3. A diet, virtually sodium-free, administered to normal and nephritic rats receiving daily injections of DCA abolished or reduced to a minimum the effects of this steroid; i.e., a liberal ingestion of NaCl was essential for the potentiation of the action of DCA. 4. The addition of KCl to the drinking water of rats receiving DCA and NaCl tended to correct the depression of the level of potassium in the serum, but had no effect upon the hypertension in nephritic animals nor upon the anatomical lesions. 5. The mechanism by which the sodium ion potentiates the activity of DCA has not been established.

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