scholarly journals Ochratoxin a and Citrinin Induced Nephrosis in Beagle Dogs III. Terminal Renal Ultrastructural Alterations

1977 ◽  
Vol 14 (4) ◽  
pp. 392-406 ◽  
Author(s):  
D. N. Kitchen ◽  
W. W. Carlton ◽  
E. J. Hinsman
Keyword(s):  
Epithelial Cells ◽  
Ochratoxin A ◽  
Ultrastructural Changes ◽  
Similar Distribution ◽  
Beagle Dogs ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Distal Tubules ◽  
Renal Tubular ◽  
Myelin Figure

The extent and type of renal ultrastructural changes in Beagle dogs varied with the administration of ochratoxin A and citrinin alone and in the two dosage combinations. The three predominant changes were cytoplasmic vacuolation, myelin figure formation and lesions designated as cytoplasmic disarray. These changes were mainly of the endomembrane system of the tubular epithelial cells. Cytoplasmic vacuoles were within proximal and distal tubules and collecting ducts and were most numerous in dogs given 10 mg/kg citrinin. Vacuolation of similar distribution, but less severe, was seen in renal tubular cells of dogs given the higher dose of the combined mycotoxins (0.2 mg/kg ochratoxin A + 10 mg/kg citrinin). This damage was limited to the proximal tubular cells in dogs given only ochratoxin A (0.1 or 0.2 mg/kg). Myelin figures were in proximal epithelial cells of dogs given ochratoxin A alone or combined with citrinin. There was cytoplasmic disarray in dogs of all groups except for dogs given 5 mg/kg citrinin. This lesion was usually limited to the proximal tubules. The lesion, however, was found in cells of the distal tubules of dogs given 10 mg/kg citrinin alone.

scholarly journals Telmisartan Attenuates Uric Acid-Induced Epithelial-Mesenchymal Transition in Renal Tubular Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Dongqing Zha ◽  
Saiqun Wu ◽  
Ping Gao ◽  
Xiaoyan Wu
Keyword(s):  
Uric Acid ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Dependent Manner ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Diphenylene Iodonium ◽  
Renal Tubular

We examined whether and how uric acid induces epithelial to mesenchymal transition (EMT) in renal tubular cells, along with the mechanism by which telmisartan acts on uric acid-induced renal injury. Rat renal proximal tubular epithelial cells (NRK-52E) were exposed to various concentrations of uric acid in the presence or absence of telmisartan. Treatment with uric acid increased the expression of α-SMA, decreased the expression of E-cadherin, and promoted EMT in NRK-52E cells. Uric acid treatment also led to increased endothelin-1 (ET-1) production, activation of extracellular-regulated protein kinase 1/2 (ERK1/2), and the upregulation of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4). Use of ET-1 receptor inhibitor (BQ123 or BQ788) could inhibit uric acid-induced EMT in NRK-52E cells. Pretreatment with the ERK inhibitor (U0126 or PD98059) suppressed the release of ET-1 and EMT induced by uric acid. Additionally, pretreatment with a traditional antioxidant (diphenylene iodonium or apocynin) inhibited the activation of ERK1/2, release of ET-1, and uric acid-induced EMT in NRK-52E cells. These findings suggested that uric acid-induced EMT in renal tubular epithelial cells occurs through NADPH oxidase-mediated ERK1/2 activation and the subsequent release of ET-1. Furthermore, telmisartan (102 nmol/L to 104 nmol/L) inhibited the expression of NOX4, intracellular reactive oxygen species (ROS), activation of ERK1/2, and the release of ET-1 in a dose-dependent manner, thereby preventing uric acid-induced EMT in NRK-52E. In conclusion, telmisartan could ameliorate uric acid-induced EMT in NRK-52E cells likely through inhibition of the NADPH oxidase/ERK1/2/ET-1 pathway.

Inhibition of prostaglandin biosynthesis in renal (MDCK) cells by cAMP

1983 ◽  
Vol 245 (1) ◽  
pp. C163-C163 ◽  
Author(s):  
A. Hassid
Keyword(s):  
Epithelial Cells ◽  
Mdck Cells ◽  
Biological Properties ◽  
Prostaglandin E ◽  
Tubular Epithelial Cells ◽  
Prostaglandin Biosynthesis ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Arachidonate Metabolite ◽  
Renal Tubular

Page C369: A. Hassid. “Inhibition of prostaglandin biosynthesis in renal (MDCK) cells by cAMP.” Page C369: in the abstract, the first sentence should read: Cultured renal tubular cells (MDCK) have many of the biological properties of cortical medullary tubular epithelial cells, including the ability to synthesize prostaglandin E2 (PGE2) as the major arachidonate metabolite. Page C373: Table 3 should read as follows: (See PDF)

scholarly journals Polarized Expression of Tamm-Horsfall Protein by Renal Tubular Epithelial Cells Activates Human Granulocytes

2002 ◽  
Vol 70 (5) ◽  
pp. 2650-2656 ◽  
Author(s):  
B. Kreft ◽  
W. J. Jabs ◽  
T. Laskay ◽  
M. Klinger ◽  
W. Solbach ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Defense ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Tubular Epithelial Cells ◽  
Bacterial Killing ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Human Granulocytes ◽  
Renal Tubular

ABSTRACT In renal bacterial infections granulocytes are of major importance in the primary immune defense against invading pathogens. However, the mechanisms of granulocytic activation in renal interstitial invasion have not been clarified. Renal tubular epithelial cell mechanisms inducing granulocytic activation and bacterial killing may include tubular cell expression of Tamm-Horsfall protein (THP), a urinary protein that is known to enhance cytokine expression in monocytes. We studied the role of THP in granulocytic activation. A strong binding of THP to human granulocytes was demonstrated by fluorescence-activated cell sorter analysis. Urinary THP and supernatants of THP-expressing cultured tubular epithelial cells (MDCK) enhanced interleukin-8 (IL-8) expression by human granulocytes. Renal tubular cells growing polarized on polycarbonate membranes were used to study apical versus basal THP expression. By electron microscopy THP immunoreactivity was exclusively found on the apical surfaces of tubular cells and was absent on the basolateral cell membrane. In the apical cell culture compartment we found significantly more stimulatory activity for granulocytic IL-8 expression. CD62L, a selectin less expressed in activated granulocytes, was decreased in granulocytes incubated with urinary THP and in supernatants of THP-producing renal tubular cells but not in supernatants from THP-negative cells. Again, the effect on CD62L expression was found only in apical culture media and was absent in the basal compartment. In summary our data give evidence that renal tubular cell THP expression may be relevant in kidney diseases since THP is a potent activator of human granulocytes. The regulation of apical versus basal THP expression and release in vivo may be crucial in the induction of the inflammatory response, e.g., in bacterial renal diseases.

Ochratoxin A induces karyomegaly and cell cycle aberrations in renal tubular cells without relation to induction of oxidative stress responses in rats

2014 ◽  
Vol 224 (1) ◽  
pp. 64-72 ◽  
Author(s):  
Eriko Taniai ◽  
Atsunori Yafune ◽  
Masahiro Nakajima ◽  
Shim-Mo Hayashi ◽  
Fumiyuki Nakane ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Ochratoxin A ◽  
Stress Responses ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Oxidative Stress Responses

Hepatocyte growth factor may function as a renotropic factor for regeneration in rats with acute renal injury

1993 ◽  
Vol 265 (1) ◽  
pp. F61-F69 ◽  
Author(s):  
T. Igawa ◽  
K. Matsumoto ◽  
S. Kanda ◽  
Y. Saito ◽  
T. Nakamura
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Dna Synthesis ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Hepatocyte Growth

Hepatocyte growth factor (HGF), a potent mitogen for mature hepatocytes, possesses mitogenic and morphogenic activities for renal epithelial cells. To examine the renotropic function of HGF, we investigated the expression of HGF mRNA and HGF activity in the rat kidney after acute renal failure. When acute renal failure was induced by ischemia or by HgCl2 administration, a DNA synthesis occurred predominantly in the renal tubular cells located in the outer medulla with a peak at 48 h after the treatments. In both renal injuries, HGF mRNA in the kidney increased markedly, reaching a maximum 6 to 12 h after the treatments. HGF activity in the kidney also increased to three- to fourfold higher level than the normal level at 12 h after ischemic treatment or HgCl2 administration. In situ hybridization and immunohistochemical analysis indicated that both HGF mRNA and HGF protein were expressed in renal interstitial cells, presumably endothelial cells and macrophages, but not in tubular epithelial cells. In addition, HGF activity in the plasma of rats with renal ischemia or HgCl2 administration rapidly increased, reaching a maximum at 6 h after the treatment. One week after these injuries, HGF mRNA and HGF activity reverted to normal levels, and renal tubular cell regeneration ceased. Moreover, intravenous injection of human recombinant HGF into mice with acute renal failure caused by HgCl2 administration stimulated DNA synthesis of renal tubular cells in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Human antigen R regulates hypoxia‐induced mitophagy in renal tubular cells through PARKIN/BNIP3L expressions

2021 ◽  
Author(s):  
Shao‐Hua Yu ◽  
Kalaiselvi Palanisamy ◽  
Kuo‐Ting Sun ◽  
Xin Li ◽  
Yao‐Ming Wang ◽  
...  
Keyword(s):  
Tubular Cells ◽  
Human Antigen R ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals Interleukin-22 attenuates renal tubular cells inflammation and fibrosis induced by TGF-β1 through Notch1 signaling pathway

Renal Failure ◽  
2020 ◽  
Vol 42 (1) ◽  
pp. 381-390 ◽  
Author(s):  
Rong Tang ◽  
Xiangcheng Xiao ◽  
Yang Lu ◽  
Huihui Li ◽  
Qiaoling Zhou ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Tubular Cells ◽  
Interleukin 22 ◽  
Renal Tubular Cells ◽  
Notch1 Signaling ◽  
Renal Tubular ◽  
Notch1 Signaling Pathway ◽  
Tgf Β1

Redistribution and dysfunction of integrins in cultured renal epithelial cells exposed to oxidative stress

1993 ◽  
Vol 264 (1) ◽  
pp. F149-F157 ◽  
Author(s):  
J. Gailit ◽  
D. Colflesh ◽  
I. Rabiner ◽  
J. Simone ◽  
M. S. Goligorsky
Keyword(s):  
Oxidative Stress ◽  
Cell Adhesion ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Cell Surface ◽  
Apical Cell ◽  
Flow Cytometric Analysis ◽  
Adhesion Properties ◽  
Renal Tubular Cells ◽  
Renal Tubular

Tubular obstruction by detached renal tubular epithelial cells is a major cause of oliguria in acute renal failure. Viable renal tubular cells can be recovered from urine of patients with acute tubular necrosis, suggesting a possible defect in cell adhesion to the basement membrane. To study this process of epithelial cell desquamation in vitro, we investigated the effect of nonlethal oxidative stress on the integrin adhesion receptors of the primate kidney epithelial cell line BS-C-1. Morphological and functional studies of cell adhesion properties included the following: interference reflection microscopy, intravital confocal microscopy and immunocytochemistry, flow cytometric analysis of integrin receptor abundance, and cell-matrix attachment assay. High levels of the integrin subunits alpha 3, alpha v, and beta 1 were detected on the cell surface by fluorescence-activated cell sorting (FACS) analysis, as well as lower levels of alpha 1, alpha 2, alpha 4, alpha 5, alpha 6, and beta 3. Exposure of BS-C-1 cells to nonlethal oxidative stress resulted in the disruption of focal contacts, disappearance of talin from the basal cell surface, and in the redistribution of integrin alpha 3-subunits from predominantly basal location to the apical cell surface. As measured in a quantitative cell attachment assay, oxidative stress decreased BS-C-1 cell adhesion to type IV collagen, laminin, fibronectin, and vitronectin. Defective adhesion was not associated with a loss of alpha 3-, alpha 4-, or alpha v-integrin subunits from the cell surface.(ABSTRACT TRUNCATED AT 250 WORDS)

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