scholarly journals Renal calcitonin receptors and adenylate cyclase in rats immunized against tubular basement membrane

1977 ◽  
Vol 12 (3) ◽  
pp. 184-192 ◽  
Author(s):  
Nadine Loreau ◽  
Jean-Pierre Cosyns ◽  
Chantal Lepreux ◽  
Pierre Verroust ◽  
Raymond Ardaillou
Keyword(s):  
Basement Membrane ◽  
Adenylate Cyclase ◽  
Tubular Basement Membrane ◽  
Calcitonin Receptors

scholarly journals Die Kaliumhydrogenphosphat-induzierte Nephropathie des Hundes. I. Pathogenese der Tubulusatrophiee [Potassium Hydrogen Phosphate Induced Nephropathy in the Dog. I. Pathogenesis of Tubular Atrophy—author's trans.]

1980 ◽  
Vol 17 (6) ◽  
pp. 699-719 ◽  
Author(s):  
P. Schneider ◽  
G. Pappritz ◽  
R. Müller-Peddinghaus ◽  
M. Bauer ◽  
H. Lehmann ◽  
...  
Keyword(s):  
Acid Phosphatase ◽  
Epithelial Cells ◽  
Basement Membrane ◽  
Basement Membranes ◽  
Tubular Epithelial Cells ◽  
Beagle Dogs ◽  
Lysosomal Degradation ◽  
Tubular Basement Membrane ◽  
Tubular Atrophy ◽  
Study Results

A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HPO4 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells. During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g K2HPO4/kg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and β-glucuronidase were found on cryostat sections. Kidneys fixed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated. Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosomes into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane. The degradation processes described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward the end of the experiment. So far, it is not clear whether the tubular basement membrane is synthesized by the tubular cells, by fibroblasts or by both cell types. The presence of basement membrane-like material in tubular epithelial cells and in parietal epithelial cells of the glomerulus favors the view that epithelial cells produce the basement membranes and that increased production of basement membrane-like material is a sign of loss of differentiation.

scholarly journals Calcitonin gene-related peptide receptor antagonist human CGRP-(8-37)

1989 ◽  
Vol 256 (2) ◽  
pp. E331-E335 ◽  
Author(s):  
T. Chiba ◽  
A. Yamaguchi ◽  
T. Yamatani ◽  
A. Nakamura ◽  
T. Morishita ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Adenylate Cyclase ◽  
Calcitonin Gene Related Peptide ◽  
Human Calcitonin ◽  
Liver Plasma Membrane ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Liver Membranes ◽  
Calcitonin Receptors ◽  
Stimulation Of

From this study, we predicted that the human calcitonin gene-related peptide (hCGRP) fragment hCGRP-(8-37) would be a selective antagonist for CGRP receptors but an agonist for calcitonin (CT) receptors. In rat liver plasma membrane, where CGRP receptors predominate and CT appears to act through these receptors, hCGRP-(8-37) dose dependently displaced 125I-[Tyr0]rat CGRP binding. However, hCGRP-(8-37) had no effect on adenylate cyclase activity in liver plasma membrane. Furthermore, hCGRP-(8-37) inhibited adenylate cyclase activation induced not only by hCGRP but also by hCT. On the other hand, in LLC-PK1 cells, where calcitonin receptors are abundant and CGRP appears to act via these receptors, the bindings of 125I-[Tyr0]rat CGRP and 125I-hCT were both inhibited by hCGRP-(8-37). In contrast to liver membranes, interaction of hCGRP-(8-37) with these receptors led to stimulation of adenosine 3',5'-cyclic monophosphate (cAMP) production in LLC-PK1 cells, and moreover, this fragment did not inhibit the increased production of cAMP induced not only by hCT but also by hCGRP. Thus hCGRP-(8-37) appears to be a useful tool for determining whether the action of CGRP as well as that of CT is mediated via specific CGRP receptors or CT receptors.

Characteristic Matrix and Tubular Basement Membrane Abnormalities in the CBA/Ca-kdkd Mouse Model of Hereditary Tubulointerstitial Disease

Nephron ◽  
1998 ◽  
Vol 80 (3) ◽  
pp. 305-313 ◽  
Author(s):  
Vladimir Sibalic ◽  
Li-kang Sun ◽  
Anita Sibalic ◽  
Beat Oertli ◽  
Theresia Ritthaler ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Mouse Model ◽  
Characteristic Matrix ◽  
Tubular Basement Membrane

Erythropoietin protects the tubular basement membrane by promoting the bone marrow to release extracellular vesicles containing tPA-targeting miR-144

2016 ◽  
Vol 310 (1) ◽  
pp. F27-F40 ◽  
Author(s):  
Yang Zhou ◽  
Li Fang ◽  
Yanting Yu ◽  
Jing Niu ◽  
Lei Jiang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Basement Membrane ◽  
Protective Effect ◽  
Extracellular Vesicles ◽  
Renal Fibrosis ◽  
Bone Marrow Cells ◽  
Circulating Microrna ◽  
Tubular Basement Membrane ◽  
Renal Tubulointerstitial Fibrosis ◽  
Metalloproteinase 9

Renal fibrosis is an inevitable outcome of chronic kidney disease (CKD). Erythropoietin (EPO) has been recently reported to be able to mitigate renal fibrosis. The mechanism underlying the protective effect of EPO, however, remains elusive. In the present study, employing a mouse model of renal tubulointerstitial fibrosis induced by unilateral ureteral obstruction (UUO), we demonstrated that EPO markedly reduced the disruption of the tubular basement membrane (TBM) through attenuating the activation of tissue plasminogen activator (tPA) and matrix metalloproteinase 9 (MMP9), the major matrix proteolytic network in the obstructed kidney. Instead of acting directly on tPA in the kidney, EPO strongly increased the level of circulating microRNA (miR)-144, which was delivered to the injured renal fibroblasts via extracellular vesicles (EVs) to target the tPA 3′-untranslated region and suppress tPA expression. The protective effect of EPO on mouse TBM was inhibited by miR-144 antagomir. Furthermore, in vitro results confirmed that EPO could stimulate bone marrow-derived Sca-1+CD44+CD11b−CD19− cells to secrete miR-144-containing EVs, which markedly suppressed tPA expression, as well as metalloproteinase 9 (MMP9) level and activity, in cultured renal fibroblasts. In conclusion, our study provides the first evidence that EPO protects mouse renal TBM through promoting bone marrow cells to generate and secrete miR-144, which, in turn, is efficiently delivered into the mouse kidney via EVs to inhibit the activation of the tPA/MMP9-mediated proteolytic network. This finding thus suggests that EPO, a hormone widely used to treat anemia in CKD, is a potential therapeutic strategy for renal fibrosis.

scholarly journals Isolation and characterization of rat tubular basement membrane

1977 ◽  
Vol 12 (4) ◽  
pp. 238-243 ◽  
Author(s):  
Istvan Krisko ◽  
Erica DeBernardo ◽  
Cliford S. Sato
Keyword(s):  
Basement Membrane ◽  
Tubular Basement Membrane ◽  
Isolation And Characterization

scholarly journals Monoclonal immunoglobulin G deposits on tubular basement membrane in renal allograft: is this significant for chronic allograft injury?

2018 ◽  
Vol 34 (4) ◽  
pp. 711-717
Author(s):  
Anri Sawada ◽  
Kunio Kawanishi ◽  
Shigeru Horita ◽  
Kazuya Omoto ◽  
Masayoshi Okumi ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Immunoglobulin G ◽  
Renal Allograft ◽  
Tubular Basement Membrane ◽  
Monoclonal Immunoglobulin

Polyclonal immunoglobulin G deposition on the tubular basement membrane in a diabetic nephropathy: A case report

2020 ◽  
Vol 70 (7) ◽  
pp. 463-469
Author(s):  
Hirofumi Watanabe ◽  
Yoichi Takeuchi ◽  
Shinji Taniuchi ◽  
Hiroshi Sato ◽  
Yasuhiro Nakamura ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Case Report ◽  
Basement Membrane ◽  
Immunoglobulin G ◽  
Tubular Basement Membrane ◽  
Polyclonal Immunoglobulin
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