scholarly journals IgG Subclass Expression in Diabetic Nephropathy

2020 ◽  
Author(s):  
Xuanli Tang ◽  
Xue Jiang ◽  
Feng Wan ◽  
Xiaohong Li ◽  
Ruchun Yang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Basement Membrane ◽  
Collagen Iv ◽  
Igg Subclasses ◽  
Igg Subclass ◽  
Tubular Injury ◽  
Tubular Basement Membrane ◽  
Cd34 Expression ◽  
Complement Deposition ◽  
Linear Expression

Abstract Background: This study aimed to analyze the distribution of IgG subclasses in diabetic nephropathy (DN) and its association with clinico-pathological features. Methods: Forty DN cases were analyzed to identify IgG subclasses, as well as collagen IV α5, CD34, and KIM-1.Results: Both IgG and its subclasses showed a linear expression and overlapped with collagen IV α5 on glomerular basement membrane (GBM) and some of tubular basement membrane (TBM), without complement deposition. Eleven cases of IgG subclass deposition along both GBM and TBM were associated with more proteinuria. Five cases of TBM-only IgG subclass deposition were accompanied with less KIM-1 positivity and more arteriosclerosis. The major IgG subclasses expressed on GBM were IgG1 and IgG2, while TBM expression was mainly IgG1 and IgG3. Glomerular IgG1-positive status was associated with less CD34 expression, while IgG2-positive status was associated with thicker GBM. Expression of multiple IgG subclasses along TBM showed less KIM-1 positivity and interstitial inflammation than those with isotype or no IgG subclass expression.Conclusions: IgG subclasses were selectively deposited along GBM and TBM in DN, which was determined by their profiles and severity of glomerular/tubular injury. IgG and its subclass deposition is not causal, but the consequence of renal injury and these positive statuses are associated with different DN injuries.

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

Cardiac myocytes cultured on a basement membrane extract of the ehs tumor

1986 ◽  
Vol 44 ◽  
pp. 270-271
Author(s):  
L. Terracio ◽  
A. Dewey ◽  
K. Rubin ◽  
T.K. Borg
Keyword(s):  
Extracellular Matrix ◽  
Basement Membrane ◽  
Cardiac Myocytes ◽  
Normal Tissue ◽  
Cell Spreading ◽  
Collagen Iv ◽  
Basement Membrane Extract ◽  
Membrane Extract ◽  
Growth Development ◽  
Multicellular Organisms

The recognition and interaction of cells with the extracellular matrix (ECM) effects the normal physiology as well as the pathology of all multicellular organisms. These interactions have been shown to influence the growth, development, and maintenance of normal tissue function. In previous studies, we have shown that neonatal cardiac myocytes specifically interacts with a variety of ECM components including fibronectin, laminin, and collagens I, III and IV. Culturing neonatal myocytes on laminin and collagen IV induces an increased rate of both cell spreading and sarcomerogenesis.

scholarly journals Basement membrane collagen IV deficiency promotes abdominal aortic aneurysm formation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
L. B. Steffensen ◽  
J. Stubbe ◽  
J. S. Lindholt ◽  
H. C. Beck ◽  
M. Overgaard ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Basement Membrane ◽  
Protective Factor ◽  
Complex Disease ◽  
Artery Bypass ◽  
Protective Role ◽  
Collagen Iv ◽  
Mammary Arteries ◽  
Abdominal Aortic

AbstractAbdominal aortic aneurysm (AAA) is a complex disease which is incompletely accounted for. Basement membrane (BM) Collagen IV (COL4A1/A2) is abundant in the artery wall, and several lines of evidence indicate a protective role of baseline COL4A1/A2 in AAA development. Using Col4a1/a2 hemizygous knockout mice (Col4a1/a2+/−, 129Svj background) we show that partial Col4a1/a2 deficiency augmented AAA formation. Although unchallenged aortas were morphometrically and biomechanically unaffected by genotype, explorative proteomic analyses of aortas revealed a clear reduction in BM components and contractile vascular smooth muscle cell (VSMC) proteins, suggesting a central effect of the BM in maintaining VSMCs in the contractile phenotype. These findings were translated to human arteries by showing that COL4A1/A2 correlated to BM proteins and VSMC markers in non-lesioned internal mammary arteries obtained from coronary artery bypass procedures. Moreover, in human AAA tissue, MYH11 (VSMC marker) was depleted in areas of reduced COL4 as assessed by immunohistochemistry. Finally, circulating COL4A1 degradation fragments correlated with AAA progression in the largest Danish AAA cohort, suggesting COL4A1/A2 proteolysis to be an important feature of AAA formation. In sum, we identify COL4A1/A2 as a critical regulator of VSMC phenotype and a protective factor in AAA formation.

scholarly journals Macrophages adhere to glucose-modified basement membrane collagen IV via their scavenger receptors.

1994 ◽  
Vol 269 (14) ◽  
pp. 10197-10200 ◽  
Author(s):  
J. el Khoury ◽  
C.A. Thomas ◽  
J.D. Loike ◽  
S.E. Hickman ◽  
L. Cao ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Collagen Iv ◽  
Scavenger Receptors ◽  
Basement Membrane Collagen ◽  
Membrane Collagen

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.

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