The structural relationship between mesangial cells and basement membrane of the renal glomerulus

1987 ◽  
Vol 176 (3) ◽  
pp. 373-386 ◽  
Author(s):  
Fatsuo Sakai ◽  
Wilhelm Kriz
Keyword(s):  
Basement Membrane ◽  
Mesangial Cells ◽  
Structural Relationship ◽  
Renal Glomerulus

scholarly journals FUNCTIONAL EVIDENCE FOR THE EXISTENCE OF A THIRD CELL TYPE IN THE RENAL GLOMERULUS

1962 ◽  
Vol 13 (1) ◽  
pp. 55-87 ◽  
Author(s):  
Marilyn G. Farquhar ◽  
George E. Palade
Keyword(s):  
Basement Membrane ◽  
Kidney Tissue ◽  
Capillary Wall ◽  
Renal Glomerulus ◽  
Sequence Of Events ◽  
Cytoplasmic Bodies ◽  
Cytoplasmic Vesicles ◽  
Spinous Processes ◽  
Luminal Side ◽  
Peripheral Areas

Two types of cells can be recognized on the luminal side of the glomerular basement membrane: the superficial endothelial cells which directly line the lumen and are comparable to endothelia lining the capillaries of other tissues, and the deep cells, ordinarily not in contact with the lumen, which are distinguished by their long cytoplasmic arms extending for some distance in several directions along the capillary wall, numerous spinous processes, and occasional intraluminal pseudopodia. Experiments carried out with electron-opaque tracers indicated that a functional distinction, based on extent of phagocytosis, can be made between the superficial and deep cells, thus supporting the existence of a distinctive "third" cell (in addition to endothelium and epithelium) in the renal glomerulus. Ferritin, colloidal gold, or thorotrast was administered intravenously to normal and, in the case of ferritin, to nephrotic rats. Kidney tissue was fixed at selected intervals from 1 hour to 10 days after the injection and studied by electron microscopy. Within 1 to 4 hours after tracer administration, the particles which did not traverse the glomerular capillary wall gradually accumulated in the less compact, inner strata of the basement membrane and the large spongy areas of axial regions. After 1 day the concentration of circulating tracer declined and the peripheral areas of the capillaries became relatively free of particles while large accumulations developed in the axial regions. During this period increasing quantities of ferritin were taken up by the deep cells and were found within large and small sized invaginations of their cell membrane or concentrated within cytoplasmic vesicles, vacuoles, multivesicular and dense bodies. At the same time the deep cells showed increased numbers of intraluminal pseudopodia. Within 2 to 4 days the deposits in the spongy areas were cleared and concomitantly increased quantities of tracer appeared in the deep cells within dense cytoplasmic bodies, some of which were more compact than before. When ferritin was given to nephrotic animals the sequence of events was generally the same except that the ferritin deposits at any given period were more massive, their incorporation into the deep cells occurred primarily by means of large pockets 1 to 2 µ in diameter and their clearance from the spongy areas was slower. In normal as well as in nephrotic animals, the phagocytic activity of the superficial endothelium was negligible when compared to that of the deep cells.

scholarly journals Maturation of the developing renal glomerulus with respect to basement membrane proteoglycans

1987 ◽  
Vol 32 (4) ◽  
pp. 498-506 ◽  
Author(s):  
Brigitte Lelongt ◽  
Hirofumi Makino ◽  
Yashpal S. Kanwar
Keyword(s):  
Basement Membrane ◽  
Renal Glomerulus

(Pro)renin receptor promotes crescent formation via the ERK1/2 and Wnt/β-catenin pathways in glomerulonephritis

2020 ◽  
Vol 319 (4) ◽  
pp. F571-F578
Author(s):  
Maki Urushihara ◽  
Shuji Kondo ◽  
Yukiko Kinoshita ◽  
Natsuko Ozaki ◽  
Ariunbold Jamba ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Mesangial Cells ◽  
Macrophage Infiltration ◽  
Crescent Formation ◽  
Sirna Treatment ◽  
Extracellular Signal ◽  
Parietal Epithelial Cells

(Pro)renin receptor [(P)RR] has multiple functions, but its regulation and role in the pathogenesis in glomerulonephritis (GN) are poorly defined. The aims of the present study were to determine the effects of direct renin inhibition (DRI) and demonstrate the role of (P)RR on the progression of crescentic GN. The anti-glomerular basement membrane nephritis rat model developed progressive proteinuria (83.64 ± 10.49 mg/day) and glomerular crescent formation (percent glomerular crescent: 62.1 ± 2.3%) accompanied by increased macrophage infiltration and glomerular expression of monocyte chemoattractant protein (MCP)-1, (P)RR, phospho-extracellular signal-regulated kinase (ERK)1/2, Wnt4, and active β-catenin. Treatment with DRI ameliorated proteinuria (20.33 ± 5.88 mg/day) and markedly reduced glomerular crescent formation (20.9 ± 2.6%), induction of macrophage infiltration, (P)RR, phospho-ERK1/2, Wnt4, and active β-catenin. Furthermore, primary cultured parietal epithelial cells stimulated by recombinant prorenin showed significant increases in cell proliferation. Notably, while the ERK1/2 inhibitor PD98059 or (P)RR-specific siRNA treatment abolished the elevation in cell proliferation, DRI treatment did not abrogate this elevation. Moreover, cultured mesangial cells showed an increase in prorenin-induced MCP-1 expression. Interestingly, (P)RR or Wnt4-specific siRNA treatment or the β-catenin antagonist XAV939 inhibited the elevation of MCP-1 expression, whereas DRI did not. These results suggest that (P)RR regulates glomerular crescent formation via the ERK1/2 signaling and Wnt/β-catenin pathways during the course of anti-glomerular basement membrane nephritis and that DRI mitigates the progression of crescentic GN through the reduction of (P)RR expression but not inhibition of prorenin binding to (P)RR.

MO070NEW ASPECTS OF THE PATHOMORPHOLOGIC SEQUENCE OF NEPHRON LOSS IN DIABETIC NEPHROPATHY

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Hermann Gröne ◽  
Wilhelm Kriz ◽  
Jana Loewen ◽  
Elisabeth Groene
Keyword(s):  
Diabetic Nephropathy ◽  
Basement Membrane ◽  
Mesangial Cells ◽  
Capillary Endothelium ◽  
Tubular Damage ◽  
Mesangial Matrix ◽  
Nephron Loss ◽  
Bowman's Capsule ◽  
Glomerular Damage ◽  
Glomerular Capillaries

Abstract Background and Aims Diabetic nephropathy (DN) is the leading cause of end-stage-renal disease in western countries. Despite of innumerable studies undertaken to elucidate the pathogenesis of DN the underlying morphologic alterations have been insufficiently analyzed. Method Re-evaluation of more than 800 biopsies was done showing several unknown features. Results: 1. Matrix accumulation in the mesangium: Thickening of the glomerular basement membrane (GBM) and expansion of the mesangial matrix are hallmarks of DN, generally considered to emerge from different sites of overproduction: GBM components from podocytes and mesangial matrix from mesangial cells. We show, that the accumulation of matrix in the mesangium emerges from an overproduction of GBM material by podocytes and endothelial cells and an impaired degradation by mesangial cells. The progressing deposition of worn-out GBM material into the mesangium accounts for the advancement from diffuse mesangial sclerosis (DMS) to nodular sclerosis (NS) and to the herniation of the tuft through the glomerular vascular pole to the outside; the latter is associated with the outgrowth of glomerular capillaries into the peri-glomerular space leading to the destruction of the juxtaglomerular apparatus. 2.The role of podocytes Podocytes have frequently been accused to play a central role in DN. This is correct, but in another way than generally assumed. Damage to podocytes cannot be seen in DMS. The albuminuria regularly seen during this stage derives, as previously suggested by others, from an increased leakiness of the glomerular capillary endothelium based on a deranged glycocalyx. Podocyte detachments start at the transition from DMS to NS, based on the loss of cross talk signals with the capillary endothelium: the increasing deposition of matrix leads to the collapse of many capillaries. These podocytes contribute little to the further progression of the damage: they are lost into primary urine or they undergo cell lysis.In addition to their role in increased matrix production, podocytes take an active role in the formation of tuft adhesions to Bowman’s capsule (BC), starting the progression to NS. Expansion of the matrix within the mesangium has led to expansion of the tuft (frequently associated with nodules) towards Bowman’s capsule (BC) or towards the urinary orifice. Podocytes on the surface of these expansions are in their majority structurally intact, exhibiting an intact pattern of foot processes. These podocytes come into contact with parietal epithelial cells and initiate DN-specific tuft adhesions to BC allowing the proliferation of glomerular capillaries into BC. There they deliver an exudate into BC that spreads around the entire circumference of the glomerulus presenting as giant insudative spaces. Moreover, this process encroaches via the glomerulo-tubular junction onto the tubule constituting the major pathway of glomerular damage extending to the tubulointerstitium. 3. Tubulointerstitial fibrosisIt is current opinion that the tubulointerstitial fibrosis may start from tubular damage resulting in an own, glomerular-independent pathway to nephron loss. However, there is scant evidence for such a mechanism. Studying 162 glomerulo-tubular transitions, we did not see a tubular epithelial or interstitial damage in those biopsies without any evidence of a glomerulo-tubular damage transfer. The only exception consists of the well-known prominent thickening of the tubular basement membrane, which may result in functional loss but does not lead to structural epithelial damage. Conclusion We consistently found that tubulo-interstitial damage develops after encroachment of the glomerular damage onto the tubule, leading first to a gradual degeneration of tubules which subsequently initiate the process of interstitial fibrosis.

scholarly journals TRANSPORT OF GLOBIN BY THE RENAL GLOMERULUS

1964 ◽  
Vol 120 (6) ◽  
pp. 1129-1138 ◽  
Author(s):  
Max G. Menefee ◽  
C. Barber Mueller ◽  
Allen L. Bell ◽  
Joseph K. Myers
Keyword(s):  
Endothelial Cells ◽  
Electron Microscope ◽  
Basement Membrane ◽  
Basement Membranes ◽  
Renal Glomerulus ◽  
Thin Sections ◽  
Characteristic Appearance ◽  
Pass Through ◽  
Surrounding Membrane ◽  
Glomerular Capillaries

Purified human globin injected into rats forms aggregates which are identifiable by their characteristic appearance in thin sections in the electron microscope and by their positive autoradiographs when the globin is tritiated before injection. Globin is taken up by endothelial cells of glomerular capillaries and is transported across the cell within the limits of a surrounding membrane. Globin is rarely seen to pass through fenestrations. Globin is also taken into the stalk region where it is seen usually within the sponge fibers and only occasionally within stalk cells. Globin is seen in all stages of passage through the basement membranes and sponge fibers, which are not deformed by its passage. On the basis of the findings presented here and by others, it is postulated that the basement membrane and sponge fibers consist of a thixotrophic gel. After traversing the basement membrane, the globin passes between foot processes of the epithelial cells. The slit membranes are deformed by this passage and thus appear to be distinctive structures. The globin is next found free in Bowman's space; the earliest aggregates are seen there within 1 minute after injection. Globin taken up in the stalk region is slowly discharged and very little is found there 6 hours postinjection.

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