scholarly journals Analysis the Detailed Process of Glomerular Capillary Formation Using Immunofluorescence Perform With Ultrathick Section

2019 ◽  
Author(s):  
Ting Yu ◽  
Chi Liu
Keyword(s):  
Developmental Biology ◽  
Complex Structure ◽  
Thick Section ◽  
Capillary Formation ◽  
Intussusceptive Angiogenesis ◽  
Glomerular Capillary ◽  
Antibody Staining ◽  
Capillary Bed ◽  
Bowman's Capsule ◽  
Glomerular Capillaries

AbstractBackgroundGlomerular capillary formation is one of the fundamental mysteries in renal developmental biology. However, there are still debates on this issue, and its detailed formation process has not been clarified.ResultsTo resolve this problem, we performed antibody staining with ultra-thick section on embryonic and postnatal mouse kidneys to detect and analyze the development of glomerular capillaries. We found that blood vessel of the fetal kidneys expanded through proliferation and sprouting. During the comma-stage and S-shaped stages, 3-4 capillaries began to bud and migrate into the glomerular cleft, forming a capillary bed in the Bowman’s capsule. Then, the capillary bed expanded into mature glomerular capillary by intussusceptive angiogenesis. The afferent and efferent arterioles were formed through pruning. The distribution of VEGFA in the nephron epithelial cells but not only in podocytes, induced multiple capillaries sprouted into the glomerular cleft. And CXCR4 played an important role in the differentiation and expansion of capillary bed into glomerular capillary.ConclusionsImmunofluorescence performed with ultra-thick section allowed us to investigate the development of complex structure tissues systematically and comprehensively.

scholarly journals Analysis the Detailed Process of Glomerular Capillary Formation Using Immunofluorescence Perform With Ultrathick Section

2019 ◽  
Author(s):  
Chi Liu ◽  
Fang Zhang ◽  
Yan Wu ◽  
Yu Ting ◽  
Lu Dai ◽  
...  
Keyword(s):  
Developmental Biology ◽  
Complex Structure ◽  
Thick Section ◽  
Capillary Formation ◽  
Intussusceptive Angiogenesis ◽  
Glomerular Capillary ◽  
Antibody Staining ◽  
Capillary Bed ◽  
Bowman's Capsule ◽  
Glomerular Capillaries

Abstract Background: Glomerular capillary formation is one of the fundamental mysteries in renal developmental biology. However, there are still debates on this issue, and its detailed formation process has not been clarified. Results: To resolve this problem, we performed antibody staining with ultra-thick section on embryonic and postnatal mouse kidneys to detect and analyze the development of glomerular capillaries. We found that blood vessel of the fetal kidneys expanded through proliferation and sprouting. During the comma-stage and S-shaped stages, 3-4 capillaries began to bud and migrate into the glomerular cleft, forming a capillary bed in the Bowman’s capsule. Then, the capillary bed expanded into mature glomerular capillary by intussusceptive angiogenesis. The afferent and efferent arterioles were formed through pruning. The distribution of VEGFA in the nephron epithelial cells but not only in podocytes, induced multiple capillaries sprouted into the glomerular cleft. And CXCR4 played an important role in the differentiation and expansion of capillary bed into glomerular capillary. Conclusions: Immunofluorescence performed with ultra-thick section allowed us to investigate the development of complex structure tissues systematically and comprehensively.

scholarly journals ELECTRON MICROSCOPY OF THE AVIAN RENAL GLOMERULUS

1957 ◽  
Vol 3 (2) ◽  
pp. 183-192 ◽  
Author(s):  
R. K. F. Pak Poy ◽  
J. S. Robertson
Keyword(s):  
Electron Microscopy ◽  
Basement Membrane ◽  
Thin Sheet ◽  
Cell Mass ◽  
Central Cell ◽  
Dense Layer ◽  
Central Mass ◽  
Capillary Basement Membrane ◽  
Glomerular Capillary ◽  
Glomerular Capillaries

Electron microscopy of sections of chicken glomeruli shows them to possess a large central cell mass, occupying the hilum and the centre of the glomerulus, and continuous with the adventitia of the afferent and efferent arterioles. The glomerular capillaries form a much simpler system than in mammals and are spread over the surface of the central cell mass. Between the capillaries the mass is limited externally by the major component of the glomerular capillary basement membrane, which continues over the surface of the mass from one capillary to the next. Projections of the central cell mass characteristically form the support for glomerular capillaries, and smaller knobs of the central mass may project actually into the lumen of the capillaries, but always carry a layer of endothelial cytoplasm before them. They are never in direct contact with blood. The basement membrane of the glomerular capillary loop has a central dense layer and two lateral less dense layers as in mammals. The central dense layer is continuous with similar appearing dense material in the intercellular spaces of the adventitiae of the arterioles, and also with that of the central cell mass. The two less dense layers can also be traced into direct continuity with the less dense regions of this intercellular substance. The endothelial cytoplasm is spread as a thin sheet over the inner surface of the capillary basement membrane, and shows scattered "pores" resembling those described in mammals. Epithelial cells with interlacing pedicels are at least as prominent as those in mammals. Bowman's capsular membrane also possesses three layers similar to but less wide than those of the capillary basement membrane, and all three layers can be traced into continuity with the dark and light regions of the intercellular material of the adventitial cells of the arterioles, and beyond them with that of the central cell mass. At the hilum Bowman's capsular membrane also fuses with the capillary basement membrane.

Glomerular surface area is normalized in mice born with a nephron deficit: no role for AT1 receptors

2009 ◽  
Vol 296 (3) ◽  
pp. F583-F589 ◽  
Author(s):  
Amany Shweta ◽  
Luise A. Cullen-McEwen ◽  
Michelle M. Kett ◽  
Roger G. Evans ◽  
Kate M. Denton ◽  
...  
Keyword(s):  
Surface Area ◽  
Time Course ◽  
Receptor Activation ◽  
Compensatory Hypertrophy ◽  
Glomerular Hypertrophy ◽  
Capillary Surface ◽  
Glomerular Capillary ◽  
Additional Group ◽  
Nephron Deficit ◽  
Glomerular Capillaries

We examined whether deficits in glomerular capillary surface area associated with a congenital nephron deficit could be corrected by glomerular hypertrophy. Using unbiased stereological techniques, we examined the time course and mode of glomerular hypertrophy in mice lacking one allele for glial cell line-derived neurotrophic factor (GDNF). These GDNF heterozygous (Het) mice are born with ∼30% less nephrons than wild-type (WT) littermates. An additional group of GDNF Het mice received the angiotensin type 1 (AT1)-receptor antagonist candesartan (Cand; 10 mg·kg−1·day−1) from 5 wk of age to determine the role of AT1 receptors in the compensatory hypertrophy. At 10 wk of age, the total volume of renal corpuscles, glomerular capillary surface area, and length of glomerular capillaries in the kidneys of GDNF Het mice were all markedly (∼45%) less than that of WT mice ( P < 0.001). However, by 30 wk, and persisting at 60 wk of age, GDNF Het and WT mice did not significantly differ in any of these parameters. Furthermore, conscious 24-h mean arterial pressure (MAP) did not differ between GDNF Het and WT mice at any time point. MAP of GDNF Het-Cand mice was 20–30 mmHg less than that of GDNF Het-vehicle mice at all three ages, but Cand treatment did not significantly alter glomerular capillary dimensions. In conclusion, we have demonstrated that the deficit in glomerular capillary surface area associated with a congenital nephron deficit can be corrected for in adulthood by an increase in the total length of glomerular capillaries. This process does not require AT1 receptor activation.

Permeability of Peritoneal and Glomerular Capillaries: What are the Differences According to Pore Theory?

2011 ◽  
Vol 31 (3) ◽  
pp. 249-258 ◽  
Author(s):  
Bengt Rippe ◽  
Simon Davies
Keyword(s):  
Glomerular Filtration ◽  
Matrix Theory ◽  
Complex Structure ◽  
Gel Filtration ◽  
Diffusion Path ◽  
Peritoneal Membrane ◽  
Glomerular Filtration Barrier ◽  
Filtration Barrier ◽  
Shed Light ◽  
Glomerular Capillaries

Pore and fiber-matrix theory can both be used to model the peritoneal and glomerular filtration barriers in an attempt to shed light on their differing structure–function relationships. The glomerular filtration barrier (GFB) is structurally more specialized, morphologically complex, and also highly dynamic; but paradoxically, because of its uniformity, it conforms more closely to the predictions of pore theory than does the peritoneum, and it in fact resembles a more simple synthetic membrane. Compared with the peritoneal capillary wall, the GFB has no transcellular “third” pores (aquaporins), and it is far less leaky and more size-selective to proteins, mainly as a result of having far fewer “large” pores. It does have charge-selective properties, although these are considered much less important in excluding albumin than was once thought, and it is also able to select polymers according to their shape and flexibility. Even this property might reflect the relative uniformity of the GFB, which has a high diffusion area and short diffusion distances, compared with the peritoneal barrier, which behaves more like a gel filtration column. Furthermore, the length of the diffusion path across the peritoneal membrane is much greater for small solutes, given the relatively high ultrafiltration coefficient for that membrane compared with the GFB—a situation that reflects both the tortuosity of the interendothelial clefts and the distribution of peritoneal capillaries within the interstitium. These comparisons reveal the peritoneal barrier as a relatively complex structure to model; and yet this model may be more representative of the general microcirculation, and thus shed light on systemic endothelial function in renal failure.

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.

Abstract 063: Impaired Myogenic Response of the Af-art Contributes to the Increased Susceptibility to Hypertension and Diabetic Induced Renal Disease in Milan Normotensive Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Ying Ge ◽  
Fan Fan ◽  
Richard J Roman
Keyword(s):  
Capillary Pressure ◽  
Perfusion Pressure ◽  
Sequence Variant ◽  
Myogenic Response ◽  
Glomerular Capillary ◽  
Protein Excretion ◽  
Glomerular Capillary Pressure ◽  
Increased Susceptibility ◽  
Glomerular Capillaries

Previous studies have indicated that Milan normotensive (MNS) rats are more susceptible to the development of hypertension and diabetic induced renal injury than Milan hypertensive (MHS) rats, but the genes and pathways involved are unknown. MNS also develop proteinuria and chronic kidney disease (CKD) as they age, whereas hypertensive MHS do not. We compared the myogenic response of isolated perfused Af-Art and autoregulation of RBF and glomerular capillary pressure in 6-9 week old MNS and MHS rats. The diameter of Af-Art of MNS rats increased from 14.0 ± 0.5 to 14.2 ± 0.6 μm (n=6) when elevation in perfusion pressure from 60 to 120 mmHg. In contrast, the diameter of the Af-Art decreased significantly from 14.3 ± 0.5 to 11.5 ± 0.6 μm (n=6) in MHS rats. In vivo, RBF increased by 26% when RPP was increased from 100 to 140 mmHg in MNS rats but it remained unchanged in MHS rats. Glomerular capillary pressure rose by 11 mmHg in MNS following the elevation in RPP from 100 to 140 mm Hg but not in MHS rats. Protein excretion increased from 8.9 ± 0.7 to 158.2 ± 23.1 mg/day in MNS rats as the increased in age from 3 to 9 months of age but it did not increase in MHS rats. In com-parison to other strains susceptible and resistant to CKD, we noticed that both MNS and Fawn Hooded hypertensive (FHH) rats that do not autoregulate RBF also share the same sequence variant in the Adducin 3 gene. We performed a genetic complementation study to test whether this mutation might be responsible for the impaired myogenic response in MNS. The diameter of the Af-Art isolated from an F1 cross of MNS &FHH rats increased from 17.2 ± 0.9 to 18.5 ± 0.9 μM (n=5) in response to increase in perfusion pressure and RBF was not efficiently autoregulated in these animals. These data indicate a mutation in Adducin 3 which impairs myogenic response of the Af-Art and increased transmission of pressure to the glomerular capillaries may contribute to the development of CKD in MNS rats similar to what is seen in FHH rats.

Pathomorphological Sequence of Nephron Loss in Diabetic Nephropathy

2021 ◽  
Author(s):  
Jana Löwen ◽  
Elisabeth Gröne ◽  
Marie-Luise Groß-Weißmann ◽  
Felix Bestvater ◽  
Hermann-Josef Gröne ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Basement Membrane ◽  
Interstitial Fibrosis ◽  
Glomerular Sclerosis ◽  
Structural Aberrations ◽  
Vascular Proliferation ◽  
Advanced Stages ◽  
Nephron Loss ◽  
Bowman's Capsule ◽  
Glomerular Capillaries

Abstract Following our reports on mesangial sclerosis and vascular proliferation in diabetic nephropathy (DN)(25,34) we now describe the advanced stages of DN terminating in glomerular obsolescence and tubulo-interstitial fibrosis based on a total of 918 biopsies. The structural aberrations emerge from two defects: First, an increased synthesis of glomerular basement membrane (GBM) components by podocytes and endothelial cells leading to an accumulation of GBM material in the mesangium. Second, a defect of glomerular vessels consisting of an increased leakiness and an increased propensity to proliferate. Both defects may lead to glomerular degeneration. The progressing compaction of the accumulated worn-out GBM-material together with the retraction of podocytes out of the tuft and the collapse and hyalinosis of capillaries results in a shrunken tuft that fuses with Bowman's capsule to glomerular sclerosis. The most frequent pathway to glomerular decay starts with local tuft expansions that result in contacts of structurally healthy podocytes to the parietal epithelium initiating the formation of tuft adhesions, which include the penetration of glomerular capillaries into BC. Exudation of plasma from such capillaries into the space between the parietal epithelium and its basement membrane causes the formation of insudative fluid accumulations within BC spreading around the glomerular circumference and, via the glomerulo-tubular junction, onto the tubule. Degeneration of the corresponding tubule develops secondarily to the glomerular damage, either due to cessation of filtration in cases of global sclerosis or due to encroachment of the insudative spaces. The degenerating tubules induce the proliferation of myo-fibroblasts resulting in interstitial fibrosis.

scholarly journals Bmp in Podocytes Is Essential for Normal Glomerular Capillary Formation

2008 ◽  
Vol 19 (4) ◽  
pp. 685-694 ◽  
Author(s):  
Hiroyuki Ueda ◽  
Yoichi Miyazaki ◽  
Taiji Matsusaka ◽  
Yasunori Utsunomiya ◽  
Tetsuya Kawamura ◽  
...  
Keyword(s):  
Capillary Formation ◽  
Glomerular Capillary

scholarly journals TGF-β–Activated Kinase 1 Is Crucial in Podocyte Differentiation and Glomerular Capillary Formation

2014 ◽  
Vol 25 (9) ◽  
pp. 1966-1978 ◽  
Author(s):  
Sung Il Kim ◽  
So-Young Lee ◽  
Zhibo Wang ◽  
Yan Ding ◽  
Nadeem Haque ◽  
...  
Keyword(s):  
Capillary Formation ◽  
Glomerular Capillary

scholarly journals On changes in the glomeruli and tubules of the kidney accompanying activity

1914 ◽  
Vol 87 (599) ◽  
pp. 593-609 ◽  
Keyword(s):  
Blood Pressure ◽  
Capsule Wall ◽  
Active Secretion ◽  
Glomerular Capillary ◽  
Before And After ◽  
The Subject ◽  
Set Up ◽  
Bowman's Capsule

The experiments described in this paper were designed to test the correctness of the view put forward by one of us, namely, that the glomerulus is a propulsor. If this view be correct, the marked dilatation of the tubules, which is so prominent a feature in a kidney after active diuresis, is simply the expression of the forcible distension of the tubule from within, effected by the discharge of fluid from the glomerulus down the tubule, the active propelling and dilating force being the intraglomerular blood-pressure transmitted through the glomerular capillary cells and epithelium. As, however, the condition of the glomerulus after active secretion has not been made the subject of extensive observation, it seemed probable that a thorough study of the alterations in size and appearance of both tubule and glomerulus might give many points of importance in criticising the propulsion theory. Thus, if the capsule be free to expand, we may find it enlarged after active diuresis; and again, if the propulsive action of the glomerulus is complete and instantaneous, we should find the glomerulus filling Bowman’s capsule completely under all conditions. But it was also possible that, after a very free secretion of water, there might be a considerable accumulation of fluid between the glomerulus and the capsule wall. We therefore measured the sizes of the capsules, the glomeruli and the tubules in kidneys, before and after diuresis had been set up under varying conditions. The more important of these states were:— 1. The kidney at rest. 2. The kidney secreting freely. This we term an “active free” kidney. 3. Decapsulated and secreting freely. This we term an “active decapsulated” kidney. The aim of the procedure was to test the explanation offered by the theory as to the meaning of the Capsule.

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