Morphometric Data on the Endothelium of Blood Capillaries

Simionescu, M; Simiónescu, N; Palade, George E.

doi:10.1083/jcb.60.1.128

Cited by 274 publications

(134 citation statements)

References 35 publications

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“…Similar images have been observed previously in other secretory systems, such as the neuromuscular junction (16,22), the adrenal medulla (45), and the pancreatic beta cells (34), and interpreted as an early event in the release process, i.e., as points of fusion between the plasmalemma and the membrane of the secretory granules. Rosettes, annuli, or localized modifications of particle distribution, which have been reported to characterize the points of membrane adhesion in some protozoa (38,39,40) as well as endothelial cells (41) and macrophages (44), were never observed around these areas. Analogous observations had been made previously in other glandular cells (34,45).…”

Section: Stimulated Cellsmentioning

confidence: 99%

Dynamic changes of the luminal plasmalemma in stimulated parotid acinar cells. A freeze-fracture study.

Camilli¹,

Peluchetti²,

Meldolesi³

1976

The Journal of Cell Biology

112

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In the acinar cells of the rat parotid gland the two membranes participating in exocytosis, i.e., the luminal plasmalemma and the secretory granule membrane, are clearly distinguishable in freeze-fracture because of their different densities in particles. In order to obtain point-specific information about the fusion-fission of these two membranes that occurs during the secretory cycle, glands were studied at various times (5 min to 6 h) after stimulation with isoproterenol. We observed that, in the course of the release of secretion products and shortly afterwards, the enlarged luminal plasmalemma exhibits a mosaic organization consisting of an alternation of membrane patches of high (original plasmalemma) and low (fused granule membrane) particle density. The transition between these two patterns is usually sharp. Later, concomitant with the reformation of acinar canaliculi, the low particle density membrane is found at the cell surface but only bounding vacuolar infoldings, and then it finally disappears.These results suggest that (a) fusion of these membranes does not result in a random intermixing of the molecular components of the participating membranes, which retain their structural identity; and (b) the enlarged luminal plasmalemma reverts to its original size by a progressive, specific removal of the regions of low particle density from the cell surface.In secretory cells the exportable proteins are known to be vectorially transported from the site of synthesis to the extracellular space through a pathway which includes a number of distinct membrane-bounded organelles (8,9,23,24): in sequence, the rough endoplasmic reticulum, the Golgi complex, and the secretion granules. The content of the latter is then discharged by exocytosis, i.e., by fusion of the granule limiting membrane with the plasmalemma followed by an opening at the point of fusion (36). Since the transport of the secretion products between adjacent cell compartments occurs in bulk, by means of membrane-bounded vesicles, a concomitant transfer of membranes must be postulated.The fate of the transferred membrane is still debated. Biochemical studies carried out on various secretory systems have clearly shown that the turnover rate of the molecular components of all the membranes involved is much slower than that of the secretory products (28,29,46,47); thus, it is most likely that these molecular components are reutilized in several secretory cycles (28,29). However, the mechanisms of this reutilization are still unclear, since it is not known whether membrane patches, after fusing with a membrane of a

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Section: Stimulated Cellsmentioning

confidence: 99%

Dynamic changes of the luminal plasmalemma in stimulated parotid acinar cells. A freeze-fracture study.

Camilli¹,

Peluchetti²,

Meldolesi³

1976

The Journal of Cell Biology

112

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“…The human ECs used were either from the microvasculature of the lung (HLMVEC) or skin (HDMVEC-Ad, HDMVEC-neo) or a large vessel such as the umbilical vein (HUVEC). We chose these cell types as none of them contain any TEC or fenestrae and their associated diaphragms in situ (Clementi and Palade, 1969a;Simionescu et al, 1974;Milici et al, 1985b). Only the lung microvascular ECs contain SDs at the mouth of their caveolae in situ (Stan et al, 1999a(Stan et al, , 1999b.…”

Section: Pma Upregulates Pv1 Mrna and Protein Levels In Ecs In Culturementioning

confidence: 99%

PV1 Is a Key Structural Component for the Formation of the Stomatal and Fenestral Diaphragms

Stan

Tkachenko²,

Niesman

2004

MBoC

122

153

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PV1 is an endothelial-specific integral membrane glycoprotein associated with the stomatal diaphragms of caveolae, transendothelial channels, and vesiculo-vacuolar organelles and the diaphragms of endothelial fenestrae. Multiple PV1 homodimers are found within each stomatal and fenestral diaphragm. We investigated the function of PV1 within these diaphragms and their regulation and found that treatment of endothelial cells in culture with phorbol myristate acetate (PMA) led to upregulation of PV1. This correlated with de novo formation of stomatal diaphragms of caveolae and transendothelial channels as well as fenestrae upon PMA treatment. The newly formed diaphragms could be labeled with anti-PV1 antibodies. The upregulation of PV1 and formation of stomatal and fenestral diaphragms by PMA was endothelium specific and was the highest in microvascular endothelial cells compared with their large vessel counterparts. By using a siRNA approach, PV1 mRNA silencing prevented the de novo formation of the diaphragms of caveolae as well as fenestrae and transendothelial channels. Overexpression of PV1 in endothelial cells as well as in cell types that do not harbor caveolar diaphragms in situ induced de novo formation of caveolar stomatal diaphragms. Lastly, PV1 upregulation by PMA required the activation of Erk1/2 MAP kinase pathway and was protein kinase C independent. Taken together, these data show that PV1 is a key structural component, necessary for the biogenesis of the stomatal and fenestral diaphragms.

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“…The specimens were transferred to the same fixative solution for 10-15 min and then immersed for 2 h at 4~ in 25% glycerol in 0.1 M HCI-Na cacodylate buffer, pH 7.2-7.4. Subsequently, the specimens were mounted on metal tissue carriers and further prepared for freeze-fracturing as previously described (24,36).…”

Section: Tissue Processingmentioning

confidence: 99%

Organization of cell junctions in the peritoneal mesothelium

Simionescu¹,

Simiónescu²

1977

The Journal of Cell Biology

104

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Intercellular junctions in the mesothelium of the visceral (mesentery and omenturn), and parietal (diaphragm, pre-aortic, and iliac region) peritoneum were examined in rats and mice by using freeze-cleaved preparations. In addition to usual intercellular junctions (cell body junctions), special junctions are found between cell processes and the surface of the neighboring cell (cell process junctions). Cell body junctions are provided with tight junctions and communicating (gap) junctions. The former consist of one to two junctional strands which show a characteristic staggered arrangement, and focal discontinuities. In cell process junctions, the strands form loops or appear as short, free-ending elements; their polymorphism suggests considerable lability, probably in connection with their assembly and disassembly. The existence of free-ending strands indicates that such structures can be used as attachment devices without being concomitantly involved in the formation of occluding zonules. In both types of junctions, the strands can be resolved into bars, -80-100 nm long, frequently provided with terminal enlargements and intercalated particles which occur singly or in small clusters. These particles are morphologically similar to those present in communicating (gap) junctions. The mesothelium is also provided with isolated composite macular junctions. Throughout the mesothelium, the cleavage plane follows the outer contour of junctional strands and particles, suggesting that strand-to-strand interactions in the apposed membranes are weaker than interactions between each strand and underlying cytoplasmic structures. In their general geometry and cleavage characteristics, the mesothelial junctions resemble the junctions found in the venular endothelium.Earlier interest in the mechanisms of transport of solutes (3,5,6,8,21,9,32), particulate material (12, 10, 16), and cells across the mesothelium has been recently renewed after the success of peritoneal dialysis as a maintenance technique in chronically uremic patients (7, 23). Despite past investigations, current views concerning the structural substrate of the high permeability of the mesothelial membrane are still markedly divergent. According to a number of studies, water-soluble toolecules cross the mesothelium by passive diffusion presumably along intercellular junctions (5, 21,9, 12, 13, 10), whereas according to other investigations transport across the mesothelium is an active process (35, 32) effected primarily via vesicles (30,42,19,17). These divergent views have broader implications than are immediately apparent, since it has been postulated that the mesothelium, due to its being morphologically and functionally similar to the vascular endothelium, can

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Morphometric Data on the Endothelium of Blood Capillaries

Cited by 274 publications

References 35 publications

Dynamic changes of the luminal plasmalemma in stimulated parotid acinar cells. A freeze-fracture study.

Dynamic changes of the luminal plasmalemma in stimulated parotid acinar cells. A freeze-fracture study.

PV1 Is a Key Structural Component for the Formation of the Stomatal and Fenestral Diaphragms

Organization of cell junctions in the peritoneal mesothelium

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