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Intercellular Matrix (intercellular + matrix)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Cellulite: nature and aetiopathogenesis

INTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 3 2006
F. Terranova
Abstract Only a limited number of studies on cellulite have been published in the international literature and many of them reach somewhat antithetical conclusions. Consequently, it is not yet possible to reconcile the extreme differences of opinion which have lingered on for years concerning the nature of this disorder, as well as its origin and even the most basic aspects of its histopathological classification. It does not even have a recognized name: in fact, the term ,cellulitis' is used in scientific English to indicate a spreading gangrenous infection of the subcutaneous cellular tissue. The other terms used from time to time [panniculitis, lipodystrophy, edematofibrosclerotic panniculitis (EFP), liposclerosis, lipoedema, etc.] have quite different morphological and pathogenetic connotations in general. Over the last few decades, three major conflicting theories have emerged in relation to the ethiopathogenesis of cellulite. These indicate, respectively, the following causes: 1. Oedema caused by excessive hydrophilia of the intercellular matrix. 2. A homeostatic alteration on a regional microcirculatory level; this pathogenetic theory is summarized in a synthetic and self-explanatory denomination: EFP. 3. A peculiar anatomical conformation of the subcutaneous tissue of women, different from male morphology. These theories must all now be updated in the light of recent advances on the sophisticated and composite physiopathology of the adipose organ , which acts not only as a control device which regulates the systematic equilibrium of energy and modulates the food intake and the metabolism of other tissue substrate through a multiple glandular secretion of hormones and parahormones. Résumé Seulement un nombre limité d'études sur la cellulite a été publié dans la littérature internationale et beaucoup de ces articles arrivent à des conclusions plutôt antithétiques. Par conséquent, actuellement il est impossible de reconcilier les opinions extrèmement différentes concernant la nature de ce désordre, ainsi que son origine, de même que les aspects les plus basilaires de sa classification histopathologique. Le nom même de cette affection n'est pas reconnu: en fait le terme ,, cellulite ''est utilisé dans le language scientifique pour indiquer une inflammation du tissu cellulaire sous-cutané, d'origine infectieuse. Les autres termes employés de temps an temps tels que panniculopathie, lipodystrophie, panniculopathie oedémato-fibroscléreuse, liposclérose, lipoedème etc. ont en general des connotations morphologiques e pathogénétiques tout à fait différentes. Au cours des dernières décennies, trois principales théories contradictoires ont émergé pour ce qui concerne l'etiopathologie dela cellulite. Chacune théorie indique respectivement les suivantes causes: 1. Oedème causé par excessive hydrophilie de la matrice intercellulaire. 2. Altération parcellaire de l'homeostase au niveau microcirculatoire ; cette théorie pathogénétique est résumée à l'intérieur de la synthétique et explicite dénomination: panniculopathie oedémato-fibroscléreuse. 3. Particulière conformation anatomique du tissu sous-cutané chez la femme, différente par rapport à l'homme. Ces théories doivent toutes être mises à jour, à la lumière des recents développements concernant la sophistiquée et composée physiopathologie de l'adipocyte, qui n'agit pas seulement comme entrepôt de stockage du matériel calorique en excès mais aussi comme dispositif de régulation de l'équilibre énergetique systémique, avec la capacitè de moduler l'ingestion d'aliments et le métabolisme d'autres substrats tissutaires. La révision de ces théories doit être faite aussi sur la base des nouvelles acquisitions concernant la modalitè attravers laquelle cet organe règle les multiples sécrétions hormonales et parahormonales. [source]

Effects of Arg-Gly-Asp Sequence Peptide and Hyperosmolarity on the Permeability of Interstitial Matrix and Fenestrated Endothelium in Joints

MICROCIRCULATION, Issue 6 2004
A. POLI
ABSTRACT Objectives: The aims were to assess the contribution of arg-gly-asp (RGD) mediated cell integrin,matrix bonds to interstitial hydraulic resistance and to fenestrated endothelial permeability in joints. Joint fluid is generated by filtration from fenestrated capillaries and drains through a fibronectin-rich synovial intercellular matrix. The role of parenchymal cell,matrix bonding in determining tissue hydraulic resistance is unknown. Methods: The knee cavity of anesthetized rabbits was infused with saline or the competitive hexapeptide blocker GRGDTP, with or without added osmotic stress (600 mosm saline). Intra-articular pressure Pj, net trans-synovial drainage rate s, and the permeation of Evans blue-labeled albumin (EVA) from plasma into the joint cavity were measured. Results: GRGDTP increased the hydraulic conductance of the synovial drainage pathway, ds/dPj, by 71% (p = .02, paired t test, n = 6 animals). Synovial plasma EVA clearance (control 7.1 ± 0.8 ,L h,1, mean ± SEM, n = 15) was unaffected by GRGDTP (7.0 ± 2.3 ,L h,1, n = 6) or hyperosmolarity (4.9 ± 1.5 ,L h,1, n = 8) but was increased by GRGDTP and hyperosmolarity together (15.9 ± 4.8 ,L h,1, n = 5) (p = .01, ANOVA). Changes in dPj/dt evoked by GRGDTP plus hyperosmolarity, but neither alone, demonstrated increased microvascular filtration into the joint cavity (p < .001, ANOVA), as did changes in fluid absorption from the infusion system at fixed Pj. Conclusions: RGD-mediated bonds between the parenchymal cells and interstitial polymers reduce the interstitial hydraulic conductance by 42%. This helps to retain the lubricating fluid inside a joint cavity. RGD-mediated bonds also support the macromolecular barrier function of fenestrated endothelium, but in vivo this is evident only in stressed endothelium (cf. in vitro). [source]

Liposomes in investigative dermatology

PHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 5 2001
Daniel B. Yarosh
Liposomes are microscopic spheres, usually composed of amphiphilic phospholipids. They may be useful without skin penetration if they simply protect or sequester compounds that would otherwise be unstable in the formulation. Liposomes that remain on the skin surface are useful as light-absorbers, agents to deliver color or sunscreens, or as depots for timed-release. Liposomes that penetrate the stratum corneum have the potential to interact with living tissue. Topically applied liposomes can either mix with the stratum corneum lipid matrix or penetrate the stratum corneum by exploiting the lipid-water interface of the intercellular matrix. There are at least four major routes of entry into the skin: pores, hair follicles, columnular spaces and the lipid:water matrix between squames. A major force driving liposome penetration is the water gradient, and flexible liposomes are best able to exploit these delivery opportunities. Some liposomes release their contents extracellularly. Topical application of photosensitizers may be enhanced by encapsulation in liposomes. Higher and longer-lasting drug concentrations may be produced in localized areas of skin, particularly at disease sites where the stratum corneum and the skin barrier function are disrupted. The liposome membrane should be designed to capture lipophilic drugs in the membrane or hydrophilic drugs in the interior. Other types of liposomes can be engineered to be taken up by cells. Once inside cells, the lysosomal sac and clatherin-coated pit are the dead-end destinations for liposomes unless an escape path has been engineered into the liposome. A novel method has been developed to allow delivery into cells of the skin, by escape from the lysosomal sac. These liposomes have been used to topical deliver active DNA repair enzymes from liposomes into epidermal cells and to enhance DNA repair of UV-irradiated skin. From these studies a tremendous amount has been learned about the relationship of DNA damage and skin cancer. Both mutations and immunosuppression appear to be essential to skin cancer and both are induced by DNA damage. DNA damage produces immediate effects by inducing the expression of cytokines, which means that DNA damage can induce signaling in neighboring, undamaged cells. The repair of only a fraction of the DNA damage has a disproportionate effect on the biological responses, clearly demonstrating that not all DNA damage is equivalent. This technology demonstrates that biologically active proteins can be delivered into the cells of skin, and opens up a new field of correcting or enhancing skin cell metabolism to improve human health. [source]

Keratin-lipid structural organization in the corneous layer of snake,

BIOPOLYMERS, Issue 12 2009
Alberto Ripamonti
Abstract The shed epidermis (molt) of snakes comprises four distinct layers. The upper two layers, here considered as ,-layer, contain essentially ,-keratin. The following layer, known as mesos-layer, is similar to the human stratum corneum, and is formed by thin cells surrounded by intercellular lipids. The latter layer mainly contains ,-keratin. In this study, the molecular assemblies of proteins and lipids contained in these layers have been analyzed in the scale of two species of snakes, the elapid Tiger snake (TS, Notechis scutatus) and the viperid Gabon viper (GV, Bitis gabonica). Scanning X-ray micro-diffraction, FTIR and Raman spectroscopies, thermal analysis, and scanning electron microscopy experiments confirm the presence of the three layers in the GV skin scale. Conversely, in the TS molt a typical ,-keratin layer appears to be absent. In the latter, experimental data suggest the presence of two domains similar to those found in the lipid intercellular matrix of stratum corneum. X-ray diffraction data also allow to determine the relative orientation of keratins and lipids. The keratin fibrils are randomly oriented inside the layers parallel to the surface of scales while the lipids are organized in lamellar structures having aliphatic chains normal to the scale surface. The high ordered lipid organization in the mature mesos layer probably increases its effectiveness in limiting water-loss. © 2009 Wiley Periodicals, Inc. Biopolymers 91: 1172,1181, 2009. This article was originally published online as an accepted preprint. The "Published Online" date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com [source]