Effect of PGE1, PGI2, and PGF2αanalogs on collagen gel compaction in vitro and interstitial pressure in vivo

Berg, Ansgar; Ekwall, Anna-Karin Hultgård; Rubin, Kristofer; Stjernschantz, Johan; Reed, Rolf K.

doi:10.1152/ajpheart.1998.274.2.h663

Cited by 37 publications

(60 citation statements)

References 24 publications

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“…Although the histamine content of these mast cells is reduced (14), other inflammatory mediators like cytokines and prostaglandins could be present, although this has not been studied in NDST-2 Ϫ/Ϫ mice. Such mediators were shown previously to lower P if in rat skin (4,30). Given our present findings in Kit W /Kit W-v mice, it seems plausible that there are enough mediators released on CTMC activation in NDST-2 Ϫ/Ϫ mice to sustain a full response in P if in response to neuropeptides.…”

Section: Discussionsupporting

confidence: 73%

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Karlsen¹,

Bletsa²,

Gjerde³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Neurogenic inflammation is known to induce lowering of interstitial fluid pressure (P if) in mouse skin. This study examined the possible role of mast cell activation secondary to neuropeptide release in lowering of P if by using , and neurokinin A, from the capsaicin-sensitive nerve endings. Capsaicin releases neuropeptides through binding to the vanilloid receptor subtype 1 (VR1) (9), which in turn induces an inflammatory response in various tissues of both rodents and humans (2, 21). This response is characterized by increased arteriolar vasodilatation and protein extravasation due to increased permeability of the postcapillary venules resulting in fluid accumulation in the tissue. Previous reports from our research group have shown that the response in the initial phase of neurogenic inflammation involves lowering of interstitial fluid pressure (P if ) as observed both in rat trachea (16) and mouse skin (25). P if is important in tissue fluid homeostasis both in the regulation of fluid filtration across the capillary and as the filling pressure for the lymphatics (1). In contrast to the classic view of P if serving as an edema-preventing mechanism, P if has been shown to play an active part in the initial phase of edema in a number of inflammatory models with a lowering of P if to more negative values (16,31,34,35). According to Starling's hypothesis, this lowering of P if will increase net filtration pressure across the capillary and hence contribute to fluid accumulation in the interstitial space.Mast cells have been thought of as possible participants in the neurogenic inflammatory response because they contain numerous inflammatory mediators and are localized in close proximity to the capsaicin-sensitive nerve endings (37,39). Alterations in the number of SP-reactive fibers and mast cell-nerve contacts have been reported as parts of the pathology of several diseases (3,19,45). SP can activate mast cells both through binding of the neurokinin-1 receptor present on these cells (8) and through receptor-independent mechanisms (10). The significance of mast cell activation as a part of neurogenic inflammation has been questioned in a number of studies, and the results are yet not conclusive. Supporting the involvement of mast cells are the findings that stimulation of the rat saphenous nerve induces mast cell degranulation (27) and that SP in high concentrations (40) as well as topical application of capsaicin (7) induce cutaneous mast cell degranulation in human forearm. In contrast, Petersen et al. (32) detected no release of SP and histamine after capsaicin injection in the same area.In light of the knowledge that capsaicin-sensitive nerve endings are localized close to connective tissue mast cells (CTMCs) in mouse skin (6) and that mast cell activation by compound 48/80 (C48/80) induces a lowering of P if in skin of both rats and mice (20,25,36), the question arises as to whether mast cells are involved in the events leading to lowering of P if in neurogenic inflammation. In a recent study (25) we exami...

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Section: Discussionsupporting

confidence: 73%

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Karlsen¹,

Bletsa²,

Gjerde³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…The same effects have been observed after administration of PGE 1 (3,17) in addition to its effects as a vasodilator (23). However, the mechanism responsible for the observed changes in protein extravasation from plasma to dialysate seems to differ between docetaxel and PGE 1 .…”

Section: Discussionsupporting

confidence: 54%

“…Many pharmacological agents and pathological conditions have been shown to alter the permeability and/or protein flux across the capillaries in subcutaneous tissue (39) Docetaxel is a microtubule fixating agent and has previously been demonstrated to lower interstitial fluid pressure (P if ) and increase the extravasation of 125 I-labeled human serum albumin ( 125 I-HSA) (5,17). The same effects have been observed after administration of PGE 1 (3,17), in addition to its effects as a vasodilator (23). Reduction of P if and increased vasodilatation are both properties that contribute to increase transcapillary fluid flux (J v ) (2,18).…”

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confidence: 96%

Changes in plasma protein extravasation in rat skin during inflammatory challenges evaluated by microdialysis

Borge

Iversen²,

Reed³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Borge, B. Å ., V. V. Iversen, and R. K. Reed. Changes in plasma protein extravasation in rat skin during inflammatory challenges evaluated by microdialysis. Am J Physiol Heart Circ Physiol 290: H2108-H2115, 2006. First published December 22, 2005 doi:10.1152/ajpheart.00395.2005.-Docetaxel and prostaglandin E 1 (PGE1) increase transcapillary albumin extravasation and reduce interstitial fluid pressure in the skin. In this study the microdialysate concentration (Cm) of 125 I-labeled human serum albumin ( 125 I-HSA) and different-sized endogenous plasma proteins (EPP) was compared to evaluate changes in transcapillary extravasation of plasma proteins.125 I-HSA was also used to estimate changes in the specific activity of albumin. Extravasation of 125 I-HSA and EPP from plasma to interstitium in the rat skin was compared during continuous administration of docetaxel and PGE 1 by using microdialysis in anesthetized rats. Also, 20 ml of Ringer solution (RS) were injected intravenously during 10 min in a separate group. Two hollow plasmapheresis fibers (3 cm, cut off 3,000 kDa), one acting as control, were placed subcutaneously on the back skin and perfused with RS (5 l/min, 140 min, collected every 10 min). The size of the different EPP was estimated to be 73, 65, 56, 47, and 39 Å , separated by a size-exclusion high-performance liquid chromatography column and quantified by UV detection (280 nm). Docetaxel (0.5 mg/ml, n ϭ 5) increased Cm of 125 I-HSA and EPP of sizes 73, 65, 56, and 39 Å significantly (P Ͻ 0.05) compared with control. PGE 1 (20 g/ml, n ϭ 6) increased Cm of 125 I-HSA significantly (P Ͻ 0.05) but none of the different-sized EPP was increased compared with control. Intravenous RS (20 ml, n ϭ 6) increased C m of 125 I-HSA and increased all the different-sized EPP significantly (P Ͻ 0.05) compared with control. Although the microdialysis method is able to monitor qualitative changes in capillary permeability, a quantitative determination of the capillary reflection coefficient or permeabilitysurface area product was not possible, because steady state between plasma and dialysate was not achieved during the measurement period. The different pattern of extravasation of EPP and 125 I-HSA after docetaxel, PGE 1, and RS indicates increased interstitial transport rate and/or increased capillary permeability after docetaxel and RS, whereas PGE 1 seems to increase transcapillary fluid flux without altering the permeability.high-performance liquid chromatography; prostaglandin E 1; docetaxel; transcapillary transport QUANTIFICATION of macromolecular passage from plasma to interstitial fluid may give important information of the integrity of the capillary barrier. Many pharmacological agents and pathological conditions have been shown to alter the permeability and/or protein flux across the capillaries in subcutaneous tissue (39) Docetaxel is a microtubule fixating agent and has previously been demonstrated to lower interstitial fluid pressure (P if ) and increase the extravasation of 125

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“…Cultured human dermal fibroblasts will compact a gel to 10% of the initial gel area in 12-24 h. The process of collagen gel compaction depends on "1-integrins (Gullberg et al 1990) and on intercellular adhesions and Gap-junctions synchronizing the work (Ehrlich et al 2000). Several studies from our laboratory have shown that the characteristics of the collagen gel compaction mimic the cellular control of interstitial fluid pressure in vivo (Wiig et al 2003;Ahlen et al 1998;Berg et al 1998;Heuchel et al 1999). We found that the human explant ED/ES fibroblasts compacted collagen gels to the same degree and with the same kinetics as dermal fibroblasts.…”

Section: Discussionmentioning

confidence: 98%

An Interstitial Network of Podoplanin-Expressing Cells in the Human Endolymphatic Duct

Ekwall

Mayerl

Rubin

et al. 2006

JARO

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The human endolymphatic duct (ED) with encompassing interstitial connective tissue (CT) is believed to be important for endolymph resorption and fluid pressure regulation of the inner ear. The periductal CT cells are interconnected via numerous cellular extensions, but do not form vessel structures. Here we report that the periductal CT is populated by two distinct cell phenotypes; one expressing podoplanin, a protein otherwise found on lymph endothelia and on epithelia involved in fluid fluxes, and a second expressing a fibroblast marker. A majority of the interstitial cells expressed podoplanin but not the lymphatic endothelial cell markers hyaluronan receptor (LYVE-1) or vascular endothelial growth factor receptor-3 (VEGFR-3). The fibroblast marker positive cells were found close to the ED epithelium. In the mid-and distal parts of the ED, these cells were enriched under folded epithelia. Furthermore, subepithelial CT cells were found to express activated platelet derived growth factor (PDGF)-" receptors. Cultured CT cells from human inner ear periductal and perisaccular explant tissues were identified as fibroblasts. These cells compacted a three-dimensional collagen lattice by a process that could be promoted by PDGF-BB, a factor involved in interstitial fluid pressure regulation. Our results are compatible with the notion that the periductal CT cells are involved in the regulation of inner ear fluid pressure. By active compaction of the periductal CT and by the formation of villous structures, the CT cells could modulate fluid fluxes over the ED epithelium as well as the longitudinal flow of endolymph in the ED.

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Effect of PGE₁, PGI₂, and PGF_2αanalogs on collagen gel compaction in vitro and interstitial pressure in vivo

Cited by 37 publications

References 24 publications

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Lowering of interstitial fluid pressure after neurogenic inflammation in mouse skin is partly dependent on mast cells

Changes in plasma protein extravasation in rat skin during inflammatory challenges evaluated by microdialysis

An Interstitial Network of Podoplanin-Expressing Cells in the Human Endolymphatic Duct

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