Cytochalasin D induces edema formation and lowering of interstitial fluid pressure in rat dermis
- 1 July 2001
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 281 (1), H7-H13
- https://doi.org/10.1152/ajpheart.2001.281.1.h7
Abstract
The increased capillary fluid filtration required to create a rapid edema formation in acute inflammation can be generated by lowering the interstitial fluid pressure (PIF). The lowering of PIFappears to involve dynamic β1-integrin-mediated interactions between dermal cells and extracellular matrix fibers. The present study specifically investigates the role of the cell cytoskeleton, i.e., the contractile apparatus of cells, in controlling PIFin rat skin as the integrins are linked to both the cytoskeleton and the extracellular matrix. PIFwas measured using a micropuncture technique in the dorsal skin of the hind paw at a depth of 0.2–0.5 mm and following the induction of circulatory arrest with the intravenous injection of KCl in pentobarbital anesthesia. This procedure prevented the transcapillary flux of fluid and protein leading to edema formation in acute inflammation, which in turn can increase the PIFand therefore potentially mask a decrease of PIF. Control PIF( n = 42) averaged −0.8 ± 0.5 (means ± SD) mmHg. In the first group of experiments, subdermal injection of 2 μl cytochalasin D, a microfilament-disrupting drug, lowered PIFto an average of −2.8 ± 0.7 mmHg within 40 min postinjection ( P< 0.05 compared with control). Subdermal injection of vehicle (10% DMSO in PBS or PBS alone) did not change the PIF( P > 0.05). Lowering of the PIFwas not observed after the injection of colchicine or nocodazole, which specifically disrupts microtubuli in cultured cells. In the second group of experiments, 2 μl of cytochalasin D injected subdermally into rats with intact circulation increased the total tissue water (TTW) and albumin extravasation rate ( EALB) by 0.7 ± 0.2 and 0.4 ± 0.3 ml/g dry wt, respectively ( P < 0.05 compared with vehicle). Nocodazole and colchicine did not significantly alter the TTW or EALBcompared with the vehicle ( P > 0.05). Taken together, these findings strongly suggest that the connective tissue cells can participate in control of PIFvia the actin filament system. In addition, the observation that subdermal injection of cytochalasin D lowered PIFindicates that a dynamic assembly and disassembly of actin filaments also occurs in the cells of dermal tissues in vivo.Keywords
This publication has 45 references indexed in Scilit:
- Cell Interactions with Collagen MatricesIn VivoandIn VitroDepend on Phosphatidylinositol 3-Kinase and Free Cytoplasmic CalciumCell Adhesion and Communication, 1998
- Integrins: Versatility, modulation, and signaling in cell adhesionCell, 1992
- Actin—membrane interaction in focal adhesionsCell Differentiation and Development, 1990
- Actions of cytochalasins on the organization of actin filaments and microtubules in a neuronal growth cone.The Journal of cell biology, 1988
- Effects of cytochalasin and phalloidin on actin.The Journal of cell biology, 1987
- Turnover rate of interstitial albumin in rat skin and skeletal muscle. Effects of limb movements and motor activityActa Physiologica Scandinavica, 1985
- Reorganization of actin filament bundles in living fibroblasts.The Journal of cell biology, 1984
- Epidermolysis Bullosa Dystrophica Recessive Fibroblasts Produce Increased Concentrations of cAMP Within a Collagen MatrixJournal of Investigative Dermatology, 1984
- Cytochalasin inhibits the rate of elongation of actin filament fragmentsThe Journal of cell biology, 1979
- Microfilaments in Cellular and Developmental ProcessesScience, 1971