Showing papers by "Andras Kapus published in 2003"
TL;DR: New research suggests that, during tubulointerstitial fibrosis, α-smooth muscle actin (SMA)-expressing mesenchymal cells might derive from the tubular epithelium via epithelial-mesenchyal transiti...
Abstract: New research suggests that, during tubulointerstitial fibrosis, α-smooth muscle actin (SMA)-expressing mesenchymal cells might derive from the tubular epithelium via epithelial-mesenchymal transiti...
240 citations
TL;DR: Hyperosmolarity activates Rho, and the Rho/ROK pathway contributes to basal and hyperosmotic MLC phosphorylation, implying that the ROK-dependent component of MLCosphorylation can be uncoupled from NKCC activation.
Abstract: Hyperosmotic stress initiates adaptive responses, including phosphorylation of myosin light chain (MLC) and concomitant activation of Na+-K+-Cl– cotransporter (NKCC). Because the small GTPase Rho i...
92 citations
TL;DR: A novel role for 25% albumin as an anti-inflammatory agent in neutrophil-mediated diseases, such as acute respiratory distress syndrome is suggested.
Abstract: ObjectiveTo evaluate novel indications for the use of human albumin solutions in the prevention and treatment of acute lung injury following shock/resuscitation and to test the hypothesis that 25% human albumin is an effective resuscitation fluid as well as an immunomodulatory agent protective again
73 citations
TL;DR: These studies show that oxidant stress is able to augment macrophage responsiveness to LPS as evidenced by earlier and increased NF-κB translocation, and provide a novel potential mechanism whereby oxidants might prime alveolar macrophages for altered responsiveness to subsequent inflammatory stimuli and suggest different cellular targets for immunomodulation following ischemia/reperfusion.
60 citations
TL;DR: HTS resuscitation exerts an immunomodulatory effect on alveolar macrophages by shifting the balance of pro- and counter-inflammatory cytokine production in favor of an anti-inflammatory response.
60 citations
TL;DR: The ability of gelsolin to remodel actin filaments is important for collagen-induced calcium entry; calcium in turn is required for rac activation, which subsequently enhances collagen binding to unoccupied alpha 2 beta 1 integrins.
Abstract: The role of gelsolin, a calcium-dependent actin-severing protein, in mediating collagen phagocytosis, is not defined. We examined α2β1 integrin-mediated phagocytosis in fibroblasts from wild-type (WT) and gelsolin knockout (Gsn-) mice. After initial contact with collagen beads, collagen binding and internalization were 60% lower in Gsn- than WT cells. This deficiency was restored by transfection with gelsolin or with β1 integrin-activating antibodies. WT cells showed robust rac activation and increased [Ca2+]i during early contact with collagen beads, but Gsn- cells showed very limited responses. Transfected gelsolin in Gsn- cells restored rac activation after collagen binding. Transfection of Gsn- cells with active rac increased collagen binding to WT levels. Chelation of intracellular calcium inhibited collagen binding and rac activation, whereas calcium ionophore induced rac activation in WT and Gsn- cells. We conclude that the ability of gelsolin to remodel actin filaments is important for collagen-induced calcium entry; calcium in turn is required for rac activation, which subsequently enhances collagen binding to unoccupied α2β1 integrins.
58 citations
01 Jan 2003
TL;DR: This article showed that focal adhesions were also required for Ca 2+ entry through store-operated channels and for IL-1-induced ERK activation in human gingival fibroblasts.
Abstract: The cellular mechanisms that modulate interleukin-1 (IL-1) signaling are not defined. In fibroblasts, IL-1 signaling is affected by the nature of cell-matrix adhesions including focal adhesions, adhesive domains that sequester IL-1 receptors. We conducted studies to elucidate which steps of cellular Ca 2+ handling are affected by focal adhesions and by which mechanisms focal adhesions modulate IL-1-induced Ca 2+ signals and ERK activation in human gingival fibroblasts. Cells were plated on poly-L-lysine or fibronectin and treated with tenascin, Hep-I, or SPARC peptides to inhibit focal adhesion formation. These treatments blocked IL-1 and thapsigargin-induced Ca 2+ release from the endoplasmic reticulum, indicating that the ER-release pathway is focal adhesion dependent. Focal adhesions were also required for Ca 2+ entry through store-operated channels and for IL-1-induced ERK activation. Thus interactions with the extracellular matrix and focal adhesion formation regulate IL-1-induced generation of intracellular Ca 2+ signals that in turn are required for ERK activation.
27 citations
TL;DR: Oxidant stress generated during global ischemia/reperfusion activates p38 MAPK in an Src-dependent manner and provides an alternative avenue to target therapy during the oxidant-induced priming of the macrophage induced by trauma resuscitation.
25 citations
TL;DR: Integrin ligation by actin filaments regulates the mobility of collagen receptors which in turn mediates the enhanced binding of collagen beads on spreading surfaces, which enhances the binding of ventral surfaces.
23 citations