Related Experiment Videos
Alterations in microtubules, intermediate filaments, and microfilaments induced by microcystin-LR in cultured cells
M L Wickstrom1, S A Khan, W M Haschek
1Department of Veterinary Biosciences, University of Illinois, Urbana 61801, USA.
Abstract:
Microcystin-LR (MCLR) is a cyanobacterial hepatotoxin that inhibits intracellular serine/threonine protein phosphatases causing disruption of actin microfilaments (MFs) and intermediate filaments (IFs) in hepatocytes. This study compared the effects of MCLR on the organization of MFs, IFs, and microtubules (MTs) in hepatocytes and nonhepatocyte cell lines and determined the sequence of toxin-induced changes in these cytoskeletal components. Rat renal epithelial cells and fibroblasts were incubated with MCLR at 100 or 200 microM for 6-18 hr. Rat hepatocytes in primary culture were exposed to the toxin at 1 or 10 microM for 2-64 min. Cells were fixed and incubated with primary antibodies against beta-tubulin, actin, and vimentin or cytokeratin IFs, followed by gold-labeled secondary antibodies with silver enhancement of the gold probe. The fraction of fibroblasts and hepatocytes with altered cytoskeletal morphology was evaluated as a function of MCLR dose and exposure time to assess the sequence of changes in cytoskeletal components. Changes in fibroblasts and some hepatocytes were characterized initially by disorganization of IFs, followed rapidly by disorganization of MTs, with the progressive collapse of both cytoskeletal components around cell nuclei. Many hepatocytes exhibited MT changes prior to effects on IF structure. Alterations in MFs occurred later and included initial aggregation of actin under the plasma membrane, followed by condensation into rosette-like structures and eventual complete collapse into a dense perinuclear bundle. The similarity of effects among different cell types suggests a common mechanism of action, but the independent kinetics of IF and MT disruption in hepatocytes suggests that there may be at least 2 sites of phosphorylation that lead to cytoskeletal alterations.
Insights
Microcystin-LR (MCLR) disrupts cellular structure by affecting actin microfilaments, intermediate filaments, and microtubules. This toxin
Area of Science:
- Cell Biology
- Toxicology
- Biochemistry
Background:
- Cyanobacterial blooms produce microcystins, potent hepatotoxins.
- Microcystin-LR (MCLR) inhibits protein phosphatases, impacting cellular structure.
- Cytoskeletal integrity is crucial for cell function and morphology.
Purpose of the Study:
- To compare MCLR effects on cytoskeletal organization in hepatocytes and non-hepatocytes.
- To determine the sequence of cytoskeletal changes induced by MCLR.
- To investigate the mechanism of MCLR-induced cytoskeletal disruption.
Main Methods:
- Incubation of rat renal epithelial cells, fibroblasts, and primary hepatocytes with MCLR.
- Immunofluorescence staining for actin, vimentin, cytokeratin, and beta-tubulin.
- Microscopic evaluation of cytoskeletal organization and quantification of altered cells.
Main Results:
- MCLR induced cytoskeletal disorganization in fibroblasts and hepatocytes.
- Intermediate filaments and microtubules were affected before actin microfilaments.
- Hepatocytes showed distinct kinetics for intermediate filament and microtubule disruption.
Conclusions:
- MCLR disrupts cytoskeletal organization through a common mechanism across cell types.
- Independent kinetics of cytoskeletal changes in hepatocytes suggest multiple phosphorylation sites.
- Further research is needed to elucidate the precise molecular targets of MCLR.