Microcystins (MCYs) are cyanobacterial heptapeptides known for their high toxicity in
eukaryotic cells and for their potential human health hazards. They are potent and specific inhibitors
of type 1 and 2A, serine-threonine protein phosphatases (PP1 and PP2A) and as such, interfere with
key cellular and metabolic events. Moreover, they induce oxidative stress involving reactive oxygen
species (ROS) generation. Their cytoskeletal effects involve both mitotic and differentiated eukaryotic
cells. The main objective of the present review is to summarize the most important cytoskeletal effects
of MCY on human, animal and plant cells known to date and to give an insight into the cellular and molecular background
of these alterations. Disruptions of microtubule (MTs), microfilament (MF) and intermediate filament (IF) organization
have all been described, having consequences on cell shape, tissue integrity and functionality and mitotic division. Most
of these subcellular changes are closely related to PP1 and PP2A inhibition and involve misfunctioning of cytoskeleton
associated proteins. However, several cytoskeletal alterations are likely to be related to the induction of oxidative stress.
MCY induced changes in MT, MF and IF assembly may have severe human health consequences. The main target of
cyanotoxin in human/ animal cells is liver and cytoskeletal disruption alters structure and functioning of hepatocytes.
However, many other cell types undergo alterations similar to those observed in hepatocytes. Both PP1/PP2A inhibition
and ROS generation are involved and the activation of mitogen activated protein kinases (MAPKs) seems to play a crucial
role in the molecular events leading to cytoskeletal disruption.
Keywords: Intermediate filaments, microcystin, microfilaments, microtubules, oxidative stress, protein phosphatase.
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