ArticlePloS one2017
p38α regulates actin cytoskeleton and cytokinesis in hepatocytes during development and aging.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Exposure ofFrontiers in veterinary science · 2025Article
- The heat shock protein Hsp27 controls mitochondrial function by modulating ceramide generation.Cell reports · 2023Article
- Cellular polyploidy in organ homeostasis and regeneration.Protein & cell · 2023Article
- Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process.Biomolecules · 2021Review
- Article
- p38α deficiency restrains liver regeneration after partial hepatectomy triggering oxidative stress and liver injury.Scientific reports · 2019Article
- The p38α Stress Kinase Suppresses Aneuploidy Tolerance by Inhibiting Hif-1α.Cell reports · 2018Article
- Defective recruitment of motor proteins to autophagic compartments contributes to autophagic failure in aging.Aging cell · 2018Article
- Age-dependent regulation of antioxidant genes by p38α MAPK in the liver.Redox biology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocyte poliploidization is an age-dependent process, being cytokinesis failure the main mechanism of polyploid hepatocyte formation. Our aim was to study the role of p38α MAPK in the regulation of actin cytoskeleton and cytokinesis in hepatocytes during development and aging.
methodsWild type and p38α liver-specific knock out mice at different ages (after weaning, adults and old) were used.
resultsWe show that p38α MAPK deficiency induces actin disassembly upon aging and also cytokinesis failure leading to enhanced binucleation. Although the steady state levels of cyclin D1 in wild type and p38α knock out old livers remained unaffected, cyclin B1- a marker for G2/M transition- was significantly overexpressed in p38α knock out mice. Our findings suggest that hepatocytes do enter into S phase but they do not complete cell division upon p38α deficiency leading to cytokinesis failure and binucleation. Moreover, old liver-specific p38α MAPK knock out mice exhibited reduced F-actin polymerization and a dramatic loss of actin cytoskeleton. This was associated with abnormal hyperactivation of RhoA and Cdc42 GTPases. Long-term p38α deficiency drives to inactivation of HSP27, which seems to account for the impairment in actin cytoskeleton as Hsp27-silencing decreased the number and length of actin filaments in isolated hepatocytes.
conclusionsp38α MAPK is essential for actin dynamics with age in hepatocytes.
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