ArticleHaematologica2012
Defective erythroid maturation in gelsolin mutant mice.
Article in Haematologica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- New insight into role of mast cells in erythrocyte homeostasis and clearance under oxidative stress conditionsBiochemistry and biophysics reports · 2026Article
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- Erythroid enucleation: a gateway into a "bloody" world.Experimental hematology · 2021Review
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- Cellular dynamics of mammalian red blood cell production in the erythroblastic island niche.Biophysical reviews · 2019Review
- Cdk6 contributes to cytoskeletal stability in erythroid cells.Haematologica · 2017Article
- Calcium Signaling Is Required for Erythroid Enucleation.PloS one · 2016Article
- The modern primitives: applying new technological approaches to explore the biology of the earliest red blood cells.ISRN hematology · 2013Review
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDuring late differentiation, erythroid cells undergo profound changes involving actin filament remodeling. One of the proteins controlling actin dynamics is gelsolin, a calcium-activated actin filament severing and capping protein. Gelsolin-null (Gsn(-/-)) mice generated in a C57BL/6 background are viable and fertile.1 DESIGN AND
methodsWe analyzed the functional roles of gelsolin in erythropoiesis by: (i) evaluating gelsolin expression in murine fetal liver cells at different stages of erythroid differentiation (using reverse transcription polymerase chain reaction analysis and immunohistochemistry), and (ii) characterizing embryonic and adult erythropoiesis in Gsn(-/-) BALB/c mice (morphology and erythroid cultures).
resultsIn the context of a BALB/c background, the Gsn(-/-) mutation causes embryonic death. Gsn(-/-) embryos show defective erythroid maturation with persistence of circulating nucleated cells. The few Gsn(-/-) mice reaching adulthood fail to recover from phenylhydrazine-induced acute anemia, revealing an impaired response to stress erythropoiesis. In in vitro differentiation assays, E13.5 fetal liver Gsn(-/-) cells failed to undergo terminal maturation, a defect partially rescued by Cytochalasin D, and mimicked by administration of Jasplakinolide to the wild-type control samples.
conclusionsIn BALB/c mice, gelsolin deficiency alters the equilibrium between erythrocyte actin polymerization and depolymerization, causing impaired terminal maturation. We suggest a non-redundant role for gelsolin in terminal erythroid differentiation, possibly contributing to the Gsn(-/-) mice lethality observed in mid-gestation.
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