ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2025
ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Ectodermal loss of ARHGAP29 alters epithelial morphology and disrupts murine palatogenesis.Development (Cambridge, England) · 2026Article
- ARHGAP29 promotes keratinocyte proliferation and migration in vitro and is dispensable for in vivo wound healing.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Keratinocyte-derived VEGF-A is an essential pro-migratory autocrine mediator, acting through the KDR/GEF-H1/RhoA pathway.Frontiers in cell and developmental biology · 2025Article
- IQGAP3 Is an Important Mediator of Skin Inflammatory Diseases.International journal of molecular sciences · 2024Article
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8 authors.
Funding
Abstract
backgroundRhoA GTPases play critical roles in actin cytoskeletal remodeling required for controlling a diverse range of cellular functions including cell proliferation, adhesion, migration and changes in cell shape, all required for cutaneous wound healing. RhoA cycles between an active GTP-bound and an inactive GDP-bound form, a process regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). ARHGAP29 is a GAP expressed in skin keratinocytes and is decreased in the absence of interferon regulator factor 6, a critical regulator of cell proliferation, migration, and wound healing. However, the role for ARHGAP29 in keratinocyte biology is unknown.
resultsWe generated ARHGAP29 knockdown keratinocyte cell lines and show they displayed increased filamentous actin, phospho-myosin regulatory light chain, cell area and population doubling time. Furthermore, we found that ARHGAP29 knockdown keratinocytes displayed significant delays in scratch wound closure in both single and collective cell migration conditions; these delays were rescued by both adding back ARHGAP29 or adding a ROCK inhibitor to ARHGAP29 knockdown cells. In vivo, however, Arhgap29 heterozygotes or keratinocyte-specific knockouts showed on-time wound healing.
conclusionsThese data demonstrate that ARHGAP29 is required for keratinocyte morphology, proliferation and migration in vitro but is dispensable during wound healing in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.