ArticlePloS one2017
Senescent Atrophic Epidermis Retains Lrig1+ Stem Cells and Loses Wnt Signaling, a Phenotype Shared with CD44KO Mice.
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 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Homeodynamic Rejuvenation: an adaptive framework for resetting skin aging.Frontiers in aging · 2026Article
- Identification of Two Distinct Stem Cell Clusters, Lrig1-Derived and Wnt/CD44-Dependent, in Corneal Epithelium.International journal of molecular sciences · 2025Article
- Review
- Senotherapeutic Effect of Retinaldehyde and Hyaluronate Fragments in Dermatoporosis.Dermatopathology (Basel, Switzerland) · 2023Article
- Long non‑coding RNA HOTAIR promotes burn wound healing by regulating epidermal stem cells.Molecular medicine reports · 2020Article
- Lrig1 Expression in Human Sebaceous Gland Tumors.Dermatopathology (Basel, Switzerland)Article
- Induction of Hyalurosome by Topical Hyaluronate Fragments Results in Superficial Filling of the Skin Complementary to Hyaluronate Filler Injections.Dermatopathology (Basel, Switzerland)Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lrig1 is known to repress the epidermal growth through its inhibitory activity on EGFR, while CD44 promotes it. We analyzed the expression of these molecules in senescent atrophic human epidermis and in the epidermis of CD44KO mice. In normal human epidermis, Lrig1+ cells form clusters located in the basal layer in which CD44 expression is downregulated and Lef1 expression reflects an active Wnt signaling. In senescent atrophic human epidermis, we found retention of Lrig1high+ cells all along the basal layer, forming no clusters, with decrease of CD44 and lef1 expression. In vitro silencing of CD44 indicated that CD44 may be required for Wnt signaling. However, if looking at the ear epidermis of CD44KO mice, we only found a limited interfollicular epidermal atrophy and unchanged Lrig1high+ cells in the hair follicle. Cell lineage tracing further revealed that interfollicular epidermis did lost its self-renewing capacity but that its homeostasis relied on Lrig1-derived keratinocytes migrating from the hair follicle. Therefore, we conclude that CD44 downregulation is part of the phenotype of senescent atrophic human epidermis, and contributes to reduce Wnt signaling and to alter Lrig1high+ stem cell distribution.
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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.