ArticlePloS one2011
Stanniocalcin-1 regulates re-epithelialization in human keratinocytes.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Intertwining of the IGF system and animal welfare.Scientific reports · 2026Article
- In Vitro Bioassay for Damage-Associated Molecular Patterns Arising from Injured Oral Cells.Bioengineering (Basel, Switzerland) · 2024Article
- Therapeutic effects of placenta derived-, umbilical cord derived-, and adipose tissue derived-mesenchymal stem cells in chronicJournal of clinical biochemistry and nutrition · 2021Article
- Parenteral lipid emulsions induce unique ileal fatty acid and metabolomic profiles but do not increase the risk of necrotizing enterocolitis in preterm pigs.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Stanniocalcin-1 Overexpression Prevents Depression-Like Behaviors Through Inhibition of the ROS/NF-κB Signaling Pathway.Frontiers in psychiatry · 2021Article
- Characterization of stanniocalcin-1 expression in macrophage differentiation.Translational oncology · 2021Article
- Endothelial Stanniocalcin 1 Maintains Mitochondrial Bioenergetics and Prevents Oxidant-Induced Lung Injury via Toll-Like Receptor 4.Antioxidants & redox signaling · 2019Article
- Effects of STC1 overexpression on tumorigenicity and metabolism of hepatocellular carcinoma.Oncotarget · 2018Article
- Article
- Renoprotective approaches and strategies in acute kidney injury.Pharmacology & therapeutics · 2016 · on this mapReview
- Kaempferol-3-O-rutinoside from Afgekia mahidoliae promotes keratinocyte migration through FAK and Rac1 activation.Journal of natural medicines · 2015Article
- Article
- Myriad Functions of Stanniocalcin-1 (STC1) Cover Multiple Therapeutic Targets in the Complicated Pathogenesis of Idiopathic Pulmonary Fibrosis (IPF).Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2015Review
- Stanniocalcin-1 controls ion regulation functions of ion-transporting epithelium other than calcium balance.International journal of biological sciences · 2015Article
- Osmoregulation in zebrafish: ion transport mechanisms and functional regulation.EXCLI journal · 2015Review
- Stanniocalcin-1 is induced by hypoxia inducible factor in rat alveolar epithelial cells.Biochemical and biophysical research communications · 2014Article
- The role of transcription-independent damage signals in the initiation of epithelial wound healing.Nature reviews. Molecular cell biology · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stanniocalcin-1 (STC1), a glycoprotein hormone, is believed to be involved in various biological processes such as inflammation, oxidative responses and cell migration. Riding on these emerging evidences, we hypothesized that STC1 may participate in the re-epithelialization during wound healing. Re-epithelialization is a critical step that involves keratinocyte lamellipodia (e-lam) formation, followed by cell migration. In this study, staurosporine (STS) treatment induced human keratinocyte (HaCaT) e-lam formation on fibronectin matrix and migration via the activation of focal adhesion kinase (FAK), the surge of intracellular calcium level [Ca²⁺]i and the inactivation of Akt. In accompanied with these migratory features, a time- and dose-dependent increase in STC1 expression was detected. STC1 gene expression was found not the downstream target of FAK-signaling as illustrated by FAK inhibition using PF573228. The reduction of [Ca²⁺]i by BAPTA/AM blocked the STS-mediated keratinocyte migration and STC1 gene expression. Alternatively the increase of [Ca²⁺]i by ionomycin exerted promotional effect on STS-induced STC1 gene expression. The inhibition of Akt by SH6 and GSK3β by lithium chloride (LiCl) could respectively induce and inhibit the STS-mediated e-lam formation, cell migration and STC1 gene expression. The STS-mediated e-lam formation and cell migration were notably hindered or induced respectively by STC1 knockdown or overexpression. This notion was further supported by the scratched wound assay. Collectively the findings provide the first evidence that STC1 promotes re-epithelialization in wound healing.
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Registered trials
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