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Updated: May 27, 2026
10:51
Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin
Published on: July 14, 2017
Stanniocalcin-1 regulates re-epithelialization in human keratinocytes
Bonnie H Y Yeung1, Chris K C Wong
1Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Plos One
|November 10, 2011
Summary
Stanniocalcin-1 (STC1) promotes wound healing by enhancing keratinocyte migration and re-epithelialization. This study reveals STC1
Area of Science:
- Cell Biology
- Biochemistry
- Dermatology
Background:
- Stanniocalcin-1 (STC1) is a glycoprotein hormone implicated in inflammation, oxidative stress, and cell migration.
- Re-epithelialization is crucial for wound healing, involving keratinocyte lamellipodia (e-lam) formation and migration.
Purpose of the Study:
- To investigate the role of STC1 in keratinocyte re-epithelialization during wound healing.
- To elucidate the signaling pathways regulating STC1 expression and function in keratinocytes.
Main Methods:
- Human keratinocyte (HaCaT) cell line treated with staurosporine (STS) to induce migration.
- Analysis of e-lam formation, cell migration, intracellular calcium levels ([Ca²⁺]i), and signaling proteins (FAK, Akt).
- STC1 gene expression modulation via knockdown or overexpression; FAK and Akt inhibition/activation.
Main Results:
- STS treatment induced keratinocyte migration and e-lam formation, associated with increased STC1 expression.
- STC1 expression was regulated by intracellular calcium levels and Akt signaling, but not FAK.
- STC1 knockdown inhibited migration, while overexpression promoted it, confirmed by wound healing assays.
Conclusions:
- STC1 plays a significant role in promoting keratinocyte migration and re-epithelialization.
- The findings provide the first evidence of STC1's function in wound healing.
- STC1 represents a potential therapeutic target for enhancing wound repair.
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