Activation of Cutaneous Protein Kinase Cα Induces Keratinocyte Apoptosis and Intraepidermal Inflammation by Independent Signaling Pathways

September 2003 in “ The Journal of Immunology ”

Christophe Cataisson, Elizabeth Joseloff, Rodolfo Murillas, Alice Wang, Coralyn Atwell, Sara Torgerson, Michael Gerdes, Jeffrey Subleski, Ji‐Liang Gao, Philip M. Murphy, Robert H. Wiltrout, Charles Vinson, Stuart H. Yuspa

protein kinase Cα PKCα keratinocyte apoptosis intraepidermal inflammation transgenic mice TPA UVB AP-1 neutrophilic inflammation epidermis hair follicles chemokine pustular psoriasis tumor promoter ultraviolet B activator protein 1

Studysummary This study found that PKCα activation in transgenic mice induces keratinocyte apoptosis and mediates neutrophilic skin inflammation via different pathways, suggesting potential mechanisms for cutaneous inflammatory diseases. Our plain-language summary of this paper — not a Tressless recommendation.

The study investigated the role of protein kinase Cα (PKCα) in skin inflammation and keratinocyte apoptosis using transgenic mice overexpressing PKCα. It was found that activation of PKCα led to severe intraepidermal neutrophilic inflammation and disruption of the epidermis and hair follicles when treated with TPA. Both TPA and UVB induced apoptosis in the skin, but only TPA caused inflammation. The apoptosis was mediated through an AP-1-dependent pathway, while the inflammation and chemokine induction occurred independently of AP-1. This research provided insights into the mechanisms of skin inflammation and could help in understanding conditions like pustular psoriasis.

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