Proteomics

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Proliferation, migration and inflammation-related signaling pathways activated in THBS4-stimulated keratinocytes characterize both wound healing and atopic dermatitis

ABSTRACT: Atopic dermatitis, which is a common inflammatory skin disease characterized by persistent epidermal barrier dysfunction, is a systemic health burden reducing overall quality of life of the person. Recently, we showed that the nonstructural extracellular matrix molecule Thrombospondin-4 (THBS4) was upregulated in psoriatic skin lesions by more than 2-fold. In addition, THBS4 contributed to both skin regeneration and wound healing in vitro and in vivo. In the present work we found that THBS4 is also abundantly expressed in atopic dermatitis (AD) patient skin biopsies. By using a proteotransciptomic approach we show that stimulation of primary keratinocytes with THBS4 activates multiple factors, including inflammation, migration, proliferation, keratinocyte differentiation, by which THBS4 could participate in AD progression and contribute to the wound healing process.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Keratinocyte, Skin

SUBMITTER: Mariliis Klaas  

LAB HEAD: Viljar Jaks

PROVIDER: PXD037593 | Pride | 2025-03-29

REPOSITORIES: Pride

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Stimulation with THBS4 activates pathways that regulate proliferation, migration and inflammation in primary human keratinocytes.

Mäemets-Allas Kristina K   Klaas Mariliis M   Cárdenas-León Claudia Griselda CG   Arak Terje T   Kankuri Esko E   Jaks Viljar V  

Biochemical and biophysical research communications 20221220

As in other mammalian tissues, the extracellular matrix (ECM) of skin functions as mechanical support and regulative environment that guides the behavior of the cells. ECM is a gel-like structure that is primarily composed of structural and nonstructural proteins. While the content of structural proteins is stable, the level of nonstructural ECM proteins, such as thrombospondin-4 (THBS4), is dynamically regulated. In a previous work we demonstrated that THBS4 stimulated cutaneous wound healing.  ...[more]

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