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Cold Atmospheric Plasma Jet Promotes Wound Healing through CK2- coordinated PI3K/AKT and MAPK Signaling Pathways

ABSTRACT: Cold atmospheric plasma jet (CAPJ) is composed of a variety of reactive species and has been demonstrated to have an effect on promoting wound healing. However, not all served-subjects respond equally to CAPJ, and indeed the underlying cellular mechanisms are rarely understood. Proteomics results clearly revealed that wound repair in keratinocytes was accelerated by plasma-activated medium (PAM) treatment through phosphorylating CK2-coordinated PI3K/AKT and MAPK signaling pathways, activating their downstream physiological responses for cell migration, proliferation and extracellular vesicles mediated cell-cell communication. Moreover, CAPJ-treated wound tissues showed a denser and well-organized extracellular matrix (ECM) architecture, implying the speed-up of epithelialization in wound healing. This study unveiled the primary cellular responses affected by CAPJ during wound repair, providing valuable insights for the treatment selection and the development of therapeutic strategies to achieve better therapy outcomes.

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Miao-Hsia Lin

PROVIDER: PXD051544 | JPOST Repository | Thu Apr 17 00:00:00 BST 2025

REPOSITORIES: jPOST

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			Action	DRS
	20200710_HaCaT_He_Ar_Prot_01.raw	Raw
	20200710_HaCaT_He_Ar_Prot_02.raw	Raw
	20200710_HaCaT_He_Ar_Prot_03.raw	Raw
	20200710_HaCaT_Prot_Ctrl_01.raw	Raw
	20200710_HaCaT_Prot_Ctrl_02.raw	Raw

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Project description:The methodology for the repair of critical-sized or non-union bone lesions has unpredictable efficacy due in part to our incomplete knowledge of bone repair and the biocompatibility of bone substitutes. Although human mesenchymal stem cells (hMSCs) differentiate into osteoblasts, which promote bone growth, their ability to repair bone has been unpredictable. We hypothesized that given the multi-stage process of osteogenesis, hMSC-mediated repair might be maximal at a specific time-point of healing. Utilizing a mouse model of calvarial healing, we demonstrate that the osteo-repair capacity of hMSCs can be substantially augmented by treatment with an inhibitor of peroxisome-proliferator-activated-receptor-γ, but efficacy is confined to the rapid osteogenic phase. Upon entry into the bone-remodeling phase, hMSC retention signals are lost, resulting in truncation of healing. To solve this limitation, we prepared a scaffold consisting of hMSC-derived extracellular matrix (ECM) containing the necessary biomolecules for extended site-specific hMSC retention. When inhibitor-treated hMSCs were co-administered with ECM, they remained at the injury well into the remodeling phase of healing, which resulted in reproducible and complete repair of critical-sized defects in 3 weeks. These data suggest that hMSC-derived ECM and inhibitor-treated hMSCs could be employed at optimal times to substantially and reproducibly improve bone repair. To gain insight into the superior healing potential of GW-hMSCs and also what might be accounting for their extended engraftment, microarray analyses on the RNA extracted from the calvarial tissue recovered after days 5 and 14 were performed. Equal amounts of total RNA from 4 animals per group and time point were pooled and animals receiving control (DMSO) or peroxisome proliferator-activated receptor-gamma inhibitor GW9662-treated hMSCs were compared with the assumption that murine cross-hybridization would be constant throughout the samples and thus be subtracted from the analysis.

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Cold Atmospheric Plasma Jet Promotes Wound Healing through CK2- coordinated PI3K/AKT and MAPK Signaling Pathways

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