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dermal cells

Logical and Experimental Modeling of Cytokine and Eicosanoid Signaling in Psoriatic Keratinocytes

[iScience] Logical model simulations describing the function of cytokine and eicosanoid signaling networks combined with experimental data suggest that T-helper (Th) 17 cytokines stimulate proinflammatory cytokine expression in psoriatic keratinocytes.

ASC Speck Formation after Inflammasome Activation in Primary Human Keratinocytes

[Oxidative Medicine and Cellular Longevity] Scientists showed that UVB provoked apoptosis-associated speck-like protein (ASC) speck formation in human primary keratinocytes prior to cell death, and that specks were, opposed to the perinuclear cytosolic localization in myeloid cells, formed in the nucleus.

The GPI-Anchored Protein CD109 Protects Hematopoietic Progenitor Cells from Undergoing Erythroid Differentiation Induced by TGF-β

[Leukemia] Investigators found that CD109 suppressed TGF-β signaling in hematopoietic stem progenitor cells (HSPCs), and increased the sensitivity of PIGA-mutated HSPCs to TGF-β, leading to the preferential commitment of erythroid progenitor cells to mature red blood cells in immune-mediated bone marrow failure.

Agrin-Matrix Metalloproteinase-12 Axis Confers a Mechanically Competent Microenvironment in Skin Wound Healing

[Nature Communications] Investigators discovered that proteoglycan Agrin was enriched within the early wound-microenvironment and was indispensable for efficient healing.

p32 Promotes Melanoma Progression and Metastasis by Targeting EMT Markers, Akt/PKB Pathway, and Tumor Microenvironment

[Cell Death & Disease] The authors identified the role of p32 in the malignancy of both murine and human melanoma and found that p32 knockdown led to reduced cell proliferation, migration, and invasion in murine and human melanoma cells.

Inhibition of Keratinocyte Ferroptosis Suppresses Psoriatic Inflammation

[Cell Death & Disease] The authors investigated a previously unrecognized role for ferroptosis in psoriasis, where ferroptosis was mediated by lipid peroxidation and iron overload. They found that ferrostatin-1 blocked inflammatory responses in vitro and in vivo, which reduced cytokine production.

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