A raised scar with the CD34<sup>-</sup> /α-SMA<sup>+</sup> /p16<sup>+</sup> phenotype with strong immunoreactivity for p16 and significant amounts of keloidal collagen, together with a thickened and strongly abnormal involucrin-stained epidermis, would sway the diagnosis towards keloid scars.
A raised scar with the CD34<sup>-</sup> /α-SMA<sup>+</sup> /p16<sup>+</sup> phenotype with strong immunoreactivity for p16 and significant amounts of keloidal collagen, together with a thickened and strongly abnormal involucrin-stained epidermis, would sway the diagnosis towards keloid scars.
Our study demonstrated that a local increase in IL-17 in keloid tissues stimulates the production of SDF-1 in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop.
The reconstructed keloid showed increased contraction, dermal thickness (trend) and α-SMA+ staining, but co-culture with monocytes did not further enhance the keloid phenotype.
Prorenin receptor and angiotensin II receptor 1 were expressed on the endothelium and the pericyte layer of the microvessels and perivascular cells, angiotensin II receptor 2 was localized to the endothelium of the microvessels and the tryptase-positive perivascular cells, and angiotensin-converting enzyme was localized to the endothelium of the microvessel, within the keloid-associated lymphoid tissues.
Identified by the IF staining of Vimentin, a classical biomarker of fibroblast, both primary culture of keloid and normal skin fibroblasts have been established.
These findings together demonstrate a tumor-suppressive role of miR-188-5p in KD proliferation and invasion via PI3K/Akt/MMP-2/9 signaling, indicating that miR-188-5p may be a potential prognostic marker and therapeutic target for KDs.
Following miR-96 antagomir treatment, a reduction in the mRNA and protein expression levels of collagen type I α 1 chain and collagen type 3 α 1 chain within keloid OC tissues was observed.
These findings indicate that TSG‑6 is a novel regulator of keloid fibrogenesis, and thus could be used/targeted TSG‑6 as a promising treatment for keloid.
We hypothesized that cathepsin B (cathB), cathepsin D (cathD) and cathepsin G (cathG) are present within the ESC-like population in KLs and contribute to bypass loops of the RAS.
Our study demonstrated that a local increase in IL-17 in keloid tissues stimulates the production of SDF-1 in KFs causing further recruitment of IL-17-producing T helper 17 (Th17) cells, which subsequently creates a positive feedback loop.
Western blotting confirmed the presence of prorenin receptor, angiotensin-converting enzyme, and angiotensin II receptor 1 in the keloid-derived primary cell lines.
The reconstructed keloid showed increased contraction, dermal thickness (trend) and α-SMA+ staining, but co-culture with monocytes did not further enhance the keloid phenotype.
These findings together demonstrate a tumor-suppressive role of miR-188-5p in KD proliferation and invasion via PI3K/Akt/MMP-2/9 signaling, indicating that miR-188-5p may be a potential prognostic marker and therapeutic target for KDs.
These findings together demonstrate a tumor-suppressive role of miR-188-5p in KD proliferation and invasion via PI3K/Akt/MMP-2/9 signaling, indicating that miR-188-5p may be a potential prognostic marker and therapeutic target for KDs.
Prorenin receptor and angiotensin II receptor 1 were expressed on the endothelium and the pericyte layer of the microvessels and perivascular cells, angiotensin II receptor 2 was localized to the endothelium of the microvessels and the tryptase-positive perivascular cells, and angiotensin-converting enzyme was localized to the endothelium of the microvessel, within the keloid-associated lymphoid tissues.
These findings together demonstrate a tumor-suppressive role of miR-188-5p in KD proliferation and invasion via PI3K/Akt/MMP-2/9 signaling, indicating that miR-188-5p may be a potential prognostic marker and therapeutic target for KDs.
We hypothesized that cathepsin B (cathB), cathepsin D (cathD) and cathepsin G (cathG) are present within the ESC-like population in KLs and contribute to bypass loops of the RAS.
In conclusion, Cthrc1 may play a role in the pathogenesis of keloid by inhibiting collagen synthesis and fibroblasts migration via suppressing TGF-β/Smad pathway and YAP nucleus translocation.
Furthermore, up-regulation of miR‑637 inhibited cell proliferation and metastasis by targeting mothers against decapentaplegic homolog (Smad)3, one of the important proteins that affects the formation of keloids.
Notably, the expression of extracellular matrix associated genes showed distinguishing profiles between all scar types and normal skin (hyaluronan synthase-1, matrix-metalloprotease-3), between keloid and normal skin (collagen type IV), between normal scar and keloid (laminin α1), and between keloid and hypertrophic scar (matrix-metalloprotease-1, integrin α5).