Expression of Components of the Renin-angiotensin System by Embryonic Stem Cell-like Population within Keloid Lesions.
Authors of this article are:
Humphries H, Brasch HD, van Schaijik B, Tan ST, Itinteang T.
A summary of the article is shown below:
BACKGROUND: This study investigated the expression of pro-renin receptor (PRR), angiotensin converting enzyme (ACE), angiotensin II receptor 1 (ATIIR1) and angiotensin II receptor (ATIIR2) by the embryonic stem cell-like population on the endothelium of the microvessels and the perivascular cells within keloid-associated lymphoid tissues (KALTs).METHODS: 3,3-Diaminobenzidine (DAB) immunohistochemical (IHC) staining for PRR, ACE, ATIIR1 and ATIIR2 was performed on 11 formalin-fixed paraffin-embedded sections of keloid tissue samples. Immunofluorescence (IF) IHC staining was performed on three keloid tissue samples by co-staining with OCT4, CD34, ERG and tryptase. RT-qPCR was performed on five keloid tissue samples and four keloid-derived primary cell lines. Western blotting (WB) was performed on the four keloid-derived primary cell lines, to investigate mRNA and protein expression of these proteins, respectively.RESULTS: DAB and IF IHC staining showed expression of PRR, ACE, ATIIR1 and ATIIR2 in all 11 keloid tissue samples. PRR and ATIIR1 were expressed on the endothelium and the outer pericyte layer of the microvessels and the perivascular cells, ATIIR2 was localized to the endothelium of the microvessels and the tryptase perivascular cells, and ACE was localized to the endothelium of the microvessel, within the KALTs. RT-qPCR showed transcriptional activation of PRR, ACE and ATIIR1 in the keloid tissue samples and keloid-derived primary cell lines, while ATIIR2 was detected in keloid tissue samples only. WB confirmed the presence of PRR, ACE and ATIIR1 in the keloid-derived primary cell lines.CONCLUSIONS: PRR, ACE, ATIIR1 and ATIIR2 were expressed by the ESC-like population within the KALTs suggesting this primitive population may be a potential therapeutic target by modulation of the RAS.
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