國家衛生研究院 NHRI:Item 3990099045/13790
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/13790


    Title: Pathogenic role of specific macrophage and fibroblast subpopulations in acne keloidalis identified by single cell RNA sequencing
    Authors: Hong, Y;Hwang, D;Yang, C;Cheng, S;Aala, W;Harn, H;Onoufriadis, A;Lu, KQ;McGrath, JA;Hsu, C
    Contributors: National Institute of Cancer Research
    Abstract: cne keloidalis (AK) is a primary form of scarring alopecia, although its etiology is not well established. Histologically, AK is characterized by a mixed leukocytic infiltrate in the acute stage induced by broken hair shafts in the upper dermis. The pattern of inflammation transitions to a more granulomatous dermatitis with extensive fibrosis in later stages. To explore the pathogenesis of AK, single cell RNA sequencing (scRNA-seq) was applied to scalp biopsy samples. After quality filtering of raw single cell RNA libraries, 4,992 cells from subacute inflammatory AK and 2,932 cells from the adjacent control skin were obtained. Following unbiased clustering, the cells were clustered into 18 distinct populations based on their differentially expressed genes. Cell communication analysis indicated that fibroblasts and myeloid cells were the major secretor and receiver in AK, respectively. We identified four distinct fibroblast subsets, from which POSTN+ cells with enriched extracellular matrix signatures were increased in AK. Among the five distinct myeloid subsets, SPP1+ cells belonging to M2 macrophages were increased in AK. Pseudotime trajectory and immunofluorescence revealed that POSTN+ fibroblasts were potentially differentiated from SPP1+ myeloid cells. In summary, our initial data indicate that communication and transdifferentiation between POSTN+ fibroblasts and SPP1+ macrophages may contribute to the pathogenesis of AK.
    Date: 2021-10
    Relation: Journal of Investigative Dermatology. 2021 Oct;141(10):S211.
    Link to: https://doi.org/10.1016/j.jid.2021.08.369
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-202X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000706854500359
    Appears in Collections:[Others] Conference Papers/Meeting Abstract

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