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    Please use this identifier to cite or link to this item: https://nccur.lib.nccu.edu.tw/handle/140.119/157339


    Title: The alterations of molecular repertoire of the RANKL-induced osteoclastogenesis in the M1 macrophage-derived inflammatory milieu
    Authors: 陳紹寬
    Chen, Shau-Kwaun;Wu, Chun-Shan;Chen, Ching-Yun;Yang, Chin-Hua;Hsu, Yu-Pao;Yu, Ching-Hsiao;Chen, Yu-Hsu
    Contributors: 神科所
    Date: 2025-05
    Issue Date: 2025-06-13 09:26:37 (UTC+8)
    Abstract: Inflammation have been linked to bone diseases such as osteoporosis or bone destruction. However, whether M1 inflammatory stimuli exert a stimulatory or inhibitory effect on the differentiation of osteoclasts remained controversial. Also, how inflammatory milieu influence cell proliferation and survival during osteoclastogenesis have not been determined. Here we reported the molecular repertoire alterations of RANKL-stimulated osteoclastogenesis from RAW264.7 at different stages in the inflammatory environments. Adding conditioned medium collected from LPS-stimulated macrophage, which are the primary source of extracellular inflammatory mediators, resulted in a biphasic change in cell number among differentiating preosteoclasts. The inflammatory milieu induced a transient proliferation of preosteoclasts during the initial 48 h, which was followed by a significant decline in cell numbers from the fourth day onwards. Proliferation-related AKT and ERK were transiently activated in the inflammatory environments, which also upregulated the expressions of c-myc, a major transcription factor for osteoclast differentiation, and pro-inflammatory genes, such as Tnf-a and Nos2. Following prolonged exposure to an inflammatory environment, undifferentiated osteoclast precursors undergo apoptosis. Our findings suggest that short-term inflammatory exposure transiently promotes the proliferation and differentiation of preosteoclasts, whereas long-term exposure leads to apoptosis, potentially due to the enhancement of inflammatory signals.
    Relation: Scientific Reports, Vol.15, No.1, Article number: 16137
    Data Type: article
    DOI 連結: https://doi.org/10.1038/s41598-025-99772-5
    DOI: 10.1038/s41598-025-99772-5
    Appears in Collections:[神經科學研究所] 期刊論文

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