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增强脂肪来源间充质干细胞的成骨分化。

enhances osteogenic differentiation in adipose-derived mesenchymal stem cells.

作者信息

Mohamad-Fauzi Nuradilla, Shaw Claire, Foutouhi Soraya H, Hess Matthias, Kong Nguyet, Kol Amir, Storey Dylan Bobby, Desai Prerak T, Shah Jigna, Borjesson Dori, Murray James D, Weimer Bart C

机构信息

Department of Animal Science, College of Agricultural and Environmental Sciences, University of California, Davis, Davis, CA, United States.

Department of Population Health and Reproduction, 100K Pathogen Genome Project, Davis, CA, United States.

出版信息

Front Cell Dev Biol. 2023 Mar 15;11:1077350. doi: 10.3389/fcell.2023.1077350. eCollection 2023.

DOI:10.3389/fcell.2023.1077350
PMID:37009487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10055666/
Abstract

The potential of mesenchymal stem cells (MSCs) for tissue repair and regeneration has garnered great attention. While MSCs are likely to interact with microbes at sites of tissue damage and inflammation, like in the gastrointestinal system, the consequences of pathogenic association on MSC activities have yet to be elucidated. This study investigated the effects of pathogenic interaction on MSC trilineage differentiation paths and mechanisms using model intracellular pathogen ssp serotype Typhimurium. The examination of key markers of differentiation, apoptosis, and immunomodulation demonstrated that altered osteogenic and chondrogenic differentiation pathways in human and goat adipose-derived MSCs. Anti-apoptotic and pro-proliferative responses were also significantly upregulated ( < 0.05) in MSCs during challenge. These results together indicate that , and potentially other pathogenic bacteria, can induce pathways that influence both apoptotic response and functional differentiation trajectories in MSCs, highlighting that microbes have a potentially significant role as influencers of MSC physiology and immune activity.

摘要

间充质干细胞(MSCs)在组织修复和再生方面的潜力已引起广泛关注。虽然MSCs可能在组织损伤和炎症部位(如胃肠道系统)与微生物相互作用,但病原体关联对MSC活性的影响尚未阐明。本研究使用细胞内病原体鼠伤寒沙门氏菌亚种血清型鼠伤寒杆菌模型,研究了病原体相互作用对MSC三系分化途径和机制的影响。对分化、凋亡和免疫调节关键标志物的检测表明,人和山羊脂肪来源的MSCs中骨生成和软骨生成分化途径发生改变。在感染过程中,MSCs的抗凋亡和促增殖反应也显著上调(P<0.05)。这些结果共同表明,鼠伤寒沙门氏菌以及潜在的其他病原菌,可诱导影响MSCs凋亡反应和功能分化轨迹的途径,突出了微生物作为MSC生理学和免疫活性影响因素的潜在重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/b11a3295ea45/fcell-11-1077350-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/e15c16e207f5/fcell-11-1077350-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/09e7f8e2f099/fcell-11-1077350-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/97dd82c6d4ba/fcell-11-1077350-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/928abff33f38/fcell-11-1077350-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/1a21b169ff74/fcell-11-1077350-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/8f0633291e1e/fcell-11-1077350-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/2891c1f30e1b/fcell-11-1077350-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/d1e83968c5af/fcell-11-1077350-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/b11a3295ea45/fcell-11-1077350-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/e15c16e207f5/fcell-11-1077350-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/09e7f8e2f099/fcell-11-1077350-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/97dd82c6d4ba/fcell-11-1077350-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/928abff33f38/fcell-11-1077350-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/1a21b169ff74/fcell-11-1077350-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/8f0633291e1e/fcell-11-1077350-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/2891c1f30e1b/fcell-11-1077350-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/d1e83968c5af/fcell-11-1077350-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7690/10055666/b11a3295ea45/fcell-11-1077350-g009.jpg

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MSC therapy in livestock models.家畜模型中的间充质干细胞疗法。
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Transl Anim Sci. 2022 Jan 27;6(1):txac012. doi: 10.1093/tas/txac012. eCollection 2022 Jan.
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