Institute of Biomedical Problems, Russian Academy of Sciences, Khoroshevskoye Shosse, 76a, 123007 Moscow, Russia.
Int J Mol Sci. 2024 May 14;25(10):5332. doi: 10.3390/ijms25105332.
The process of aging is intimately linked to alterations at the tissue and cellular levels. Currently, the role of senescent cells in the tissue microenvironment is still being investigated. Despite common characteristics, different cell populations undergo distinctive morphofunctional changes during senescence. Mesenchymal stem cells (MSCs) play a pivotal role in maintaining tissue homeostasis. A multitude of studies have examined alterations in the cytokine profile that determine their regulatory function. The extracellular matrix (ECM) of MSCs is a less studied aspect of their biology. It has been shown to modulate the activity of neighboring cells. Therefore, investigating age-related changes in the MSC matrisome is crucial for understanding the mechanisms of tissue niche ageing. This study conducted a broad proteomic analysis of the matrisome of separated fractions of senescent MSCs, including the ECM, conditioned medium (CM), and cell lysate. This is the first time such an analysis has been conducted. It has been established that there is a shift in production towards regulatory molecules and a significant downregulation of the main structural and adhesion proteins of the ECM, particularly collagens, fibulins, and fibrilins. Additionally, a decrease in the levels of cathepsins, galectins, S100 proteins, and other proteins with cytoprotective, anti-inflammatory, and antifibrotic properties has been observed. However, the level of inflammatory proteins and regulators of profibrotic pathways increases. Additionally, there is an upregulation of proteins that can directly cause prosenescent effects on microenvironmental cells (SERPINE1, THBS1, and GDF15). These changes confirm that senescent MSCs can have a negative impact on other cells in the tissue niche, not only through cytokine signals but also through the remodeled ECM.
衰老过程与组织和细胞水平的改变密切相关。目前,衰老细胞在组织微环境中的作用仍在研究中。尽管具有共同特征,但不同的细胞群在衰老过程中会经历独特的形态和功能变化。间充质干细胞(MSCs)在维持组织内稳态方面发挥着关键作用。大量研究已经研究了决定其调节功能的细胞因子谱的改变。MSCs 的细胞外基质(ECM)是其生物学中研究较少的方面。它已被证明可以调节相邻细胞的活性。因此,研究 MSC 基质体与年龄相关的变化对于理解组织龛位老化的机制至关重要。本研究对分离的衰老 MSC 各部分的基质体进行了广泛的蛋白质组学分析,包括 ECM、条件培养基(CM)和细胞裂解物。这是第一次进行这样的分析。已经确定,生产向调节分子的转移,以及 ECM 的主要结构和粘附蛋白,特别是胶原蛋白、纤维连接蛋白和原纤维蛋白的显著下调。此外,还观察到组织蛋白酶、半乳糖凝集素、S100 蛋白和其他具有细胞保护、抗炎和抗纤维化特性的蛋白质水平下降。然而,炎症蛋白和促纤维化途径调节剂的水平增加。此外,还上调了可以直接对微环境细胞产生促衰老作用的蛋白质(SERPINE1、THBS1 和 GDF15)。这些变化证实衰老的 MSC 不仅可以通过细胞因子信号,还可以通过重塑的 ECM 对组织龛位中的其他细胞产生负面影响。