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Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [MOVAS]

ABSTRACT: Atherosclerosis (AS) is an age-related disease whose incidence increases with advancing age. During disease pathogenesis, vascular smooth muscle cells (VSMCs) undergo senescence within the plaques and secrete senescence-associated secretory phenotype (SASP) factors, which contributes to the development and destabilization of atherosclerotic plaques. As key effector cells of the innate immune system, natural killer (NK) cells can specifically recognize and eliminate senescent cells; however, their role in inhibiting AS progression and the underlying mechanisms remain unclear. Isoliensinine (IsoL) is a bisbenzylisoquinoline alkaloid extracted from lotus plumule, which exerts anti-inflammatory and immunomodulatory effects. Studies have shown that IsoL can effectively enhance the immune clearance of tumor cells by NK cells, suggesting that this compound may also have the potential to inhibit AS progression by regulating the recognition and elimination of abnormal target cells by immune cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE318401 | GEO | 2026/02/07

REPOSITORIES: GEO

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Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [VSMC]

Project description:Atherosclerosis (AS) is an age-related disease whose incidence increases with advancing age. During disease pathogenesis, vascular smooth muscle cells (VSMCs) undergo senescence within the plaques and secrete senescence-associated secretory phenotype (SASP) factors, which contributes to the development and destabilization of atherosclerotic plaques. As key effector cells of the innate immune system, natural killer (NK) cells can specifically recognize and eliminate senescent cells; however, their role in inhibiting AS progression and the underlying mechanisms remain unclear. Isoliensinine (IsoL) is a bisbenzylisoquinoline alkaloid extracted from lotus plumule, which exerts anti-inflammatory and immunomodulatory effects. Studies have shown that IsoL can effectively enhance the immune clearance of tumor cells by NK cells, suggesting that this compound may also have the potential to inhibit AS progression by regulating the recognition and elimination of abnormal target cells by immune cells.

2026-02-07 | GSE318399 | GEO

Effects of isoliensinine on gene expression in Jurkat cells

Project description:To investigate the effects of isoliensinine (IsoL) on gene expression in Jurkat cells.

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Isoliensinine induces vasorelaxation by regulating Calcium Channel in Hypertension：An in vitro and in vivo approach [vascular tissue]

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Isoliensinine ameliorates renal injury via the TGF-β1/SMAD2/3 pathway in spontaneously hypertensive rats [kidney tissue]

Project description:The goals of this study is to compare the differently expressed genes in renal tissues of WKY and SHR with or without isoliensinine treatment. The SHRs (n=12) were randomly divided into 2 groups: SHR, and SHR + isoliensinine (5mg/kg/d) groups (n=6 for each group). WKY rats (n=6) were set as control. Rats in WKY and SHR groups were intragastrically with double distilled water (dd H2O); while rats in SHR + isoliensinine (5mg/kg/d) group were intragastrically with 5mg/kg/d of isoliensinine for 10 weeks. Then the renal tissues were used to identify differentially expressed genes among different groups.

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Effects of isoliensinine on gene expression in Jurkat cells

Project description:Effects of isoliensinine on gene expression in Jurkat cells

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Cellular senescence reprograms human NK cells to promote vascular remodeling

Project description:Natural killer (NK) cells are lymphocytes that participate in immune responses through their cytotoxic activity and secretion of cytokines and chemokines. They can be activated by interaction with ligands on target cells or by soluble mediators such as cytokines. In addition, soluble HLA-G, a major histocompatibility complex molecule secreted by fetal trophoblast cells during early pregnancy, stimulates resting NK cells to secrete proinflammatory and proangiogenic factors. Human NK cells are abundant in uterus, where they remain after implantation. Soluble HLA-G is endocytosed into early endosomes of NK cells where its receptor, CD158d, initiates a signaling cascade through DNA-PKcs, Akt and NF-kB3. The physiological relevance of this endosomal signaling pathway, and how the fate and function of NK cells during early pregnancy is regulated, is unknown. Here we show that soluble agonists of CD158d trigger DNA damage response signaling and p21 (CIP1/WAF1) expression to promote senescence in primary NK cells. CD158d engagement resulted in morphological alterations in cell size and shape, chromatin remodeling, and survival in the absence of proliferation, all hallmarks of senescence. Microarray analysis revealed a senescence signature of upregulated genes upon sustained activation through CD158d. The proinflammatory and proangiogenic factors secreted by these metabolically active NK cells are part of a senescence associated secretory phenotype (SASP) that promoted tissue remodeling and angiogenesis as assessed by functional readouts of vascular permeability and endothelial cell tube formation. We propose that ligand-induced senescence is a molecular switch for the sustained activation of NK cells in response to soluble HLA-G for the purpose of remodeling the maternal vasculature in early pregnancy. Time series (4 hr, 16 hr, 64 hr) of NK cells treated with agonist (anti-CD158d mAb) or control. NK cells were from 4 donors.

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Proteomic characterization of CD56posCD57 NK cell subsets

Project description:NK cells are lymphocytes that provide a first defense against viral infections and cancer. They act (i) cytotoxic by killing virus-infected and tumorigenic cells and (ii) immune regulatory by releasing cytokines and chemokines. These innate immune cells are commonly further classified as CD56bright and CD56dim NK cells. Former studies confirmed immune regulatory CD56bright NK cells as progenitors of cytotoxic CD56dim NK cells. CD57 was previously described as T cell marker for senescence and terminal differentiation. Recent studies detected CD57+ and CD57- NK cells among the CD56dim NK cell population and suggested a fully mature developmental status for CD57+ NK cells. The recent NK cell maturation model includes CD34+ hematopoietic stem cells (HSC), which develop into CD56bright NK cells, later into CD56dimCD57- and finally into terminally maturated CD56dimCD57+ (1) (2) (3). The molecular mechanisms of human NK cell differentiation and maturation remain unknown to this date. We performed for the first time a proteomic analysis of these distinct developmental stages of human primary NK cells, isolated from overall 10 healthy human blood donors. CD56bright NK cells versusCD56dim and CD56dimCD57- versus CD56dimCD57+ NK cells were analyzed by using quantitative peptide sequencing, which revealed individual protein signatures (3400 proteins) of these different NK cell developmental stages. Notably, our data support the current NK cell differentiation model by highlighting both strong distinctions between CD56dim/bright NK cells and close relationships between CD57+/- NK cells on the proteomic level. Among the most prominent and conserved regulated proteins, we detected myosin IIa, Calvasculin and Calcyclin with very similar expression patterns. We investigated their sub-cellular localization and observed specific recruitment- and accumulation-events at the NK cell immunological synapse (NKIS) after NK activation.

2013-01-23 | PRD000666 | Pride

Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [MOVAS]

Project description:Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [MOVAS]

| PRJNA1418687 | ENA

Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [VSMC]

Project description:Isoliensinine promotes the clearance of senescent vascular smooth muscle cells by natural killer cells [VSMC]

| PRJNA1418685 | ENA

Cancer immune control needs senescence induction by Stat1 dependent cell cycle regulator pathways in tumours

Project description:Immune checkpoint bloackade (ICB)-based or natural cancer immune responses largely eliminate tumours. Yet, they require additional mechanisms to arrest those cancer cells that are not rejected. Cytokine-induced senescence (CIS) can stably arrest cancer cells, suggesting that interferon-dependent induction of senescence-inducing cell cycle regulators is needed to control those cancer cells that escape from killing. Here we report in two different cancers sensitive to T cell-mediated rejection, we show that deletion of the senescence-inducing cell cycle regulators p16Ink4a/p19Arf (Cdkn2a) or p21Cip1 (Cdkn1a) in the tumour cells abrogated both, the natural and the ICB-induced cancer immune control. Also in humans, melanoma metastases that progressed rapidly during ICB have losses of senescence-inducing genes and amplifications of senescence inhibitors. Metastatic cells also resist CIS. Such genetic and functional alterations are infrequent in metastatic melanomas regressing during ICB. Thus, activation of tumour-intrinsic, senescence-inducing cell cycle regulators is required to stably arrest those cancer cells that escape from eradication.

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