Stable CAD patients show higher levels of platelet-borne TGF-β1 associated with a superior pro-inflammatory state than the pro-aggregatory status; Evidence highlighting the importance of platelet-derived TGF-β1 in atherosclerosis

Ahmadi, Javad; Hosseini, Ehteramolsadat; Kargar, Faranak; Ghasemzadeh, Mehran

doi:10.1007/s11239-022-02729-y

Cited by 10 publications

(7 citation statements)

References 75 publications

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“…However, we need more work to explore the mechanism behind this. As we all know, cellular TGF- β 1 exists in a biologically inactive (latent) form by combing with latency-associated peptide (LAP) [ 35 ]. Unexpectedly, our results showed that several manipulation platelet concentrates contain only mature TGF- β 1.…”

Section: Discussionmentioning

confidence: 99%

Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells

Jin

Pan

Lin

et al. 2023

Oxidative Medicine and Cellular Longevity

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As a critical member in wound healing, vascular endothelial cells (ECs) impaired under high levels of reactive oxygen species (ROS) would hamper neovascularization. Mitochondria transfer can reduce intracellular ROS damage under pathological condition. Meanwhile, platelets can release mitochondria and alleviate oxidative stress. However, the mechanism by which platelets promote cell survival and reduce oxidative stress damage has not been clarified. Here, first, we selected ultrasound as the best method for subsequent experiments by detecting the growth factors and mitochondria released from manipulation platelet concentrates (PCs), as well as the effect of manipulation PCs on the proliferation and migration of HUVECs. Then, we found that sonicate platelet concentrates (SPC) decreased the level of ROS in HUVECs treated with hydrogen peroxide in advance, increased mitochondrial membrane potential, and reduced apoptosis. By transmission electron microscope, we saw that two kinds of mitochondria, free or wrapped in vesicles, were released by activated platelets. In addition, we explored that platelet-derived mitochondria were transferred to HUVECs partly by means of dynamin-dependent clathrin-mediated endocytosis. Consistently, we determined that platelet-derived mitochondria reduced apoptosis of HUVECs caused by oxidative stress. What is more, we screened survivin as the target of platelet-derived mitochondria via high-throughput sequencing. Finally, we demonstrated that platelet-derived mitochondria promoted wound healing in vivo. Overall, these findings revealed that platelets are important donors of mitochondria, and platelet-derived mitochondria can promote wound healing by reducing apoptosis caused by oxidative stress in vascular endothelial cells. And survivin is a potential target. These results further expand the knowledge of the platelet function and provide new insights into the role of platelet-derived mitochondria in wound healing.

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Section: Discussionmentioning

confidence: 99%

Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells

Jin

Pan

Lin

et al. 2023

Oxidative Medicine and Cellular Longevity

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“…Patients' platelets also had significantly higher levels of latent TGF-β1 than controls. Moreover, platelet-active TGF-β1 levels correlated with P-selectin (r = 0.7299, p < 0.0001), CD40L (r = 0.6397, p = 0.001), C-reactive protein (CRP, r = 0.5483, p = 0.002), and erythrocyte sedimentation rate (ESR, r = 0.5296, p = 0.003) in CAD [20]. These correlations may indicate proinflammatory and pro-aggregatory properties and their relationship with platelet active TGF-β1 levels.…”

Section: Role Of Tgf-β1 In Atherosclerosismentioning

confidence: 97%

“…J. Ahmadi and colleagues found that platelet-borne and soluble TGF-β1 levels are higher in CAD patients compared to healthy controls (30 patients and 30 healthy volunteers) [20]. The amount of mature TGF-β1 was eight-fold higher in the platelets of patients.…”

Section: Role Of Tgf-β1 In Atherosclerosismentioning

confidence: 97%

“…In most studies, TGF-β1 has been presented as a protective anti-inflammatory cytokine, inhibiting IL-1 β, TNF-α, and interferon-γ, leading to reduced VCAM-1 expression, leukocyte adhesion, and macrophage activity. TGF-β1 is reported to be present in endothelium, vascular smooth muscle cells (VSMCs), macrophages, platelets [20], and haematopoietic cells. It is the best-studied isoform and is considered to be the most important in the cardiovascular system [12].…”

Section: Role Of Tgf-β1 In Atherosclerosismentioning

confidence: 99%

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TGF-β Isoforms and GDF-15 in the Development and Progression of Atherosclerosis

Liuizė (Abramavičiūtė),

Mongirdienė

2024

IJMS

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The effect of oxidised lipoproteins on the endothelium, monocytes, platelets, and macrophages is a key factor in the initiation and development of atherosclerosis. Antioxidant action, lipoprotein metabolism, and chronic inflammation are the fields of research interest for better understanding the development of the disease. All the fields are related to inflammation and hence to the secretion of cytokines, which are being investigated as potential diagnostic markers for the onset of atherosclerosis. Pathways of vascular damage are crucial for the development of new laboratory readouts. The very early detection of endothelial cell damage associated with the onset of atherosclerosis, allowing the initiation of therapy, remains a major research goal. This article summarises the latest results on the relationship of tumour growth factor beta (TGF-β) isoforms and growth differentiation factor 15 (GDF-15) to the pathogenesis of atherosclerosis: which cells involved in atherosclerosis produce them, which effectors stimulate their synthesis and secretion, how they influence atherosclerosis development, and the relationship between the levels of TGF-β and GDF-15 in the blood and the development and extent of atherosclerosis.

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“…[61,62] In atherosclerotic lesions with activated vascular endothelium, there are also other components expressing CD40/ CD40L besides immune cells, such as vascular smooth muscle cells, endothelial cells, and platelets. [33,52,63] The surface expression of both CD40 and CD40L on these cells can lead to similar biological functions as that of monocytes/macrophages in atherosclerotic lesions, including the secretion of proinflammatory cytokines, adhesion, and co-stimulatory molecules expression, and the production of prothrombotic tissue factors. [64,65] For vascular smooth muscle cells, ligation of CD40 can induce the production of metalloproteinases to promote plaque rupture, [66] and CD40 signaling can activate the Src family kinase pathway, leading to the induction of MAPK activities.…”

Section: Cd40-cd40l and Atherosclerosismentioning

confidence: 99%

Co-stimulators CD40-CD40L, a potential immune-therapy target for atherosclerosis: A review

Tian,

Wang,

Wan

et al. 2024

Medicine

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The interaction between CD40 and CD40 ligand (CD40L) a crucial co-stimulatory signal for activating adaptive immune cells, has a noteworthy role in atherosclerosis. It is well-known that atherosclerosis is linked to immune inflammation in blood vessels. In atherosclerotic lesions, there is a multitude of proinflammatory cytokines, adhesion molecules, and collagen, as well as smooth muscle cells, macrophages, and T lymphocytes, particularly the binding of CD40 and CD40L. Therefore, research on inhibiting the CD40-CD40L system to prevent atherosclerosis has been ongoing for more than 30 years. However, it’s essential to note that long-term direct suppression of CD40 or CD40L could potentially result in immunosuppression, emphasizing the critical role of the CD40-CD40L system in atherosclerosis. Thus, specifically targeting the CD40-CD40L interaction on particular cell types or their downstream signaling pathways may be a robust strategy for mitigating atherosclerosis, reducing potential side effects. This review aims to summarize the potential utility of the CD40-CD40L system as a viable therapeutic target for atherosclerosis.

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Stable CAD patients show higher levels of platelet-borne TGF-β1 associated with a superior pro-inflammatory state than the pro-aggregatory status; Evidence highlighting the importance of platelet-derived TGF-β1 in atherosclerosis

Cited by 10 publications

References 75 publications

Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells

Platelets Facilitate Wound Healing by Mitochondrial Transfer and Reducing Oxidative Stress in Endothelial Cells

TGF-β Isoforms and GDF-15 in the Development and Progression of Atherosclerosis

Co-stimulators CD40-CD40L, a potential immune-therapy target for atherosclerosis: A review

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