Atrial fibrillation is associated with high levels of monocyte-platelet-aggregates and increased CD11b expression in patients with aortic stenosis

Pfluecke, Christian; Berndt, K.; Wydra, Sandy; Tarnowski, Daniel; Barthel, Peggy; Quick, Silvio; Ulbrich, Stefan; Christoph, Marian; Waessnig, Nadine; Speiser, Uwe; Wunderlich, Carsten; Poitz, David M.; Strasser, Ruth H.; Ibrahim, Karim

doi:10.1160/th15-06-0477

Cited by 19 publications

(7 citation statements)

References 44 publications

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“…We concluded that the protective effects of LIF occur during early period following stroke. It is known that various immune cells contribute to inflammation and that these cells can express inflammation-related proteins on their surface or release inflammation-related factors to their extracellular environments [ 24 , 25 ]. Pro-inflammatory genes accelerate the damage of ischemic tissue while anti-inflammation related genes promote the repair of ischemic tissue.…”

Section: Discussionmentioning

confidence: 99%

Temporal Gene Expression Profiles after Focal Cerebral Ischemia in Mice

et al. 2018

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A cascade of pathological processes is triggered in the lesion area after ischemic stroke. Unfortunately, our understanding of these complicated molecular events is incomplete. In this investigation, we sought to better understand the detailed molecular and inflammatory events occurring after ischemic stroke. RNA-seq technology was used to identify whole gene expression profiles at days (D1, D3, D7, D14, D21) after focal cerebral ischemia in mice. Enrichment analyses based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) terms for the differentially expressed genes (DEGs) were then analyzed. Inflammation-related genes that were significantly expressed after stroke were selected for analysis and the temporal expression patterns of pro-inflammatory and anti-inflammatory genes were reported. These data illustrated that the number of DEGs increased accumulatively after cerebral ischemia. In summary, there were 1967 DEGs at D1, 2280 DEGs at D3, 2631 DEGs at D7, 5516 DEGs at D14 and 7093 DEGs at D21. The significantly enriched GO terms also increased. 58 GO terms and 18 KEGG pathways were significantly enriched at all inspected time points. We identified 87 DEGs which were functionally related to inflammatory responses. The expression levels of pro-inflammation related genes CD16, CD32, CD86, CD11b, Tumour necrosis factor α (TNF-α), Interleukin 1β (IL-1β) increased over time and peaked at D14. Anti-inflammation related genes Arginase 1 (Arg1) and Chitinase-like 3 (Ym1) peaked at D1 while IL-10, Transforming growth factor β (TGF-β) and CD206, which were induced at 1 day after cerebral ischemia, peaked by 7 to 14 days. These gene profile changes were potentially linked to microglia/macrophage phenotype changes and could play a role in astroglial activation. This study supplies new insights and detailed information on the molecular events and pathological mechanisms that occur after experimental ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

Temporal Gene Expression Profiles after Focal Cerebral Ischemia in Mice

et al. 2018

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“…It also permits expression analysis of various platelet activation markers as well as platelet receptors on distinct platelets. Furthermore, flow cytometry allows the quantification analysis of the associates that link platelet to the other blood cells [211–215]. …”

Section: Platelets Hyperactivity In T2dmmentioning

confidence: 99%

Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies

Kaur

Singh

2018

Cardiovasc Diabetol

530

363

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The incidence and prevalence of diabetes mellitus is rapidly increasing worldwide at an alarming rate. Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes, accounting for approximately 90–95% of the total diabetes cases worldwide. Besides affecting the ability of body to use glucose, it is associated with micro-vascular and macro-vascular complications. Augmented atherosclerosis is documented to be the key factor leading to vascular complications in T2DM patients. The metabolic milieu of T2DM, including insulin resistance, hyperglycemia and release of excess free fatty acids, along with other metabolic abnormalities affects vascular wall by a series of events including endothelial dysfunction, platelet hyperactivity, oxidative stress and low-grade inflammation. Activation of these events further enhances vasoconstriction and promotes thrombus formation, ultimately resulting in the development of atherosclerosis. All these evidences are supported by the clinical trials reporting the importance of endothelial dysfunction and platelet hyperactivity in the pathogenesis of atherosclerotic vascular complications. In this review, an attempt has been made to comprehensively compile updated information available in context of endothelial and platelet dysfunction in T2DM.

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“…Leukocyte infiltration into tissue can promote collagen breakdown and structural remodeling processes, triggering oxidative stress 41 , leading in turn to ischemic heart failure 42 . Infiltrating leukocytes and PLA seem to promote structural and electrical remodeling in patients with atrial fibrillation 43 , which may also result in heart dysfunction and even failure.…”

Section: Discussionmentioning

confidence: 99%

Platelet-leukocyte aggregate is associated with adverse events after surgical intervention for rheumatic heart disease

Liu

Yang

et al. 2019

Sci Rep

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Platelet-leukocyte aggregate (PLA) is implicated in the etiology of both vascular lesions and cardiovascular events. This prospective cohort study aimed to examine the prognostic value of PLA for major adverse cardiac and cerebrovascular events (MACCE) and perioperative adverse events (AEs) in patients with rheumatic heart disease undergoing surgical intervention by Cox proportional hazard regression and logistic regression. A total of 244 patients were included, of whom 7 were lost to follow-up. Among the analyzed 237 subjects who completed 3-year follow-up, 30 experienced MACCE and 38 experienced perioperative AEs. Preoperative PLA was higher in subjects who developed MACCE (13.32%) than in those who did not (8.69%, p = 0.040). In multivariate regression, elevated PLA was associated with increased MACCE (hazard ratio 1.51 for each quartile, 95% CI 1.07–2.13; p = 0.020), and perioperative AEs (odds ratio 1.61, 95% CI 1.14–2.26; p = 0.007). The optimal PLA cut-off for predicting MACCE was 6.8%. Subjects with PLA > 6.8% had a higher prevalence of MACCE (17.1% vs. 5.5%, p = 0.009) and perioperative AEs (19.9% vs. 8.6%, p = 0.018). Kaplan-Meier analysis showed shorter MACCE-free survival in patients with PLA > 6.8% (p = 0.007, log rank). Elevated preoperative PLA is associated with increased MACCE and perioperative AEs in patients with rheumatic valve disease undergoing surgical intervention.

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Atrial fibrillation is associated with high levels of monocyte-platelet-aggregates and increased CD11b expression in patients with aortic stenosis

Cited by 19 publications

References 44 publications

Temporal Gene Expression Profiles after Focal Cerebral Ischemia in Mice

Temporal Gene Expression Profiles after Focal Cerebral Ischemia in Mice

Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies

Platelet-leukocyte aggregate is associated with adverse events after surgical intervention for rheumatic heart disease

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