Human platelet antigens in disease

Wen, Yu‐Chuan; Chen, Ding‐Ping

doi:10.1016/j.cca.2018.05.009

Cited by 9 publications

(6 citation statements)

References 68 publications

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“…Platelet glycoprotein receptor polymorphisms, named human platelet antigens (HPAs), modulate receptor density and, subsequently, platelet function and thrombus formation [153]. The association of HPAs with pediatric and perinatal AIS is poorly investigated and, in most studies, only HPA-1 antigen variants on glycoprotein IIIa are included.…”

Section: Genetic Risk Factors In Pediatric Strokementioning

confidence: 99%

The Genetic Basis of Strokes in Pediatric Populations and Insight into New Therapeutic Options

Janković

Petrović²,

Novaković

et al. 2022

IJMS

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Strokes within pediatric populations are considered to be the 10th leading cause of death in the United States of America, with over half of such events occurring in children younger than one year of life. The multifactorial etiopathology that has an influence on stroke development and occurrence signify the importance of the timely recognition of both modifiable and non-modifiable factors for adequate diagnostic and treatment approaches. The early recognition of a stroke and stroke risk in children has the potential to advance the application of neuroprotective, thrombolytic, and antithrombotic interventions and rehabilitation strategies to the earliest possible timepoints after the onset of a stroke, improving the outcomes and quality of life for affected children and their families. The recent development of molecular genetic methods has greatly facilitated the analysis and diagnosis of single-gene disorders. In this review, the most significant single gene disorders associated with pediatric stroke are presented, along with specific therapeutic options whenever they exist. Besides monogenic disorders that may present with stroke as a first symptom, genetic polymorphisms may contribute to the risk of pediatric and perinatal stroke. The most frequently studied genetic risk factors are several common polymorphisms in genes associated with thrombophilia; these genes code for proteins that are part of the coagulation cascade, fibrolysis, homocystein metabolism, lipid metabolism, or platelets. Single polymorphism frequencies may not be sufficient to completely explain the stroke causality and an analysis of several genotype combinations is a more promising approach. The recent steps forward in our understanding of the disorders underlying strokes has given us a next generation of therapeutics and therapeutic targets by which to improve stroke survival, protect or rebuild neuronal connections in the brain, and enhance neural function. Advances in DNA sequencing and the development of new tools to correct human gene mutations have brought genetic analysis and gene therapy into the focus of investigations for new therapeutic options for stroke patients.

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Section: Genetic Risk Factors In Pediatric Strokementioning

confidence: 99%

The Genetic Basis of Strokes in Pediatric Populations and Insight into New Therapeutic Options

Janković

Petrović²,

Novaković

et al. 2022

IJMS

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“…The aggregation of platelet is driven by the interaction between surface specific glycoprotein antigens IIb/IIIa. [7] Therefore, it is well recognized that the application of antagonists of specific glycoprotein antigen can play an anti-platelet function via the inhibition of IIb/IIIa. [7] As the only clinically available specific antagonist of IIb/IIIa, tirofiban has the advantages of short biological half-life and high specificity.…”

Section: Introductionmentioning

confidence: 99%

“…[7] Therefore, it is well recognized that the application of antagonists of specific glycoprotein antigen can play an anti-platelet function via the inhibition of IIb/IIIa. [7] As the only clinically available specific antagonist of IIb/IIIa, tirofiban has the advantages of short biological half-life and high specificity. [8] The administration can block thrombus formation and attenuate coronary vessel obstruction by inhibiting the aggregation of platelets, [8] which ameliorates coronary micro-cycle conditions.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effect of recombinant human pro-urokinase and tirofiban on myocardial blood flow perfusion in ST elevation myocardial infarction patients receiving primary percutaneous coronary intervention

Yao¹,

Li²,

Cheng³

et al. 2019

Medicine

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Ischemia/reperfusion (I/R) injury is associated with primary percutaneous coronary intervention (PPCI). The current study was performed to compare the effect of tirofiban and recombinant human pro-urokinase (rh-proUK) on the improvement of coronary slow blood after PPCI. Sixty-five ST elevation myocardial infarction (STEMI) patients treated with rh-proUK and an equal number treated with tirofiban after PPCI were employed in the current study. The clinicopathological information regarding the biochemical parameters, thrombolysis in myocardial infarction (TIMI) grade, hemodynamics parameters, thrombus core (TS), sum-STR, left ventricular ejection fraction (LVEF), blood routine parameters, high-sensitivity C-reactive protein (CRP) level, uric acid, hepatorenal function, electrocardiogram (ECG), and echocardiography before and after the interventions were collected. The differences in those parameters between the 2 groups then compared with assess the treatment effect and side effects associated with the both therapies. The results showed that the TIMI level post-intervention ( P = .03), the proportion of TIMI myocardial perfusion grade level III ( P = .04), the changes in thrombus score ( P < .001) in rh-proUK group were significantly higher than those in tirofiban group while the corrected TIMI Frame Count (CTFC) ( P = .02), the incidence of slow flow ( P = .02), the thrombus score post-intervention ( P < .001), the stent length ( P = .02), and the number of receiving administration of sodium nitroprusside ( P = .01) were significantly lower than those in tirofiban group. Moreover, the levels of CK ( P < .001), CK-MB ( P = .01), and NT-proBNP 24-hour post-intervention ( P < .02) were significantly lower in rh-proUK group than those in tirofiban group and the sum-STR right after the intervention ( P < .03) of rh-proUK group was significantly higher than that of tirofiban group. No significant difference was detected between the 2 therapies regarding major adverse cardiac events (MACE). The findings outlined in the current study showed that the improvement effect of rh-proUK on blood flow condition was stronger right after the intervention and the therapy had a similar safety when compared with tirofiban during a 30-day follow-up.

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“…Platelets play a fundamental role in the progression, instability, and rupture of coronary plaques [2][3][4]. Moreover, platelet surface glycoproteins participate in platelet activation, adhesion, and aggregation, indirectly mediating the pathogenesis and clinical manifestations of ACS [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Platelet Carcinoembryonic Antigen Cell Adhesion Molecule 5 (CEACAM5) as a Possible Novel Diagnostic Tool for Evaluation of Acute Coronary Syndrome

Wan

Wang

et al. 2019

Med Sci Monit

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Background:Acute coronary syndrome (ACS) occurs approximately every 40 seconds, and was an underlying cause of death in 1 out of every 7 deaths. More accurate indicators are needed to distinguish patients with ACS from patients manifesting negative changes in electrocardiogram (ECG) and myocardial enzymes. This study aimed to investigate whether the expression of platelet carcinoembryonic antigen cell adhesion molecule-5 (CEACAM5/CEA/ CD66e) could help predict ACS. Material/Methods:We enrolled 82 participants (mean age 60 years, 33 females and 49 males). The expression of CEA on washed human platelets was assessed using two-color flow cytometry. The CEA levels on platelets and in serum of these 82 consecutive patients were detected using two-color whole-blood flow cytometry analysis and a custom-made Luminex multiplex assay, respectively. Results:CEA was expressed on the surface of human platelets. The expression of platelet CEA (P<0.01), but not serum CEA (P=0.30), was significantly higher in patients with ACS compared to patients with normal coronary artery. Increased platelet CEA levels could serve as a new independent indicator for ACS (P=0.0003). Platelet CEA testing (P=0.000002), as well as cardiac troponin I (cTnI) (P=0.0005), can diagnose ACS with high sensitivity and specificity, and, combined with cTnI (P<0.0001), can improve the diagnostic value. Conclusions:Platelet CEA expression was higher in individuals presenting with ACS. Hence, platelet CEA might be a novel and reliable biomarker for ACS. Large-scale studies are needed to confirm this hypothesis.

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Human platelet antigens in disease

Cited by 9 publications

References 68 publications

The Genetic Basis of Strokes in Pediatric Populations and Insight into New Therapeutic Options

The Genetic Basis of Strokes in Pediatric Populations and Insight into New Therapeutic Options

Comparison of the effect of recombinant human pro-urokinase and tirofiban on myocardial blood flow perfusion in ST elevation myocardial infarction patients receiving primary percutaneous coronary intervention

Platelet Carcinoembryonic Antigen Cell Adhesion Molecule 5 (CEACAM5) as a Possible Novel Diagnostic Tool for Evaluation of Acute Coronary Syndrome

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