Transcript profiling of human platelets using microarray and serial analysis of gene expression

Gnatenko, Dmitri V.; Dunn, John J.; McCorkle, S.; Weissmann, David; Perrotta, Peter L.; Bahou, Wadie F.

doi:10.1182/blood-2002-09-2797

Cited by 352 publications

(407 citation statements)

References 37 publications

Supporting

Mentioning

383

Contrasting

Unclassified

Order By: Relevance

“…The present study demonstrates that PMP express complement regulatory proteins, C1-INH, CD55 and CD59. In addition, clusterin, a regulator of the assembly of the terminal complement complex, is packaged in platelet alpha granules [37], and is expressed on the surface of platelets [38] and microparticles [39].…”

Section: Discussionmentioning

confidence: 99%

Expression of complement components and inhibitors on platelet microparticles

2008

View full text Add to dashboard Cite

Platelet microparticles (PMP) are released from activated platelets and play an important role in hemostasis, thrombosis and inflammation. Since platelets were recently found to demonstrate an intrinsic capacity for activating both classical and alternative pathways of the complement system, the present study extended these observations to PMP. PMP were generated by treating platelets with 10 µM A23187 (37°C, 5 min). PMP were identified by flow cytometry, based on size, Annexin V binding, and expression of P-selectin and GPIIb (CD41). PMP expressed gC1qR/p33, a multifunctional cellular protein that was recently described to activate the classical complement cascade. PMP also expressed the classical pathway and contact system regulator, CI inhibitor (C1-INH), as well as CD55 and CD59. Despite C1-INH expression, PMP supported classical pathway C4 activation in the presence of purified C1 and C4. Moreover, statistically significant deposition of C3b and C5b-9 was detected on PMP exposed to plasma, concurrently with expression of CD55 and CD59. These data provide the first evidence for the ability of PMP to support in situ complement activation. Complement activation contributes to a variety of vascular and inflammatory disease states including atherosclerosis and ischemia/reperfusion injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Expression of complement components and inhibitors on platelet microparticles

2008

View full text Add to dashboard Cite

show abstract

“…Under physiologic conditions, platelet damage or lysis by C5b-9 assembly is regulated by surface membrane CD55, CD59, and clusterin. Apparently clusterin is more highly expressed on platelets than on other mammalian cell types (Gnatenko, Dunn, McCorkle, Weissmann, Perrotta, and Bahou 2003). If stimulated platelets are indeed actively engaged in the initiation and propagation of both classical and alternative pathways, the arming of platelets with potent complement regulatory mechanisms would be necessary to prevent uncontrolled cytolysis and production of inflammatory mediators.…”

Section: Regulation Of Complement Activity On Plateletsmentioning

confidence: 99%

Platelet Mediated Complement Activation

Peerschke

Ghebrehiwet

2008

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

show abstract

“…8,9 Sequencing-based approaches, SAGE and CAGE, allow quantitative analysis of gene expression by counting the number of tags (corresponding to the number of mRNA transcripts) rather than measuring signal intensities as in hybridization-based approaches. 10 These technologies have been successfully employed to simultaneously study the expression levels of thousand genes, leading to promising results for Down syndrome (DS), 11 cardiovascular diseases 12 and diabetes. 13 However, the laborious concatenation and cloning of such tags, and the high costs of automated Sanger sequencing, have thus far limited their use.…”

Section: Introductionmentioning

confidence: 99%