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International Angiology 2004 September;23(3):246-54


lingua: Inglese

Biomarker profiling of plasma from acute coronary syndrome patients. Application of ProteinChip Array analysis

Florian-Kujawski M., Hussain W., Chyna B., Kahn S., Hoppensteadt D., Leya F., Fareed J.

Loyola University Medical Center, Maywood, IL, USA


Aim. Acute cor­o­nary syn­drome (ACS) is one of the lead­ing caus­es of death in the world and ­remains a com­plex path­o­phy­sio­log­ic pro­cess involv­ing inflam­ma­to­ry, hemo­stat­ic and vas­cu­lar pro­cess­es. The pur­pose of this study was to iden­ti­fy ­unique prot­e­om­ic bio­mark­ers ­present in ­patients with ACS using a newly devel­oped prot­e­om­ic pro­fil­ing tech­nique, sur­face ­enhanced laser desorp­tion/ion­iza­tion (SELDI).
Meth­ods. Citrat­ed plas­ma sam­ples ­obtained from clin­i­cal­ly con­firmed cases of ACS (n=100) and age ­matched con­trols (n=25) were pro­filed using SELDI-time of ­flight (TOF)-mass spec­trom­e­try (Cipher­gen Bio­systems, Free­mont, CA, USA). A ­strong anion ­exchange (SAX) Pro­tein­Chip Array was used to pro­file these sam­ples. In addi­tion to spec­tra pro­files, pro­tein den­sity plots were be ­obtained from the gen­er­at­ed molec­u­lar pro­file.
­Results. The SELDI pro­file in the molec­u­lar ­weight (MW) range of 0-150 kDa ­revealed a prom­i­nent 66.3 kDa albu­min peak along with sev­er­al dis­tinct com­po­nents at 28 kDa, 13.7 kDa and 6.5 kDa. Addi­tion­al minor molec­u­lar com­po­nents were also noted in the lower MW range (<6 kDa). There was a clus­ter of peaks ­between 10 and 12 kDa that were ­unique to the ­patients with ACS; about 1/3 of the ACS ­patients exhib­it­ed these peaks as evi­dent in the Pro­tein­Chip Array spec­trum. None of the age-­matched con­trols exhib­it­ed the peaks in this MW range, nor did the nor­mal human plas­ma pool that was used as an addi­tion­al con­trol. The rel­a­tive inten­sity of these novel molec­u­lar com­po­nents in the range of 10-12 kDa rep­re­sent ­unique pro­teins/pep­tides which are gen­er­at­ed in spe­cif­ic path­o­log­ic ­states asso­ciat­ed with ACS.
Con­clu­sion. These obser­va­tions sug­gest that ­patients with ACS have a ­unique clus­ter of molec­u­lar com­po­nents that are ­present in their SELDI pro­file. It might be pos­sible to use these pat­terns to iden­ti­fy high-risk ­patients who may be more sus­cep­ti­ble to the devel­op­ment of ­unstable ­plaque, which may even­tu­al­ly lead to myo­car­dial infarc­tion. Iden­tifi­ca­tion and char­ac­ter­iza­tion of these molec­u­lar com­po­nents will also help in the under­stand­ing of the path­o­gen­e­sis of ACS. These ­unique peaks may rep­re­sent path­o­log­ic pro­teins, novel inflam­ma­to­ry medi­a­tors or pro­tease cleav­age prod­ucts. Fur­ther stud­ies need to be done to bet­ter char­ac­ter­ize and iden­ti­fy these molec­u­lar com­po­nents and their path­o­log­ic role in ACS.

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