Open AccessRistocetin induces phosphorylated‑HSP27 (HSPB1) release from the platelets of type 2 DM patients: Anti‑platelet agent‑effect on the release
Author(s) -
Harukuni Tokuda,
Gen Kuroyanagi,
Takashi Onuma,
Yukiko Enomoto,
Tomoaki Doi,
Hiroki Iida,
Takanobu Otsuka,
Shinji Ogura,
Toru Iwama,
Kumi Kojima,
Osamu Kozawa
Publication year - 2018
Publication title -
biomedical reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.607
H-Index - 25
eISSN - 2049-9442
pISSN - 2049-9434
DOI - 10.3892/br.2018.1058
Subject(s) - platelet , ristocetin , chemistry , hsp27 , endocrinology , medicine , platelet membrane glycoprotein , pharmacology , biochemistry , heat shock protein , platelet aggregation , hsp70 , gene
It has been previously reported that HSP27 is released from platelets in type 2 diabetes mellitus (DM) patients according to phosphorylation. In the present study, we investigated the effect of ristocetin, a glycoprotein (GP)Ib/IX/V activator, on the release of HSP27 and the effect of anti-platelet agents, such as acetylsalicylic acid (ASA), on this release. Forty-six patients with type 2 DM were recruited, and classified into two groups depending on administration of anti-platelet agents, resulting in 31 patients without these agents (control group) and 15 patients with them (anti-platelet group). Ristocetin potently induced the aggregation of platelets in the two groups. Ristocetin-induced changes of the area under the curve of light transmittance and the ratio of the size of platelet aggregates in the anti-platelet group were slightly different from those in the control group. On the other hand, the levels of phosphorylated-HSP27 induced by ristocetin in the platelets from a patient of the anti-platelet group taking ASA were significantly lower than those from a patient of the control group. The levels of HSP27 release from the ristocetin-stimulated platelets were significantly correlated with the levels of phosphorylated-HSP27 in the platelets from patients in the two groups. The levels of HSP27 release and those of platelet-derived growth factor-AB (PDGF-AB) secretion stimulated by ristocetin in the anti-platelet group were lower than those in the control group. In addition, the levels of HSP27 release and those of PDGF-AB secretion stimulated by ADP in the anti-platelet group were lower than those in the control group. These results strongly suggest that anti-platelet agents inhibit the HSP27 release from platelets stimulated by ristocetin but not the aggregation in type 2 DM patients.