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- Peng, XiangLinköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet,Jinan University, Guangdong, China (author)
The neutrophil serine protease PR3 induces shape change of platelets via the Rho/Rho kinase and Ca2+ signaling pathways
- Article/chapterEnglish2014
Publisher, publication year, extent ...
- Oxon, United Kingdom :Elsevier,2014
- printrdacarrier
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- LIBRIS-ID:oai:DiVA.org:oru-37561
- https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-37561URI
- https://doi.org/10.1016/j.thromres.2014.06.001DOI
- https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-111292URI
Supplementary language notes
- Language:English
- Summary in:English
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- SwePubSwePub
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- Funding Agencies:Swedish Renal FoundationAsp Foundation
- Funding Agencies|Swedish Renal Foundation; Asp Foundation
- Introduction: Proteinase 3 (PR3) is released from neutrophil azurophilic granules and exerts complex effects on the inflammatory process. PR3 catalyzes the degradation of a number of macromolecules, but the consequences on blood cells are less well defined. In the present study, the effect of PR3 on human platelets was thoroughly investigated.Methods: The experiments were performed on washed platelets freshly isolated from blood donated by healthy human volunteers. Platelets shape change and aggregation was measured on a Chrono-Log aggregometer. The phosphorylated form of MYPT1 was visualized by immunostaining. Platelet activation was further evaluated by flow cytometry.Results: PR3 induced platelet shape change but not aggregation. Flow cytometry analysis showed that PR3 induced no P-selectin expression or binding of fibrinogen to the platelets, and it did not change the activation in response to PAR1- or PAR4-activating peptides or to thrombin. Furthermore, Fura-2 measurement and immuno-blotting analysis, respectively, revealed that PR3 stimulated small intracellular Ca2+ mobilization and Thr696-specific phosphorylation of the myosin phosphatase target subunit 1 (MYPT1). Separate treatment of platelets with the Rho/Rho kinase inhibitor Y-27632 and the intracellular Ca2+ chelator BAPTA/AM reduced the shape change induced by PR3 whereas concurrent treatment completely inhibited it.Conclusion: The data shows that the neutrophil protease PR3 is a direct modulator of human platelets and causes shape change through activation of the Rho/Rho kinase and Ca2+ signaling pathways. This finding highlights an additional mechanism in the complex interplay between neutrophils and platelets.
Subject headings and genre
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Hematologi hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine Hematology hsv//eng
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng
- ANCA-associated vasculitis
- Proteinase PR3
- Platelet shape change
- Rho/Rho kinase signaling pathway
- Ca2+ signaling pathway
- Medicine
- Medicin
Added entries (persons, corporate bodies, meetings, titles ...)
- Ramström, Sofia,1973-Linköpings universitet,Avdelningen för mikrobiologi och molekylär medicin,Hälsouniversitetet(Swepub:liu)sofra86 (author)
- Kurz, TinoLinköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet(Swepub:liu)tinku34 (author)
- Grenegård, Magnus,1963-Linköpings universitet,Örebro universitet,Institutionen för läkarutbildning,Department of Medical and Health Sciences, Linköping University, Linköping, Sweden;,Avdelningen för läkemedelsforskning,Hälsouniversitetet,University of Örebro, Sweden(Swepub:liu)maggr06 (author)
- Segelmark, MårtenÖstergötlands Läns Landsting,Linköpings universitet,Avdelningen för läkemedelsforskning,Hälsouniversitetet,Njurmedicinska kliniken US(Swepub:liu)marse71 (author)
- Linköpings universitetAvdelningen för läkemedelsforskning (creator_code:org_t)
Related titles
- In:Thrombosis ResearchOxon, United Kingdom : Elsevier134:2, s. 418-4250049-38481879-2472
Internet link
- http://liu.diva-portal.org/smash/get/diva2:755332/FULLTEXT01
- https://liu.diva-portal.org/smash/get/diva2:755332/FULLTEXT01.pdffulltext:postprint
- https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-37561
- https://doi.org/10.1016/j.thromres.2014.06.001
- https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-111292
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