Proteome analysis of testis from infertile protein C inhibitor‐deficient mice reveals novel changes in serpin processing and prostaglandin metabolism

Yang, Hanjiang; Wahlmüller, Felix C.; Uhrín, Pavel; Baumgartner, Roland; Mitulović, Goran; Sarg, Bettina; Geiger, Margarethe; Zellner, Maria

doi:10.1002/elps.201500218

Cited by 8 publications

(1 citation statement)

References 23 publications

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“…Murine platelets were isolated from ACD-anticoagulated blood by gel-filtration and analyzed by two-dimensional (2D)-difference gel electrophoresis (DIGE) as previously published. 23,24 Study Approval All performed animal experimentations were approved by the Animal Care and Use Committee of the Medical University of Vienna and by the Austrian Ministry of Sciences (BMWF-66.009/0320-II/3b/2013, BMWF-66.009/0254-ll/3b/2013).…”

Section: Platelet Proteomicsmentioning

confidence: 99%

Platelet PI3K Modulates Innate Leukocyte Extravasation during Acid-Induced Acute Lung Inflammation

et al. 2019

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Introduction Blood platelets are increasingly recognized as modulators of leukocyte effector functions in various pathologies including acute lung injury (ALI). ALI is a life-threatening disease, caused by damage to the alveolar epi- and endothelium. Excessive accumulation of leukocytes leads to severe lung inflammation, resulting in impaired lung function and hypoxemia. Objective Since leukocyte migration is modulated by activated platelets and phosphatidylinositol 3-kinase (PI3K) signaling is involved in platelet function, we aimed to elucidate the effect of PI3K on platelet-mediated immune responses. Materials and Methods We generated a mouse model with a platelet-specific deletion of p85α, the most important regulatory subunit of the class IA PI3K, and evaluated platelet function and platelet–leukocyte interactions. Moreover, we analyzed the impact of platelet-specific p85α gene deficiency during sterile peritonitis and acid-induced ALI. Results In vitro analyses of platelets revealed that lack of p85α led to decreased downstream signaling and diminished expression of surface activation markers, for example, CD62P and CD63, as well as reduced platelet aggregation. Moreover, platelet PI3K essentially mediated direct interactions of platelets with monocytes and neutrophils. In mice, platelet-specific p85α deficiency prevented leukocyte infiltration into the peritoneum and the bronchoalveolar compartment during sterile peritonitis and ALI, respectively. Additionally, the release of the inflammatory cytokine interleukin-12/23 was diminished in platelet p85α-deficient mice during ALI. In contrast to PI3K, neither overexpression nor depletion of platelet phosphatase and tensin homolog, the endogenous antagonist of PI3K, significantly modulated platelet function. Conclusion Our data indicate a crucial role of platelet PI3K signaling for leukocyte extravasation upon inflammatory stimuli in various diseases models.

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Section: Platelet Proteomicsmentioning

confidence: 99%