Hck/Fgr Kinase Deficiency Reduces Plaque Growth and Stability by Blunting Monocyte Recruitment and Intraplaque Motility

Medina, Indira; Cougoule, Céline; Drechsler, Maik; Bermúdez, Beatriz; Koenen, Rory R.; Sluimer, Judith C.; Wolfs, Ine M.J.; Döring, Yvonne; Hérias, Veronica; Gijbels, Marion; Bot, Ilze; Jager, Saskia C.A. de; Weber, Christian; Cleutjens, Jack P.M.; Berkel, Theo J.C. Van; Sikkink, Kees Jan; Mócsai, Atilla; Maridonneau‐Parini, Isabelle; Soehnlein, Oliver; Biessen, Erik A. L.

doi:10.1161/circulationaha.114.012316

Cited by 31 publications

(24 citation statements)

References 32 publications

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“…The current findings supported the idea that inflammation played a part in the pathophysiological mechanisms involved in ST-segment elevation myocardial infarction (STEMI) [88]. Two recent animal studies demonstrated the role of inflammation and neutrophils in the atherosclerotic process, in healing after myocardial infarction, and in cardiac remodeling [89,90].…”

Section: Hbp In Acute Bacterialsupporting

confidence: 84%

A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction

Yang

Liu

et al. 2019

Journal of Immunology Research

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Sepsis is a systemic inflammatory response syndrome caused by infection. With high morbidity and mortality of this disease, there is a need to find early effective diagnosis and assessment methods to improve the prognosis of patients. Heparin-binding protein (HBP) is a granular protein derived from polynuclear neutrophils. The biosynthetic HBP in neutrophils is rapidly released under the stimulation of bacteria, resulting in increased vascular permeability and edema. It is reasonable to speculate that the HBP in plasma may serve as a novel diagnostic marker for sepsis, bacterial skin infection, acute bacterial meningitis, leptospirosis, protozoan parasites, and even some noncommunicable diseases. It implies that in the detection and diagnosis of sepsis, it will be possible to make relevant diagnosis through this new indicator in the future. In this review, we summarize the typical biological function of HBP and its latest research progress to provide theoretical basis for clinical prediction and diagnosis of sepsis.

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Section: Hbp In Acute Bacterialsupporting

confidence: 84%

A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction

Yang

Liu

et al. 2019

Journal of Immunology Research

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“…Although Hck and Fgr only show overlapping localization at the cell membrane, compound Hck KO ; Fgr KO mice are unable to clear Listeria infection (Lowell et al, 1994), and show blunted recruitment of myeloid cells to arterial plaques or to LPS-challenged lungs (Mazzi et al, 2015; Medina et al, 2015). By contrast, excessive activation of endogenous SFK results in a lethal autoimmune response in Lyn CA mice (Hibbs et al, 1995) and inflammatory lung disease in Hck CA mice (Ernst et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Hematopoietic Cell Kinase Activity Suppresses Myeloid Cell-Mediated Colon Cancer Progression

Poh¹,

Love²,

Masson³

et al. 2017

Cancer Cell

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SUMMARY Aberrant activation of the SRC family kinase hematopoietic cell kinase (HCK) triggers hematological malignancies as a tumor cell-intrinsic oncogene. Here we find that high HCK levels correlate with reduced survival of colorectal cancer patients. Likewise, increased Hck activity in mice promotes the growth of endogenous colonic malignancies and of human colorectal cancer cell xenografts. Furthermore, tumor-associated macrophages of the corresponding tumors show a pronounced alternatively activated endotype, which occurs independently of mature lymphocytes or of Stat6-dependent Th2 cytokine signaling. Accordingly, pharmacological inhibition or genetic reduction of Hck activity suppresses alternative activation of tumor-associated macrophages and the growth of colon cancer xenografts. Thus, Hck may serve as a promising therapeutic target for solid malignancies.

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“…Upon migration into infected tissue, monocytes differentiate into dendritic cells and classically activated M1 macrophages, and migrate though the dense extracellular matrix to confront pathogens. The ability of monocytes/macrophages to undergo transendothelial migration and invade target tissues depends on podosomes ( Medina et al. , 2015 ).…”

Section: Introductionmentioning

confidence: 99%

S100A4 regulates macrophage invasion by distinct myosin-dependent and myosin-independent mechanisms

Dulyaninova

Ruiz

Gamble

et al. 2018

MBoC

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S100A4, a member of the S100 family of Ca2+-binding proteins, is a key regulator of cell migration and invasion. Our previous studies showed that bone marrow–derived macrophages from S100A4−/− mice exhibit defects in directional motility and chemotaxis in vitro and reduced recruitment to sites of inflammation in vivo. We now show that the loss of S100A4 produces two mechanistically distinct phenotypes with regard to macrophage invasion: a defect in matrix degradation, due to a disruption of podosome rosettes caused by myosin-IIA overassembly, and a myosin-independent increase in microtubule acetylation, which increases podosome rosette stability and is sufficient to inhibit macrophage invasion. Our studies point to S100A4 as a critical regulator of matrix degradation, whose actions converge on the dynamics and degradative functions of podosome rosettes.

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Hck/Fgr Kinase Deficiency Reduces Plaque Growth and Stability by Blunting Monocyte Recruitment and Intraplaque Motility

Cited by 31 publications

References 32 publications

A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction

A Promising Candidate: Heparin-Binding Protein Steps onto the Stage of Sepsis Prediction

Inhibition of Hematopoietic Cell Kinase Activity Suppresses Myeloid Cell-Mediated Colon Cancer Progression

S100A4 regulates macrophage invasion by distinct myosin-dependent and myosin-independent mechanisms

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