1. Activated protein C ameliorates diabetic nephropathy by epigenetically inhibiting the redox enzyme p66Shc.

    PNAS 110(2):648 (2013) PMID 23267072 PMCID PMC3545757

    The coagulation protease activated protein C (aPC) confers cytoprotective effects in various in vitro and in vivo disease models, including diabetic nephropathy. The nephroprotective effect may be related to antioxidant effects of aPC. However, the mechanism through which aPC may convey these an...
  2. Activated protein C ameliorates diabetic nephropathy by epigenetically inhibiting the redox enzyme p66Shc.

    PNAS 110(2):648 (2013) PMID 23267072 PMCID PMC3545757

    The coagulation protease activated protein C (aPC) confers cytoprotective effects in various in vitro and in vivo disease models, including diabetic nephropathy. The nephroprotective effect may be related to antioxidant effects of aPC. However, the mechanism through which aPC may convey these an...
  3. Role of the coagulation system in development

    Thrombosis Research 131:S14 (2013)

    The generation of knock out mice urged researchers, not always voluntarily, to newly define developmental functions of the gene knocked out. Among others, this has led to the establishment of the field of developmental haemostasis. The work in this field identified a role of coagulatio...
  4. Role of the coagulation system in development.

    Thrombosis Research 131 Suppl 1:S14 (2013) PMID 23452732

    The generation of knock out mice urged researchers, not always voluntarily, to newly define developmental functions of the gene knocked out. Among others, this has led to the establishment of the field of developmental haemostasis. The work in this field identified a role of coagulation protease...
  5. Role of the coagulation system in development.

    Thrombosis Research 131 Suppl 1:S14 (2013) PMID 23452732

    The generation of knock out mice urged researchers, not always voluntarily, to newly define developmental functions of the gene knocked out. Among others, this has led to the establishment of the field of developmental haemostasis. The work in this field identified a role of coagulation protease...
  6. The lectin-like domain of thrombomodulin ameliorates diabetic glomerulopathy via complement inhibition.

    Thrombosis and Haemostasis 108(6):1141 (2012) PMID 23014597

    Coagulation and complement regulators belong to two interactive systems constituting emerging mechanisms of diabetic nephropathy. Thrombomodulin (TM) regulates both coagulation and complement activation, in part through discrete domains. TM's lectin like domain dampens complement activation, whi...
  7. The lectin-like domain of thrombomodulin ameliorates diabetic glomerulopathy via complement inhibition.

    Thrombosis and Haemostasis 108(6):1141 (2012) PMID 23014597

    Coagulation and complement regulators belong to two interactive systems constituting emerging mechanisms of diabetic nephropathy. Thrombomodulin (TM) regulates both coagulation and complement activation, in part through discrete domains. TM's lectin like domain dampens complement activation, whi...
  8. Nuclear factor erythroid-derived 2 (Nfe2) regulates JunD DNA-binding activity via acetylation: a novel mechanism regulating trophoblast differentiation.

    Journal of Biological Chemistry 287(8):5400 (2012) PMID 22174410 PMCID PMC3285319

    We recently demonstrated that the bZip transcription factor nuclear factor erythroid-derived 2 (Nfe2) represses protein acetylation and expression of the transcription factor glial cell missing 1 (Gcm1) in trophoblast cells, preventing excess syncytiotrophoblast formation and permitting normal p...
  9. Nuclear factor erythroid-derived 2 (Nfe2) regulates JunD DNA-binding activity via acetylation: a novel mechanism regulating trophoblast differentiation.

    Journal of Biological Chemistry 287(8):5400 (2012) PMID 22174410 PMCID PMC3285319

    We recently demonstrated that the bZip transcription factor nuclear factor erythroid-derived 2 (Nfe2) represses protein acetylation and expression of the transcription factor glial cell missing 1 (Gcm1) in trophoblast cells, preventing excess syncytiotrophoblast formation and permitting normal p...
  10. Targeting activation of specific NF-κB subunits prevents stress-dependent atherothrombotic gene expression.

    Molecular Medicine 18:1375 (2012) PMID 23114885 PMCID PMC3533647

    Psychosocial stress has been shown to be a contributing factor in the development of atherosclerosis. Although the underlying mechanisms have not been elucidated entirely, it has been shown previously that the transcription factor nuclear factor-κB (NF-κB) is an important component of stress-act...
  11. Targeting activation of specific NF-κB subunits prevents stress-dependent atherothrombotic gene expression.

    Molecular Medicine 18:1375 (2012) PMID 23114885 PMCID PMC3533647

    Psychosocial stress has been shown to be a contributing factor in the development of atherosclerosis. Although the underlying mechanisms have not been elucidated entirely, it has been shown previously that the transcription factor nuclear factor-κB (NF-κB) is an important component of stress-act...
  12. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  13. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  14. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  15. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  16. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  17. Minocycline reduces plaque size in diet induced atherosclerosis via p27(Kip1).

    Atherosclerosis 219(1):74 (2011) PMID 21719015

    Minocycline, a tetracycline derivate, mediates vasculoprotective effects independent of its antimicrobial properties. Thus, minocycline protects against diabetic nephropathy and reduces neointima formation following vascular injury through inhibition of apoptosis or migration, respectively. Whet...
  18. p45NF-E2 represses Gcm1 in trophoblast cells to regulate syncytium formation, placental vascularization and embryonic growth.

    Development 138(11):2235 (2011) PMID 21558372

    Absence of the leucine zipper transcription factor p45NF-E2 results in thrombocytopenia, impaired placental vascularization and intrauterine growth restriction (IUGR) in mice. The mechanism underlying the p45NF-E2-dependent placental defect and IUGR remains unknown. Here, we show that the placen...
  19. p45NF-E2 represses Gcm1 in trophoblast cells to regulate syncytium formation, placental vascularization and embryonic growth.

    Development 138(11):2235 (2011) PMID 21558372

    Absence of the leucine zipper transcription factor p45NF-E2 results in thrombocytopenia, impaired placental vascularization and intrauterine growth restriction (IUGR) in mice. The mechanism underlying the p45NF-E2-dependent placental defect and IUGR remains unknown. Here, we show that the placen...
  20. Low but sustained coagulation activation ameliorates glucose-induced podocyte apoptosis: protective effect of factor V Leiden in diabetic nephropathy.

    Blood 117(19):5231 (2011) PMID 21389321

    Whereas it is generally perceived to be harmful, enhanced coagulation activation can also convey salutary effects. The high prevalence of the prothrombotic factor V Leiden (FVL) mutation in whites has been attributed to a positive selection pressure (eg, resulting from reduced blood loss or impr...