Search | Engineering

Subscribe Submit

Home Journals Focus Achievement Fronts About Us 中文版

Resource Type

Journal Article 4

Year

2017 2

2010 1

2008 1

Keywords

F10 1

PML/RARα fusion protein 1

acute promyelocytic leukemia 1

annexin A2-S100A10 heterotetramer 1

biomarker 1

cell invasion 1

chemoattractant 1

chemotactic activity 1

nanomedicine 1

plasmin 1

plasminogen activator inhibitor type-1 1

plasminogen activators 1

polymorphism 1

prothrombin 1

receptor 1

risk factor 1

stroke 1

thrombolytics 1

thrombophilia 1

uPA inhibitor 1

open ︾

Search scope:

排序： Display mode:

Translational initiatives in thrombolytic therapy

Melvin E. Klegerman

Frontiers of Medicine 2017, Volume 11, Issue 1, Pages 1-19 doi: 10.1007/s11684-017-0497-8

Abstract: clinically meaningful thrombolytic agents available for reversing the thrombogenic process are various plasminogenactivators.enzymes that reverse fibrin polymerization underlying the coagulation process by converting endogenous plasminogenFor the most part, the major clinically used thrombolytics, tissue plasminogen activator, urokinase and

Keywords： thrombolytics nanomedicine plasminogen activators

HTML PDF Collect

Chemotactic effect of urokinase-type plasminogen activator on mouse spermatozoa

DING Xiaofang, LI Honggang, XIONG Chengliang

Frontiers of Medicine 2008, Volume 2, Issue 2, Pages 195-199 doi: 10.1007/s11684-008-0037-7

Abstract: The aim of this study is to investigate the chemotactic effect of urokinase-type plasminogen activator

Keywords： chemotactic activity receptor uPA inhibitor F10 chemoattractant

HTML PDF Collect

Annexin A2-S100A10 heterotetramer is upregulated by PML/RARα fusion protein and promotes plasminogen-dependent

Dan Huang, Yan Yang, Jian Sun, Xiaorong Dong, Jiao Wang, Hongchen Liu, Chengquan Lu, Xueyu Chen, Jing Shao, Jinsong Yan

Frontiers of Medicine 2017, Volume 11, Issue 3, Pages 410-422 doi: 10.1007/s11684-017-0527-6

Abstract:

Aberrant expression of annexin A2-S100A10 heterotetramer (AIIt) associated with PML/RARα fusion protein causes lethal hyperfibrinolysis in acute promyelocytic leukemia (APL), but the mechanism is unclear. To facilitate the investigation of regulatory association between ANXA2 and promyelocytic leukemia/retinoic acid receptor a (PML/RARα) fusion protein, this work was performed to determine the transcription start site of ANXA2 promoter with rapid amplification of 5′-cDNA ends analysis. Zinc-induced U937/PR9 cells expressed PML/RARα fusion protein, and resultant increases in ANXA2 transcripts and translational expressions of both ANXA2 and S100A10, while S100A10 transcripts remained constitutive. The transactivation of ANXA2 promoter by PML/RARα fusion protein was 3.29±0.13 fold higher than that by control pSG5 vector or wild-type RARα. The overexpression of ANXA2 in U937 transfected with full-length ANXA2 cDNA was associated with increased S100A10 subunit, although S100A10 transcripts remained constitutive. The tPA-dependent initial rate of plasmin generation (IRPG) in zinc-treated U937/PR9 increased by 2.13-fold, and cell invasiveness increased by 27.6%. Antibodies against ANXA2, S100A10, or combination of both all remarkably inhibited the IRPG and invasiveness in U937/PR9 and NB4. Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Thus, PML/RARα fusion protein transactivated the ANXA2 promoter to upregulate ANXA2 and accumulate S100A10. Increased AIIt promoted IRPG and invasiveness, both of which were partly abolished by antibodies against ANXA2 and S100A10 or by ATRA.

Keywords： annexin A2-S100A10 heterotetramer PML/RARα fusion protein plasmin cell invasion acute promyelocytic leukemia

HTML PDF Collect

Clinical and genetic risk factors for venous thromboembolism in Chinese population

Chen WANG PhD, MD, Zhen-Guo ZHAI PhD, MD, Ying H. SHEN PhD, MD, Lan ZHAO PhD, MD,

Frontiers of Medicine 2010, Volume 4, Issue 1, Pages 29-35 doi: 10.1007/s11684-010-0012-y

Abstract: Venous thromboembolism (VTE), including deep vein thrombosis and pulmonary embolism, carries significant mortality and morbidity. The most important and effective way to reduce VTE incidence is to identify the patients at risk and give necessary prevention. VTE is a multifactorial and complicated disorder. Major risk factors for VTE include surgery and trauma, acute medical illness, active cancer and pregnancy. Genetic factors increase susceptibility to the disease and are useful in predicting the development of VTE. Gene-gene and gene-environment interactions alter and magnify the clinical picture in this disorder. This brief review summarizes some selected clinical and genetic risk factors for VTE based on the current research in China.

Keywords： risk factor stroke prothrombin plasminogen activator inhibitor type-1 polymorphism thrombophilia biomarker