Binding of upstream stimulatory factor 1 to the E-Box regulates the 4G/5G polymorphism–dependent plasminogen activator inhibitor 1 expression in mast cells

Ma, Zejun; Jhun, Bong Sook; Jung, Sandy; Oh, Chad K.

doi:10.1016/j.jaci.2007.11.015

Cited by 23 publications

(46 citation statements)

References 32 publications

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“…However, the results of this study show that Usf1 and Usf2 exert opposing regulatory effects on the expression of the same gene. Consistent with this notion, similarly opposing effects of Usf1 and Usf2 on the E-box of plasminogen activator inhibitor-1 gene, a key regulator of the fibrinolytic system, have been reported (62, 63). With respect to an interaction between Usf and other transcription factors, a previous study reported a contrasting functional and physical interaction between Usf and Sp1, a GC-box binding transcription factor, in the transcriptional regulation of the deoxycytidine kinase gene in liver-derived HepG2 cells (64).…”

Section: Discussionsupporting

confidence: 54%

Upstream Stimulatory Factors 1 and 2 Mediate the Transcription of Angiotensin II Binding and Inhibitory Protein

Matsuda

Tamura

Wakui

et al. 2013

Journal of Biological Chemistry

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Background: Regulation of angiotensin II type 1 receptor-interacting and inhibitory protein (ATRAP/Agtrap) is important in pathophysiology.Results: Gene knockdown in cells and unilateral ureteral obstruction in mice indicate that Usf1 decreases and Usf2 increases Agtrap expression.Conclusion: Interplay between E-box and Usf1/Usf2 is important for Agtrap regulation.Significance: A strategy of modulating the E-box-Usf1/Usf2 interaction may have novel therapeutic potential.

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Section: Discussionsupporting

confidence: 54%

Upstream Stimulatory Factors 1 and 2 Mediate the Transcription of Angiotensin II Binding and Inhibitory Protein

Matsuda

Tamura

Wakui

et al. 2013

Journal of Biological Chemistry

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“…86 The 4G/5G polymorphism regulates the extent of PAI-1 release on exposure to allergen: a challenge with house dust mite caused an increase in plasma PAI-1 levels in all patients with asthma with the 4G allele and in only one-third of 5G homozygotes, 87 a clinical finding further corroborated by in vitro studies showing that in stimulated human mast cells the transcriptional activity of the 4G-PAI-1 promoter is higher than that of the 5G-PAI-1 promoter. 88 Remarkably, plasminogen-deficient mice demonstrated attenuated leukocyte recruitment into the lungs and reduced early histologic changes, including collagen deposition in the peribronchial areas and mucus metaplasia in allergic pulmonary inflammation induced by ovalbumin sensitization and challenge. 89 In accordance, administration of the plasminogen inhibitor tranexamic acid reduced eosinophil and lymphocyte numbers, mucus production, and collagen deposition in the lungs of ovalbumin-treated wild-type mice.…”

Section: Fibrinolysis In Asthmamentioning

confidence: 97%

Asthma and coagulation

Boer

Majoor²,

Veer

et al. 2012

Blood

145

140

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Asthma is a chronic airway disease characterized by paroxysmal airflow obstruction evoked by irritative stimuli on a background of allergic lung inflammation. Currently, there is no cure for asthma, only symptomatic treatment. In recent years, our understanding of the involvement of coagulation and anticoagulant pathways, the fibrinolytic system, and platelets in the pathophysiology of asthma has increased considerably. Asthma is associated with a procoagulant state in the bronchoalveolar space, further aggravated by impaired local activities of the anticoagulant protein C system and fibrinolysis. Protease-activated receptors have been implicated as the molecular link between coagulation and allergic inflammation in asthma. This review summarizes current knowledge of the impact of the disturbed hemostatic balance in the lungs on asthma severity and manifestations and identifies new possible targets for asthma treatment. (Blood. 2012;119(14):3236-3244) IntroductionAsthma is a disease of chronic airway inflammation causing symptoms of paroxysmal airflow obstruction, airway hyperresponsiveness to irritative stimuli, wheezing, chest tightness, and coughing. 1 These symptoms occur against a background of allergic inflammation, characterized by infiltration of mast cells, eosinophils, and T-helper 2 (Th2) lymphocytes into the airway wall and mucus hypersecretion. Many patients with chronic asthma show progressive decline of lung function that is thought to be the result of structural remodeling of the airway wall 2 and have frequent exacerbations and steroid resistance, 3 posing a major clinical challenge and health problem. 4 New therapeutic approaches need to be developed targeting the inflammatory background that triggers asthma symptoms. 5 Historically, coagulation and fibrinolysis have been considered as processes that take place in the vascular compartment. It is now appreciated that the airways represent a body compartment in which coagulation and anticoagulant mechanisms can be initiated and regulated locally. 6 In addition to the activation of coagulation in lung inflammatory disorders that is probably induced by leakage of plasma proteins into the bronchoalveolar space, essential mediators of coagulation can be found locally in the lung, including tissue factor (TF) that initiates coagulation and thrombin, which transforms fibrinogen to fibrin. 7 Several diseases associated with abundant lung inflammation, including acute respiratory distress syndrome, pneumonia, and lung fibrosis, 6,8 have been shown to result in similar changes in bronchoalveolar levels of proteins implicated in coagulation and fibrinolysis, tipping the physiologic equilibrium of preventing fibrin clot formation toward a net procoagulant state. In particular, for asthma this disturbed hemostatic balance in the airways is of importance for the perpetuation of allergic inflammation (Figure 1) in which cytokines and protease-activated receptors (PARs) play an important role. In addition, platelets have been found to actively participate in ma...

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“…been observed during the differentiation of osteoclasts, Sertoli cells, and mast cells (85,144,152).…”

Section: Usf1 and Usf2mentioning

confidence: 99%

Role of Helix-Loop-Helix Proteins during Differentiation of Erythroid Cells

Anantharaman

Lin

Barrow

et al. 2011

Molecular and Cellular Biology

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2Helix-loop-helix (HLH) proteins play a profound role in the process of development and cellular differentiation. Among the HLH proteins expressed in differentiating erythroid cells are the ubiquitous proteins Myc, USF1, USF2, and TFII-I, as well as the hematopoiesis-specific transcription factor Tal1/SCL. All of these HLH proteins exhibit distinct functions during the differentiation of erythroid cells. For example, Myc stimulates the proliferation of erythroid progenitor cells, while the USF proteins and Tal1 regulate genes that specify the differentiated phenotype. This minireview summarizes the known activities of Myc, USF, TFII-I, and Tal11/ SCL and discusses how they may function sequentially, cooperatively, or antagonistically in regulating expression programs during the differentiation of erythroid cells.Adult erythroid cells differentiate from hematopoietic stem cells (HSCs) through a cascade of steps (18,132). The most primitive HSC is called a long-term HSC (LT-HSC) for its ability to reconstitute HSCs in the bone marrow of irradiated mice over a long period of time. These slowly dividing cells are attached to a niche in the bone marrow and give rise to shortterm HSCs, which then differentiate into common lymphoid progenitors (CLPs) or common myeloid progenitors (CMPs). The CMPs go on to differentiate into granulocyte/monocyte precursors (GMPs) or into megakaryocyte/erythroid cell precursors (MEPs). MEPs further differentiate into erythropoietin-responsive BFU-E (blast-forming unit-erythroid) and then CFU-E (CFU-erythroid). The CFU-E cells differentiate to form orthochromatic normoblasts, then reticulocytes, and finally enucleated mature erythrocytes (125). The process of erythropoiesis has been extensively studied in vitro and in vivo and led to the identification of key erythroid cell transcription factors that regulate gene expression programs at the various steps of differentiation. The availability of erythroid cells representing different stages of maturation has rendered this system ideal for studying gene regulatory mechanisms.Transcription factors are classified based on the presence of specific protein-protein and protein-DNA interaction motifs which allow them to regulate gene expression by binding to DNA in a sequence-specific manner and to recruit coregulator complexes (98). The class of helix-loop-helix (HLH) transcription factors encompasses many proteins that play important roles during development and differentiation (89). The HLH motif is a characteristic dimerization domain which is accompanied by a basic (b) DNA-binding domain. Some HLH proteins contain an additional leucine zipper (ZIP) protein interaction module; these proteins are referred to as bHLHZIP proteins (89). Erythroid cells express many different HLH proteins. Here, we will review the well-characterized proteins USF1, USF2, Myc, TFII-I, and Tal1/SCL but will also discuss how inhibitor of DNA binding (ID) proteins, which only contain the HLH domain, may interfere with the function of HLH transcription factors in erythro...

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Binding of upstream stimulatory factor 1 to the E-Box regulates the 4G/5G polymorphism–dependent plasminogen activator inhibitor 1 expression in mast cells

Cited by 23 publications

References 32 publications

Upstream Stimulatory Factors 1 and 2 Mediate the Transcription of Angiotensin II Binding and Inhibitory Protein

Upstream Stimulatory Factors 1 and 2 Mediate the Transcription of Angiotensin II Binding and Inhibitory Protein

Asthma and coagulation

Role of Helix-Loop-Helix Proteins during Differentiation of Erythroid Cells

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