Role of the Transcription Factor HIF‐2α in Promoting the Ischemia‐Tolerant Phenotype in Cerebral Endothelial Cells

Blood vessels are essential for the formation and maintenance of almost all functional tissues. They play fundamental roles in the supply of oxygen and nutrition, as well as development and morphogenesis. Vascular endothelial cells are the main factor in blood vessel formation. Recently, research findings showed heterogeneity in vascular endothelial cells in different tissue/organs. Endothelial cells alter their gene expressions depending on their cell fate or angiogenic states of vascular development in normal and pathological processes. Studies on gene regulation in endothelial cells demonstrated that the activator protein 1 (AP-1) transcription factors are implicated in angiogenesis and vascular development. In particular, it has been revealed that JunB (a member of the AP-1 transcription factor family) is transiently induced in endothelial cells at the angiogenic frontier and controls them on tip cells specification during vascular development. Moreover, JunB plays a role in tissue-specific vascular maturation processes during neurovascular interaction in mouse embryonic skin and retina vasculatures. Thus, JunB appears to be a new angiogenic factor that induces endothelial cell migration and sprouting particularly in neurovascular interaction during vascular development. In this review, we discuss the recently identified role of JunB in endothelial cells and blood vessel formation.

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Transcriptional regulation of endothelial-to-mesenchymal transition in cardiac fibrosis: role of myocardin-related transcription factor A and activating transcription factor 3

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2016-0634 ◽

2017 ◽

Vol 95 (10) ◽

pp. 1263-1270 ◽

Cited By ~ 9

Author(s):

Vibhuti Sharma ◽

Nilambra Dogra ◽

Uma Nahar Saikia ◽

Madhu Khullar

Keyword(s):

Endothelial Cells ◽

Transcription Factor ◽

Cardiac Fibrosis ◽

Activating Transcription Factor 3 ◽

Mesenchymal Transition ◽

Related Transcription Factor ◽

Endothelial To Mesenchymal Transition ◽

Activating Transcription Factor ◽

Transcription Factor 3

The etiology of cardiac fibrogenesis is quite diverse, but a common feature is the presence of activated fibroblasts. Experimental evidence suggests that a subset of cardiac fibroblasts is derived via transition of vascular endothelial cells into fibroblasts by endothelial-to-mesenchymal transition (EndMT). During EndMT, endothelial cells lose their endothelial characteristics and acquire a mesenchymal phenotype. Molecular mechanisms and the transcriptional mediators controlling EndMT in heart during development or disease remain relatively undefined. Myocardin-related transcription factor A facilitates the transcription of cytoskeletal genes by serum response factor during fibrosis; therefore, its specific role in cardiac EndMT might be of importance. Activation of activating transcription factor 3 (ATF-3) during cardiac EndMT is speculative, since ATF-3 responds to a transforming growth factor β (TGF-β) stimulus and controls the expression of the primary epithelial-to-mesenchymal transition markers Snail, Slug, and Twist. Although the role of TGF-β in EndMT-mediated cardiac fibrosis has been established, targeting of the TGF-β ligand has not proven to be a viable anti-fibrotic strategy owing to the broad functional importance of this ligand. Thus, targeting of downstream transcriptional mediators may be a useful therapeutic approach in attenuating cardiac fibrosis. Here, we discuss some of the transcription factors that may regulate EndMT-mediated cardiac fibrosis and their involvement in type 2 diabetes.

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CD97/ADGRE5 Inhibits LPS Induced NF-κB Activation through PPAR-γUpregulation in Macrophages

Mediators of Inflammation ◽

10.1155/2016/1605948 ◽

2016 ◽

Vol 2016 ◽

pp. 1-10 ◽

Cited By ~ 2

Author(s):

Shuai Wang ◽

Zewei Sun ◽

Wenting Zhao ◽

Zhen Wang ◽

Mingjie Wu ◽

...

Keyword(s):

Endothelial Cells ◽

Transcription Factor ◽

Immunofluorescence Staining ◽

Inflammatory Factor ◽

Negative Role ◽

Anti Inflammatory

CD97/ADGRE5 protein is predominantly expressed on leukocytes and belongs to the EGF-TM7 receptors family. It mediates granulocytes accumulation in the inflammatory tissues and is involved in firm adhesion of PMNC on activated endothelial cells. There have not been any studies exploring the role of CD97 in LPS induced NF-κB activation in macrophages. Therefore, we first measured the CD97 expression in LPS treated human primary macrophages and subsequently analyzed the levels of inflammatory factor TNF-αand transcription factor NF-κB in these macrophages that have been manipulated with either CD97 knockdown or overexpression. We found that a reported anti-inflammatory transcription factor, PPAR-γ, was involved in the CD97 mediated NF-κB suppression. Furthermore, by immunofluorescence staining, we established that CD97 overexpression not only inhibited LPS induced p65 expression in the nucleus but also promoted the PPAR-γexpression. Moreover, using CD97 knockout THP-1 cells, we further demonstrated that CD97 promoted PPAR-γexpression and decreased LPS induced NF-κB activation. In conclusion, CD97 plays a negative role in LPS induced NF-κB activation and TNF-αsecretion, partly through PPAR-γupregulation.

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Hhex regulates the specification and growth of the hepatopancreatic ductal system

10.1101/330779 ◽

2018 ◽

Cited By ~ 1

Author(s):

Alethia Villasenor ◽

Sébastien Gauvrit ◽

Michelle M. Collins ◽

Silvia Parajes ◽

Hans-Martin Maischein ◽

...

Keyword(s):

Endothelial Cells ◽

Transcription Factor ◽

Bile Duct ◽

Common Bile Duct ◽

Blood Vessels ◽

Molecular Mechanisms ◽

Distinct Population ◽

System Formation ◽

Shed Light

SUMMARYSignificant efforts have advanced our understanding of foregut-derived organ development; however, little is known about the molecular mechanisms that underlie the formation of the hepatopancreatic ductal (HPD) system. Here, we report a role for the homeodomain transcription factor Hhex in directing HPD progenitor specification in zebrafish. Loss of Hhex function results in impaired HPD system formation. We found that Hhex specifies a distinct population of HPD progenitors that gives rise to the cystic duct, common bile duct, and extra-pancreatic duct. Since hhex is not uniquely expressed in the HPD region but is also expressed in endothelial cells and the yolk syncytial layer (YSL), we tested the role of blood vessels as well as the YSL in HPD formation. We found that blood vessels are required for HPD patterning, but not for HPD progenitor specification. In addition, we found that Hhex is required in both the endoderm and the YSL for HPD development. Our results shed light on the mechanisms necessary to direct endodermal progenitors towards the HPD fate and also advance our understanding of HPD system formation.

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The Role of Second Messenger Molecules in the Regulation of Permeability in the Cerebral Endothelial Cells

Frontiers in Cerebral Vascular Biology - Advances in Experimental Medicine and Biology ◽

10.1007/978-1-4615-2920-0_25 ◽

1993 ◽

pp. 155-164 ◽

Cited By ~ 8

Author(s):

Ferenc Joó

Keyword(s):

Endothelial Cells ◽

Second Messenger ◽

Cerebral Endothelial Cells ◽

Messenger Molecules

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Role of Aβ-receptor for advanced glycation endproducts interaction in oxidative stress and cytosolic phospholipase A2 activation in astrocytes and cerebral endothelial cells

Neuroscience ◽

10.1016/j.neuroscience.2011.09.038 ◽

2011 ◽

Vol 199 ◽

pp. 375-385 ◽

Cited By ~ 50

Author(s):

S. Askarova ◽

X. Yang ◽

W. Sheng ◽

G.Y. Sun ◽

J.C.-M. Lee

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Phospholipase A2 ◽

Advanced Glycation Endproducts ◽

Cytosolic Phospholipase A2 ◽

Advanced Glycation ◽

Glycation Endproducts ◽

Cerebral Endothelial Cells ◽

Cytosolic Phospholipase

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Cdc42p GTPase Regulates the Budded-to-Hyphal-Form Transition and Expression of Hypha-Specific Transcripts in Candida albicans

Eukaryotic Cell ◽

10.1128/ec.3.3.724-734.2004 ◽

2004 ◽

Vol 3 (3) ◽

pp. 724-734 ◽

Cited By ~ 37

Author(s):

Alysia L. vandenBerg ◽

Ashraf S. Ibrahim ◽

John E. Edwards ◽

Kurt A. Toenjes ◽

Douglas I. Johnson

Keyword(s):

Saccharomyces Cerevisiae ◽

Endothelial Cells ◽

Transcription Factor ◽

Candida Albicans ◽

Opportunistic Pathogen ◽

Integral Function ◽

Morphological Transition ◽

Strongly Correlated ◽

Hypha Formation

ABSTRACT The yeast Candida albicans is a major opportunistic pathogen of immunocompromised individuals. It can grow in several distinct morphological states, including budded and hyphal forms, and the ability to make the dynamic transition between these forms is strongly correlated with virulence. Recent studies implicating the Cdc42p GTPase in hypha formation relied on cdc42 mutations that affected the mitotic functions of the protein, thereby precluding any substantive conclusions about the specific role of Cdc42p in the budded-to-hypha-form transition and virulence. Therefore, we took advantage of several Saccharomyces cerevisiae cdc42 mutants that separated Cdc42p's mitotic functions away from its role in filamentous growth. The homologous cdc42-S26I, cdc42-E100G, and cdc42-S158T mutations in C. albicans Cdc42p caused a dramatic defect in the budded-to-hypha-form transition in response to various hypha-inducing signals without affecting normal budded growth, strongly supporting the conclusion that Cdc42p has an integral function in orchestrating the morphological transition in C. albicans. In addition, the cdc42-S26I and cdc42-E100G mutants demonstrated a reduced ability to damage endothelial cells, a process that is strongly correlated to virulence. The three mutants also had reduced expression of several hypha-specific genes, including those under the regulation of the Efg1p transcription factor. These data indicate that Cdc42p-dependent signaling pathways regulate the budded-to-hypha-form transition and the expression of hypha-specific genes.

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