Transcription factor HIF1A: downstream targets, associated pathways, polymorphic hypoxia response element (HRE) sites, and initiative for standardization of reporting in scientific literature

Tumor Biology ◽  
2016 ◽  
Vol 37 (11) ◽  
pp. 14851-14861 ◽  
Author(s):  
Lucija Slemc ◽  
Tanja Kunej
Keyword(s):  
Transcription Factor ◽  
Scientific Literature ◽  
Hypoxia Response Element ◽  
Response Element ◽  
Hypoxia Response ◽  
Downstream Targets

scholarly journals AAV2-mediated and hypoxia response element-directed expression of bFGF in neural stem cells showed therapeutic effects on spinal cord injury in rats

2021 ◽  
Vol 12 (3) ◽  
Author(s):  
Sipin Zhu ◽  
Yibo Ying ◽  
Jiahui Ye ◽  
Min Chen ◽  
Qiuji Wu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Clinical Trials ◽  
Control Group ◽  
Therapeutic Effects ◽  
Hypoxia Response Element ◽  
Neurofilament Protein ◽  
Response Element ◽  
Hypoxia Response ◽  
Cord Injury

AbstractNeural stem cell (NSCs) transplantation has been one of the hot topics in the repair of spinal cord injury (SCI). Fibroblast growth factor (FGF) is considered a promising nerve injury therapy after SCI. However, owing to a hostile hypoxia condition in SCI, there remains a challenging issue in implementing these tactics to repair SCI. In this report, we used adeno-associated virus 2 (AAV2), a prototype AAV used in clinical trials for human neuron disorders, basic FGF (bFGF) gene under the regulation of hypoxia response element (HRE) was constructed and transduced into NSCs to yield AAV2-5HRE-bFGF-NSCs. Our results showed that its treatment yielded temporally increased expression of bFGF in SCI, and improved scores of functional recovery after SCI compared to vehicle control (AAV2-5HRE-NSCs) based on the analyses of the inclined plane test, Basso–Beattie–Bresnahan (BBB) scale and footprint analysis. Mechanistic studies showed that AAV2-5HRE-bFGF-NSCs treatment increased the expression of neuron-specific neuronal nuclei protein (NeuN), neuromodulin GAP43, and neurofilament protein NF200 while decreased the expression of glial fibrillary acidic protein (GFAP) as compared to the control group. Further, the expressions of autophagy-associated proteins LC3-II and Beclin 1 were decreased, whereas the expression of P62 protein was increased in AAV2-5HRE-bFGF-NSCs treatment group. Taken together, our data indicate that AAV2-5HRE-bFGF-NSCs treatment improved the recovery of SCI rats, which is accompanied by evidence of nerve regeneration, and inhibition of SCI-induced glial scar formation and cell autophagy. Thus, this study represents a step forward towards the potential use of AAV2-5HRE-bFGF-NSCs for future clinical trials of SCI repair.

Hypoxia response element of the human vascular endothelial growth factor gene mediates transcriptional regulation by nitric oxide: control of hypoxia-inducible factor-1 activity by nitric oxide

Blood ◽  
2000 ◽  
Vol 95 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Hideo Kimura ◽  
Alessandro Weisz ◽  
Yukiko Kurashima ◽  
Kouichi Hashimoto ◽  
Tsutomu Ogura ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Hypoxia Inducible Factor ◽  
Vascular Endothelial ◽  
Hypoxia Response Element ◽  
Response Element ◽  
Hypoxia Response ◽  
Hypoxia Inducible Factor 1 ◽  
Endothelial Growth Factor

Abstract Nitric oxide (NO) regulates production of vascular endothelial growth factor (VEGF) by normal and transformed cells. We demonstrate that NO donors may up-regulate the activity of the human VEGF promoter in normoxic human glioblastoma and hepatoma cells independent of a cyclic guanosine monophosphate–mediated pathway. Deletion and mutation analysis of the VEGF promoter indicates that the NO-responsive cis-elements are the hypoxia-inducible factor-1 (HIF-1) binding site and an adjacent ancillary sequence that is located immediately downstream within the hypoxia-response element (HRE). This work demonstrates that the HRE of this promoter is the primary target of NO. In addition, VEGF gene regulation by NO, as well as by hypoxia, is potentiated by the AP-1 element of the gene. Our study also reveals that NO and hypoxia induce an increase in HIF-1 binding activity and HIF-1 protein levels, both in the nucleus and the whole cell. These results suggest that there are common features of the NO and hypoxic pathways of VEGF induction, while in part, NO mediates gene transcription by a mechanism distinct from hypoxia. This is demonstrated by a difference in sensitivity to guanylate cyclase inhibitors and a different pattern of HIF-1 binding. These results show that there is a primary role for NO in the control of VEGF synthesis and in cell adaptations to hypoxia. (Blood. 2000;95:189-197)

scholarly journals Epigenetic regulation of HIF-1α in renal cancer cells involves HIF-1α/2α binding to a reverse hypoxia-response element

Oncogene ◽  
2011 ◽  
Vol 31 (8) ◽  
pp. 1065-1072 ◽  
Author(s):  
J Xu ◽  
B Wang ◽  
Y Xu ◽  
L Sun ◽  
W Tian ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Renal Cancer ◽  
Epigenetic Regulation ◽  
Hypoxia Response Element ◽  
Response Element ◽  
Hypoxia Response

Absence of mutations in the hypoxia response element ofVEGF in ALS

2003 ◽  
Vol 28 (6) ◽  
pp. 774-775 ◽  
Author(s):  
Francois Gros-Louis ◽  
Sandra Laurent ◽  
Ana Amelia Simoes Lopes ◽  
Jawad Khoris ◽  
Vincent Meininger ◽  
...  
Keyword(s):  
Hypoxia Response Element ◽  
Response Element ◽  
Hypoxia Response

scholarly journals Hypoxia Response Element-Regulated MMP-9 Promotes Neurological Recovery via Glial Scar Degradation and Angiogenesis in Delayed Stroke

2017 ◽  
Vol 25 (6) ◽  
pp. 1448-1459 ◽  
Author(s):  
Hongxia Cai ◽  
Yuanyuan Ma ◽  
Lu Jiang ◽  
Zhihao Mu ◽  
Zhen Jiang ◽  
...  
Keyword(s):  
Glial Scar ◽  
Neurological Recovery ◽  
Hypoxia Response Element ◽  
Response Element ◽  
Hypoxia Response

scholarly journals Zebrafish Hif3α modulates erythropoiesis via regulation of gata1 to facilitate hypoxia tolerance

Development ◽  
2020 ◽  
Vol 147 (22) ◽  
pp. dev185116
Author(s):  
Xiaolian Cai ◽  
Ziwen Zhou ◽  
Junji Zhu ◽  
Qian Liao ◽  
Dawei Zhang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cellular Response ◽  
Transcriptional Activity ◽  
Hypoxia Tolerance ◽  
Cell Maturation ◽  
Marker Genes ◽  
Hypoxia Inducible Factors ◽  
Hypoxia Response Element ◽  
Hypoxia Response ◽  
Master Regulators

ABSTRACTThe hypoxia-inducible factors 1α and 2α (HIF1α and HIF2α) are master regulators of the cellular response to O2. In addition to HIF1α and HIF2α, HIF3α is another identified member of the HIFα family. Even though the question of whether some HIF3α isoforms have transcriptional activity or repressive activity is still under debate, it is evident that the full length of HIF3α acts as a transcription factor. However, its function in hypoxia signaling is largely unknown. Here, we show that loss of hif3a in zebrafish reduced hypoxia tolerance. Further assays indicated that erythrocyte number was decreased because red blood cell maturation was impeded by hif3a disruption. We found that gata1 expression was downregulated in hif3a null zebrafish, as were several hematopoietic marker genes, including alas2, band3, hbae1, hbae3 and hbbe1. Hif3α recognized the hypoxia response element located in the promoter of gata1 and directly bound to the promoter to transactivate gata1 expression. Our results suggested that hif3a facilities hypoxia tolerance by modulating erythropoiesis via gata1 regulation.

Sign in / Sign up

Export Citation Format

Share Document