scholarly journals Evaluation of Hypoxia-Inducible Factor-1 Alpha (HIF-1α) in Equine Sarcoid: An Immunohistochemical and Biochemical Study

Pathogens ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 58
Author(s):  
Manuela Martano ◽  
Gennaro Altamura ◽  
Karen Power ◽  
Brunella Restucci ◽  
Francesca Carella ◽  
...  
Keyword(s):  
Biochemical Study ◽  
Hypoxia Inducible Factor ◽  
Hypoxic Condition ◽  
Vegf Expression ◽  
Cytoplasmic Staining ◽  
Hypoxia Inducible Factor 1 ◽  
Equine Sarcoid ◽  
Relevant Role ◽  
Causative Agents ◽  
Pathway Regulation

Background: equine sarcoids are the most frequent skin tumors in equidae worldwide. It is well known that delta bovine papillomaviruses are their causative agents. We have recently shown the presence in equine sarcoids of abnormal vessel structures, which could cause a hypoxic condition. The aim of this study was to analyze the expression of hypoxia-inducible factor-1 alpha (HIF-1α) in a subset of BPV positive equine sarcoids and explore the relationship with vascular endothelial growth factor (VEGF) expression. Results: 80% of equine sarcoids showed strong cytoplasmic staining in >60% of neoplastic fibroblasts, while 20% of samples showed a moderate cytoplasmic staining in 40–60% of neoplastic fibroblasts for HIF-1α. Results of Western blotting (WB) were consistent with immunohistochemistry (IHC). Moreover, a positive correlation between HIF-1α and VEGF expression (r = 0.60, p < 0.01) was observed. Conclusion: we have shown that HIF-1α was strongly expressed in equine sarcoid. The upregulation of HIF-1α has been described in numerous tumors and can be modulated by many proteins encoded by transforming viruses. Thus, it is also possible that BPV could have a relevant role in HIF-1α pathway regulation, contributing to the development of equine sarcoids by promoting HIF-1α/VEGF mediated tumor angiogenesis.

scholarly journals Hypoxia Inducible Factor-1-Alpha Expression on Preeclampsia Mice Model With L-Arginine Administration

2021 ◽  
Vol 57 (3) ◽  
pp. 226
Author(s):  
Nutria Widya Purna Anggraini ◽  
Sri Sulistyowati ◽  
Muhammad Adrianes Bachnas ◽  
Eric Edwin Yuliantara ◽  
Wisnu Prabowo ◽  
...  
Keyword(s):  
Treatment Group ◽  
Statistical Tests ◽  
Hypoxia Inducible Factor ◽  
Data Distribution ◽  
Hypoxic Condition ◽  
Control Group ◽  
Mice Model ◽  
Hypoxia Inducible Factor 1 ◽  
Minimum Value ◽  
Maximum Value

Preeclampsia is hypertension in pregnancy that affects 2% to 8% of pregnancies worldwide and causes significant maternal and perinatal morbidity and mortality. In the pathogenesis of preeclampsia, placental hypoxia plays an important role, associated with excessive trophoblast apoptosis resulting in decreased trophoblast and spiral arteries invasion. This placental hypoxic condition will induce increased expression of Hypoxia Inducible Factor -1-Alpha (HIF-1-A). L-Arginine is a potent vasodilator presumably to improve preeclampsia placental hypoxic conditions and reduce HIF-1-A expression. This study was an experimental study with a parallel-group post-test only design. Thirty-six preeclamptic mice models were divided into 2 groups. The control group (K1) 18 preeclamptic mice model without treatment and the treatment group (K2) 18 preeclamptic mice given L-Arginine. The independent variable was the administration of L-Arginine and the dependent variable is the placental HIF-1-A expression. Statistical analysis used unpaired t-test on normal data distribution, and Mann Whitney test on abnormal data distribution. The mean of placental HIF-1-A expression K1 was 2.47 ± 1.65 with a minimum value of 0.4 and a maximum value of 6.6. At K2 0.93 ± 0.55 with a minimum value of 0.0 and a maximum value of 2.0. Statistical tests showed that the placental HIF-1-A expression in the treatment group was significantly lower than that in the control group (p <0.001). In conclusion, the expression of HIF-1-A in preeclamptic mice model placenta decreased with L-Arginine administration.

scholarly journals SEMAPHORINS and their receptors: focus on the crosstalk between melanoma and hypoxia

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Elisabetta Valentini ◽  
Marta Di Martile ◽  
Donatella Del Bufalo ◽  
Simona D’Aguanno
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Progression ◽  
Stromal Cells ◽  
Hypoxia Inducible Factor ◽  
Cell Communication ◽  
Hypoxic Condition ◽  
Response To Therapy ◽  
Hypoxia Inducible Factor 1 ◽  
Shed Light

AbstractHypoxia, a condition of oxygen deprivation, is considered a hallmark of tumor microenvironment regulating several pathways and promoting cancer progression and resistance to therapy. Semaphorins, a family of about 20 secreted, transmembrane and GPI-linked glycoproteins, and their cognate receptors (plexins and neuropilins) play a pivotal role in the crosstalk between cancer and stromal cells present in the tumor microenvironment. Many studies reported that some semaphorins are involved in the development of a permissive tumor niche, guiding cell-cell communication and, consequently, the development and progression, as well as the response to therapy, of different cancer histotypes, including melanoma.In this review we will summarize the state of art of semaphorins regulation by hypoxic condition in cancer with different origin. We will also describe evidence about the ability of semaphorins to affect the expression and activity of transcription factors activated by hypoxia, such as hypoxia-inducible factor-1. Finally, we will focus our attention on findings reporting the role of semaphorins in melanocytes transformation, melanoma progression and response to therapy. Further studies are necessary to understand the mechanisms through which semaphorins induce their effect and to shed light on the possibility to use semaphorins or their cognate receptors as prognostic markers and/or therapeutic targets in melanoma or other malignancies.

scholarly journals HIF-1-miR-219-SMC4 Regulatory Pathway Promoting Proliferation and Migration of HCC under Hypoxic Condition

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Yang Chen ◽  
Fei Huang ◽  
liang Deng ◽  
Xiaowei Yuan ◽  
Qiang Tao ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Hypoxia Inducible Factor ◽  
Hypoxic Condition ◽  
Regulatory Pathway ◽  
Mesenchymal Transition ◽  
Hypoxia Inducible Factor 1 ◽  
Structural Maintenance Of Chromosome ◽  
And Migration ◽  
Hcc Cells ◽  
Proliferation And Migration

This paper aims to investigate the function of structural maintenance of chromosome 4 (SMC4) in the progression of hepatocellular carcinoma (HCC) under hypoxic condition. In this study, we found that suppression of SMC4 could inhibit proliferation and migration of HCC cells through inducing G1 phase arrest and affecting process of epithelial-mesenchymal transition (EMT) under hypoxic condition. Moreover, we demonstrated that SMC4 was transcriptionally regulated by hypoxia-inducible factor-1 (HIF-1) under hypoxic condition. As SMC has been shown to be a target gene of miR-219, we observed that miR-219 was downregulated under hypoxic condition and suppression of HIF-1a could lead to the upregulation of miR-219. We also proved that miR-219 could affect the proliferation and migration of HCC cells under hypoxic condition. In conclusion, our study demonstrated a novel HIF-1-miR-219-SMC4 regulatory pathway under hypoxic condition in HCC cells.

Vascular adaptations to hypoxia: molecular and cellular mechanisms regulating vascular tone

2007 ◽  
Vol 43 ◽  
pp. 105-120 ◽  
Author(s):  
Michael L. Paffett ◽  
Benjimen R. Walker
Keyword(s):  
Vascular Tone ◽  
Cellular Proliferation ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Hypoxia Inducible Factor ◽  
Systemic Circulation ◽  
Cellular Mechanisms ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Vasoconstriction ◽  
Adaptive Mechanisms ◽  
Adaptive Processes

Several molecular and cellular adaptive mechanisms to hypoxia exist within the vasculature. Many of these processes involve oxygen sensing which is transduced into mediators of vasoconstriction in the pulmonary circulation and vasodilation in the systemic circulation. A variety of oxygen-responsive pathways, such as HIF (hypoxia-inducible factor)-1 and HOs (haem oxygenases), contribute to the overall adaptive process during hypoxia and are currently an area of intense research. Generation of ROS (reactive oxygen species) may also differentially regulate vascular tone in these circulations. Potential candidates underlying the divergent responses between the systemic and pulmonary circulations may include Nox (NADPH oxidase)-derived ROS and mitochondrial-derived ROS. In addition to alterations in ROS production governing vascular tone in the hypoxic setting, other vascular adaptations are likely to be involved. HPV (hypoxic pulmonary vasoconstriction) and CH (chronic hypoxia)-induced alterations in cellular proliferation, ionic conductances and changes in the contractile apparatus sensitivity to calcium, all occur as adaptive processes within the vasculature.

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