A narrative review of research progress on the relationship between hypoxia-inducible factor-2α and wound angiogenesis.

OBJECTIVE: This article aims to pay attention to the latest research on the expression, activation and function of hypoxia-inducible factor-2α (HIF-2α) under hypoxia and non-hypoxia conditions, and summarizes the current knowledge about the interaction between hypoxia-inducible factor-2 and angiogenesis, hoping to understand its actions in physiology and disease, with the goal of providing a new strategy for the diagnosis and treatment of wounds. BACKGROUND: Wound healing is a complex and continuous process, involving coagulation, inflammation, angiogenesis, new tissue formation and extracellular matrix remodeling. Of these, angiogenesis is an essential step. One of the main reasons for non-healing or delayed healing of wounds in peripheral vascular diseases and diabetes is the reduced ability to regenerate microvessels through the process of angiogenesis, which has become the focus of new methods for treating chronic wounds. HIF-2α regulates many aspects of angiogenesis, including vascular maturation, cell migration, proliferation and metastasis. METHODS: Throughout extensive search of PubMed, summarize the medical research on HIF-2α to 2020. CONCLUSIONS: HIF-2α is necessary for normal embryonic development by stimulating the expression of angiogenic factors, such as vascular endothelial growth factor (VEGF). It is essential for the formation of new blood vessels in physiological and pathophysiological environments. Targeting HIF-2α in wound healing has much clinical significance for tissue repair.

Potentially fatal electrolyte imbalance caused by severe hydrofluoric acid burns combined with inhalation injury: A case report.

BACKGROUND: Hydrofluoric acid (HF) is one of the most common causes of chemical burns. HF burns can cause wounds that deepen and progress aggressively. As a result, HF burns are often severe even if they involve a small area of the skin. Published cases of HF burns have mostly reported small HF burn areas. Few cases of HF inhalation injury have been reported to date. CASE SUMMARY: A 24-year-old man suffered from extensive hydrofluoric acid burns covering 60% of the total body surface area (TBSA), including deep second degree burns on 47% and third degree burns on 13% of the TBSA, after he fell into a pickling pool containing 15% HF. Comprehensive treatments were carried out after the patient was admitted. Ventricular fibrillation occurred 9 times within the first 2 h, and the lowest serum Ca2+ concentration was 0.192 mmol/L. A dose of calcium gluconate (37 g) was intravenously supplied during the first 24 h, and the total amount of calcium gluconate supplementation was 343 g. Extracorporeal membrane oxygenation (ECMO) was applied for 8 d to handle the acute respiratory distress syndrome (ARDS) induced by the HF inhalation injury. The patient was discharged after 99 d of comprehensive treatment, including skin grafting. CONCLUSION: Extensive HF burns combined with an inhalation injury led to a potentially fatal electrolyte imbalance and ARDS. Adequate and timely calcium supplementation and ECMO application were the keys to successful treatment of the patient.

Involvement of NF-kappaB activation in the apoptosis induced by extracellular adenosine in human hepatocellular carcinoma HepG2 cells.

Adenosine can exhibit cytotoxic activity in vivo and in vitro, though its mechanisms are still uncertain. In this study, we investigated the adenosine-mediated apoptotic signaling pathway and the role of NF-kappaB in human hepatocellular carcinoma HepG2 cells. HepG2 cells were treated with different concentrations of adenosine for 12-48 h, and the effect of adenosine on cell proliferation was evaluated by MTT assay. The cytotoxicity of adenosine alone or in combination with an NF-kappaB inhibitor, pyrrolidine dithiocarbamate (PDTC), was also evaluated by MTT assay and the mode of cell death was detected by Hoechst 33342 staining. Cell cycle progress was performed by flow cytometry with PI staining. The protein expressions of Bcl-2, p53, NF-kappaB subunit p65, and caspase-3 were assayed by Western blot. Caspase-3 activity was measured by spectrophotomteric assay. The results showed that adenosine significantly reduced the viability of HepG2 cells in a dose- and time-dependent manner, with IC 50 (24 and 48 h) of 2.52 and 1.89 mmol x L(-1), respectively. The apoptotic index (percentage of sub-G1 phase) of HepG2 cells in adenosine treatment alone for 12 and 24 h or in combination with PDTC were 8.30%, 22.32% and 20.18%, 30.89%, respectively. All of them were higher than that in the control group (0.81%, p < 0.01). The characteristic changes of cell apoptosis (chromatin condensation and sub-G1 peak) were observed under fluorescent microscopy and flow cytometry. We also found that the apoptotic process triggered by adenosine was involved in G0-G1 cell-cycle arrest, enhanced the activity of caspase-3, upregulated p53 and NF-kappaB p65 expression, and downregulated Bcl-2 expression. Inhibition of NF-kappaB by PDTC decreased NF-kappaB p65 expression, enhanced cell apoptosis ratio, and increased caspase-3 activity. NF-kappaB may play an anti-apoptosis role in adenosine-induced HepG2 cytotoxicity.