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Data on hypoxia-induced VEGF, leptin and NF-kB p65 expression
Azizah Al-Anazi1, Ranjit Parhar1, Soad Saleh1
1Department of Cell Biology, Riyadh 11211, Saudi Arabia.
Data in Brief
|December 15, 2018
Summary
Hypoxia triggers leptin and VEGF release in human fat cells, a process regulated by intracellular calcium and NF-κB signaling pathways. Blocking these pathways reduces the hypoxia-induced secretion of these key molecules.
Area of Science:
- Cell Biology
- Endocrinology
- Molecular Biology
Background:
- Hypoxia, a state of low oxygen, influences various cellular functions.
- Leptin and VEGF are crucial adipokines involved in metabolism and angiogenesis.
- NF-κB is a key transcription factor regulating inflammatory and stress responses.
Purpose of the Study:
- To investigate the role of intracellular calcium and NF-κB in hypoxia-induced secretion of leptin, VEGF, IL-6, and adiponectin.
- To elucidate the molecular mechanisms linking hypoxia to adipokine regulation in human adipocytes.
Main Methods:
- Human adipocytes were subjected to hypoxic conditions (0.5-1.5% oxygen).
- Cells were treated with BAPTA-AM (calcium chelator) or SN50 (NF-κB inhibitor).
- Gene expression analysis was performed using RNA isolation and PCR.
Main Results:
- Hypoxia induced the expression of VEGF and leptin in human adipocytes.
- Treatment with BAPTA-AM reduced hypoxia-induced VEGF and leptin expression.
- Hypoxia also induced NF-κB p65 expression, suggesting its involvement.
Conclusions:
- Intracellular calcium and NF-κB signaling are critical regulators of hypoxia-induced leptin and VEGF secretion in human adipocytes.
- These findings provide insights into the cellular response to low oxygen environments.
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