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<p>We studied the effect of hypoxic stress on the efficiency of intercellular communication through gap junctions (GJ) in cultured endothelial cells. The cells were maintained under conditions of normoxia (20% O<sub>2</sub>; group 1), after which GJ were either pharmacologically blocked (group 2), exposed to hypoxic stress (&lt; 0.1% O2, 24 h; group 3), or simultaneously blocked and exposed to hypoxic stress (group 4). Carbenoxolone, a specific GJ inhibitor, was used to suppress connexin-mediated signaling. Hypoxic stress induced a 2.1-fold increase in <i>HIF1A</i> expression (<i>p</i> ⩽ 0.05) and stimulated directed cell migration (by 1.6 times), without significantly affecting the formation of capillary-like structures. In contrast, inhibition of GJ reduced both directed and random migration (by more than 2 times; <i>p</i> ⩽ 0.05), completely suppressed the formation of capillary-like networks, and was accompanied by reduced expression of <i>HIF1A</i> (by 1.6 times) and <i>GJA1</i> (by 2 times; <i>p</i> ⩽ 0.05). Hypoxia moderately increased the proportion of necrotic cells without substantially influencing overall viability, whereas GJ blockade reduced necrosis, possibly due to disruption of intercellular transmission of death signals. These findings indicate a critical role of functionally active GJ in mediating the hypoxia-induced angiogenic response of endothelial cells, including modulation of key gene expression, migration, and capillary-like structure formation <i>in vitro</i>.</p>

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Regulation of the Angiogenic Potential of Endothelial Cells In Vitro under Conditions of Acute Hypoxic Stress: The Role of Homotypic Communication via Gap Junctions

  • 期刊论文

  • 发表日期：

    2025年11月1日

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  • M. I. Ezdakova

摘要

We studied the effect of hypoxic stress on the efficiency of intercellular communication through gap junctions (GJ) in cultured endothelial cells. The cells were maintained under conditions of normoxia (20% O2; group 1), after which GJ were either pharmacologically blocked (group 2), exposed to hypoxic stress (< 0.1% O2, 24 h; group 3), or simultaneously blocked and exposed to hypoxic stress (group 4). Carbenoxolone, a specific GJ inhibitor, was used to suppress connexin-mediated signaling. Hypoxic stress induced a 2.1-fold increase in HIF1A expression (p ⩽ 0.05) and stimulated directed cell migration (by 1.6 times), without significantly affecting the formation of capillary-like structures. In contrast, inhibition of GJ reduced both directed and random migration (by more than 2 times; p ⩽ 0.05), completely suppressed the formation of capillary-like networks, and was accompanied by reduced expression of HIF1A (by 1.6 times) and GJA1 (by 2 times; p ⩽ 0.05). Hypoxia moderately increased the proportion of necrotic cells without substantially influencing overall viability, whereas GJ blockade reduced necrosis, possibly due to disruption of intercellular transmission of death signals. These findings indicate a critical role of functionally active GJ in mediating the hypoxia-induced angiogenic response of endothelial cells, including modulation of key gene expression, migration, and capillary-like structure formation in vitro.