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Objective <p>Alteration of the expression of vascular endothelial growth factor (VEGF) and its receptors, VEGFR-1 and VEGFR-2, leads to aberrant angiogenesis in cancer; this is exacerbated by chronic stress. Our main aim was to determine the effect of chronic restraint stress on the expression of <i>Vegfr2</i>, the gene encoding VEGFR-2, in tumor, fat, skeletal muscle and brain in a murine model of lymphoma.</p> Results <p>We found that both chronic stress and tumor burden alter <i>Vegfr2</i> expression. Under chronic stress, <i>Vegfr2</i> is differentially expressed in inguinal adipose tissue, decreasing in tumor-free, and increasing in tumor-bearing animals. In skeletal muscle, brain, and tumor, <i>Vegfr2</i> expression was upregulated by chronic stress. Adipose tissue, brain and skeletal muscle of tumor-bearing animals also showed changes in <i>Vegfr2</i> expression during tumor progression. We also found that for skeletal muscle the combination of chronic stress and tumor burden enhances <i>Vegfr2</i> expression (23-folds).</p> Conclusion <p>Chronic stress and tumor burden influence <i>Vegfr2</i> expression in normal and tumoral tissues and their co-occurrence enhances its effect on skeletal muscle.</p>

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Tissue-specific changes in expression of Vegfr2 in tumor and normal tissues of lymphoma-bearing BALB/c mice under chronic restraint stress

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月14日

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  • Alonso A. Orozco-Flores,
  • Gloria Romero-Beltrán,
  • Diana Caballero-Hernández,
  • Deyanira Quistián-Martínez,
  • Ricardo Gomez-Flores,
  • Patricia Tamez-Guerra,
  • Cristina Rodríguez-Padilla

摘要

Objective

Alteration of the expression of vascular endothelial growth factor (VEGF) and its receptors, VEGFR-1 and VEGFR-2, leads to aberrant angiogenesis in cancer; this is exacerbated by chronic stress. Our main aim was to determine the effect of chronic restraint stress on the expression of Vegfr2, the gene encoding VEGFR-2, in tumor, fat, skeletal muscle and brain in a murine model of lymphoma.

Results

We found that both chronic stress and tumor burden alter Vegfr2 expression. Under chronic stress, Vegfr2 is differentially expressed in inguinal adipose tissue, decreasing in tumor-free, and increasing in tumor-bearing animals. In skeletal muscle, brain, and tumor, Vegfr2 expression was upregulated by chronic stress. Adipose tissue, brain and skeletal muscle of tumor-bearing animals also showed changes in Vegfr2 expression during tumor progression. We also found that for skeletal muscle the combination of chronic stress and tumor burden enhances Vegfr2 expression (23-folds).

Conclusion

Chronic stress and tumor burden influence Vegfr2 expression in normal and tumoral tissues and their co-occurrence enhances its effect on skeletal muscle.