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Updated: Jan 31, 2026

Isolation of Human Umbilical Vein Endothelial Cells HUVEC
Published on: April 28, 2007
Effects of thyroid-stimulating hormone on adhesion molecules and pro-inflammatory cytokines secretion in human
Attabak Toofani Milani1, Mohammad Hassan Khadem-Ansari1, Yousef Rasmi1
1Department of Biochemistry, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, I.R. Iran.
Insights
Thyroid-stimulating hormone (TSH) showed anti-inflammatory effects by down-regulating tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). However, TSH also increased markers of endothelial dysfunction and leukocyte adhesion, suggesting a complex role in atherosclerosis.
Area of Science:
- Endocrinology
- Cardiovascular Biology
- Cell Biology
Background:
- Atherosclerosis is a complex arterial disease linked to cardiovascular disorders, with endothelial dysfunction playing a key role.
- Hypothyroidism and thyroid hormone deficiency are associated with increased cardiovascular risks.
- Thyroid-stimulating hormone (TSH) effects on endothelial cells in the context of atherosclerosis require further elucidation.
Purpose of the Study:
- To investigate the impact of TSH on pro-inflammatory cytokines (TNF-α, IL-6), angiogenic factors (VEGF), and adhesion molecules (ICAM-1, E-selectin) in human umbilical vein endothelial cells (HUVECs).
- To assess the role of TSH in endothelial dysfunction and leukocyte adhesion, critical processes in atherogenesis.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) were treated with varying concentrations (1 and 2 μM) of TSH for different durations.
- Gene and protein expression of ICAM-1, VEGF, and E-selectin were analyzed using real-time PCR and Western blotting.
- Protein levels of TNF-α and IL-6 were quantified using ELISA.
Main Results:
- TSH treatment led to the downregulation of pro-inflammatory cytokines TNF-α and IL-6.
- Conversely, TSH significantly upregulated the expression of ICAM-1, E-selectin, and VEGF, indicating increased leukocyte adhesion and angiogenesis.
- These markers of endothelial dysfunction and angiogenic potential were elevated in TSH-treated HUVECs.
Conclusions:
- TSH exhibits a dual role in atherogenesis: it possesses anti-inflammatory properties but also promotes pathways involved in angiogenesis and leukocyte adhesion.
- The findings suggest that TSH influences vascular cell proliferation and adhesion, contributing to the complex pathophysiology of atherosclerosis.
- Further research is warranted to fully understand the implications of TSH's multifaceted actions in the context of vascular disease.
Abstract:
Atherosclerosis is a multifactorial disorder, which affects the arterial wall. It has been reported that, hypothyroidism and thyroid hormone deficiency are related to cardiovascular disorders. Also, endothelial dysfunction plays an essential role in the development of atherosclerosis. We aimed to evaluate the effects of thyroid-stimulating hormone (TSH) on pro-inflammatory tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), angiogenic vascular endothelial growth factor (VEGF) and leukocyte adhesion, intercellular adhesion molecule 1 (ICAM-1) and E-selectin in human umbilical vein endothelial cells (HUVECs). In this study, HUVEC cells were treated with 1 and 2 μM of TSH in different treatment times. The gene and protein expression of ICAM-1, VEGF, and E-selectin were performed by real-time polymerase chain reaction and western blotting, respectively. Likewise, TNF-α and IL-6 protein levels were determined by the ELISA method. VEGF, ICAM-1, and E-selectin as endothelial dysfunction markers and also, TNF-α and IL-6 as pro-inflammatory cytokines were detectable in HUVEC. Besides, the results of this study revealed that TSH treatment down-regulates TNF-α and IL-6. Evaluating the gene and protein expression data revealed the upregulation of ICAM-1, E-selectin, and VEGF in TSH treated cases in different periods of exposure. Considering the multiple actions of TSH, it could be concluded that TSH plays a controversial role in atherogenesis by anti-inflammatory effects and on the other side, angiogenesis and leukocyte adhesion induction which is related to vascular cell proliferation.
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