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Title

A genetic polymorphism in the pannexin1 gene predisposes for the development of endothelial dysfunction with increasing BMI.

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Published in Biomolecules. 2020, vol. 10, no. 2, p. 208
Abstract Endothelial dysfunction worsens when body mass index (BMI) increases. Pannexin1 (Panx1) ATP release channels regulate endothelial function and lipid homeostasis in mice. We investigated whether the Panx1-400A>C single nucleotide polymorphism (SNP), encoding for a gain-of-function channel, associates with endothelial dysfunction in non-obese and obese individuals. Myocardial blood flow (MBF) was measured by 13N-ammonia positron emission/computed tomography at rest, during cold pressor test (CPT) or dipyridamole-induced hyperemia. Myocardial flow reserve (MFR) and endothelial function were compared in 43 non-obese (BMI < 30 kg/m2) vs. 29 obese (BMI 30 kg/m2) participants and genotyping for the Panx1-400A>C SNP was performed. Groups comprised subjects homozygous for the C allele (n = 40) vs. subjects with at least one A allele (n = 32). MBF (during CPT or hyperemia), MFR and endothelial function correlated negatively with BMI in the full cohort. BMI correlated negatively with MFR and endothelial function in non-obese Panx1-400C subjects, but not in Panx1-400A individuals nor in obese groups. BMI correlated positively with serum triglycerides, insulin or HOMA. MFR correlated negatively with these factors in non-obese Panx1-400C but not in Panx1-400A individuals. Here, we demonstrated that Panx1-400C SNP predisposes to BMI-dependent endothelial dysfunction in non-obese subjects. This effect may be masked by excessive dysregulation of metabolic factors in obese individuals.
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PMID: 32023876
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Article (Published version) (1.6 MB) - public document Free access
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Research group L'athérosclérose (665)
Projects FNS: 310030_182573
FNS: 3200B0_122237
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(ISO format)
MOLICA, Filippo et al. A genetic polymorphism in the pannexin1 gene predisposes for the development of endothelial dysfunction with increasing BMI. In: Biomolecules, 2020, vol. 10, n° 2, p. 208. doi: 10.3390/biom10020208 https://archive-ouverte.unige.ch/unige:130346

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Deposited on : 2020-02-11

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