Key result
Increased ganglioside GM1 on senescent arterial endothelial cells contributes to impaired insulin signaling.
Why the study?
Does ganglioside GM1 abundance contribute to insulin resistance in senescent human arterial endothelial cells?
Does ganglioside GM1 abundance contribute to insulin resistance in senescent human arterial endothelial cells?
Ganglioside GM1 accumulation on senescent human arterial endothelial cells causes insulin resistance, identifying it as a potential therapeutic target for aging-related vascular diseases.
May identify GM1 as a target in vascular senescence; hypothesis-generating from animal data and requires human validation.
Vascular endothelial cells (ECs) play central roles in physiologically important functions of blood vessels and contribute to the maintenance of vascular integrity. Therefore, it is considered that the impairment of EC functions leads to the development of vascular diseases. However, the molecular mechanisms of the EC dysfunctions that accompany senescence and aging have not yet been clarified. The carbohydrate antigens carried by glycoconjugates (e.g. glycoproteins, glycosphingolipids, and proteoglycans) mainly present on the cell surface serve not only as marker molecules but also as functional molecules. In this study, we have investigated the abundance and functional roles of glycosphingolipids in human ECs during senescence and aging. Among glycosphingolipids, ganglioside GM1 was highly expressed in abundance on the surface of replicatively and prematurely senescent ECs and also of ECs derived from an elderly subject. Insulin signaling, which regulates important functions of ECs, is impaired in senescent and aged ECs. Actually, by down-regulating GM1 on senescent ECs and overloading exogenous GM1 onto non-senescent ECs, we showed that an increased abundance of GM1 functionally contributes to the impairment of insulin signaling in ECs. Taken together, these findings provide the first evidence that GM1 increases in abundance on the cell surface of ECs under the conditions of cellular senescence and aging and causes insulin resistance in ECs. GM1 may be an attractive target for the detection, prevention, and therapy of insulin resistance and related vascular diseases, particularly in older people.
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Sasaki et al. (2015) studied Insulin resistance in senescent endothelial cells. Ganglioside GM1 modulation vs. Non-senescent endothelial cells or normal GM1 levels was evaluated on Insulin signaling impairment. Increased abundance of ganglioside GM1 on the surface of senescent human arterial endothelial cells functionally contributes to the impairment of insulin signaling.
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