ArticleScientific reports2022
Modified lipid metabolism and cytosolic phospholipase A2 activation in mesangial cells under pro-inflammatory conditions.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 13 citations in OpenAlex.
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- Comparative analysis of commercial human primary mesangial cell, implications for experimental design.BMC nephrology · 2025Article
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- Proteomic analysis of human kidney biopsies unveils emerging acute kidney injury very early after liver graft reperfusion.Journal of translational medicine · 2025Article
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- Cytosolic phospholipase A2 links tau pathology to insulin signaling impairment in Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Transcriptomic Profile of LinBMC genomics · 2024Article
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- The Use of Palmitoylethanolamide in the Treatment of Long COVID: A Real-Life Retrospective Cohort Study.Medical sciences (Basel, Switzerland) · 2022Article
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
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5 authors at 2 institutions in 1 country.
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Abstract
Diabetic kidney disease is a consequence of hyperglycemia and other complex events driven by early glomerular hemodynamic changes and a progressive expansion of the mesangium. The molecular mechanisms behind the pathophysiological alterations of the mesangium are yet to be elucidated. This study aimed at investigating whether lipid signaling might be the missing link. Stimulation of human mesangial cells with high glucose primed the inflammasome-driven interleukin 1 beta (IL-1β) secretion, which in turn stimulated platelet-derived growth factor (PDGF-BB) release. Finally, PDGF-BB increased IL-1β secretion synergistically. Both IL-1β and PDGF-BB stimulation triggered the formation of phosphorylated sphingoid bases, as shown by lipidomics, and activated cytosolic phospholipase cPLA2, sphingosine kinase 1, cyclooxygenase 2, and autotaxin. This led to the release of arachidonic acid and lysophosphatidylcholine, activating the secretion of vasodilatory prostaglandins and proliferative lysophosphatidic acids. Blocking cPLA2 release of arachidonic acid reduced mesangial cells proliferation and prostaglandin secretion. Validation was performed in silico using the Nephroseq database and a glomerular transcriptomic database. In conclusion, hyperglycemia primes glomerular inflammatory and proliferative stimuli triggering lipid metabolism modifications in human mesangial cells. The upregulation of cPLA2 was critical in this setting. Its inhibition reduced mesangial secretion of prostaglandins and proliferation, making it a potential therapeutical target.
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