Lamin A is involved in the development of vascular calcification induced by chronic kidney failure and phosphorus load

Bone
Isabel Quirós-GonzálezJosé Luis Fernández-Martín

Abstract

Vascular calcification remains one of the main factors associated to morbidity and mortality in both ageing and chronic kidney disease. Both hyperphosphataemia, a well-known promoter of vascular calcification, and abnormal processing defects of lamin A/C have been associated to ageing. The main aim of this study was to analyse the effect of phosphorus load in the differential expression pattern of genes and proteins, particularly of lamin A/C, which are involved in phenotypic change of the vascular smooth muscle cells to osteoblast-like cells. The in vivo study of the calcified abdominal aortas from nephrectomized rats receiving a high phosphorus diet showed among others, a repression of muscle related proteins and overexpression of lamin A/C. Similar results were observed in vitro, where primary vascular smooth muscle cells cultured in calcifying medium showed increased expression of prelamin A and lamin A and abnormalities in the nuclear morphology. Co-immunoprecipitation assays showed novel and important physical interactions between lamin A and RUNX2 during the process of calcification. In fact, the knockdown of prelamin A and lamin A inhibited the increase of Runx2, osteocalcin and osteopontin gene expression, calcium depo...Continue Reading

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Jan 14, 2017·Current Opinion in Cell Biology·Beatriz Dorado, Vicente Andrés
Dec 26, 2018·Frontiers in Cardiovascular Medicine·David NgaiMichelle P Bendeck
Sep 22, 2017·Annual Review of Physiology·Magda R HamczykVicente Andrés
Jan 6, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Yongjiang QianZhongqun Wang
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Oct 24, 2020·Clinica Chimica Acta; International Journal of Clinical Chemistry·Meng DuanKai Yin
Jun 18, 2021·International Urology and Nephrology·Jun PengJia-Qing Peng

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