Role of Na/K-ATPase α1 caveolin-binding motif in adipogenesis
American Journal of Physiology - Cell Physiology, ISSN: 1522-1563, Vol: 327, Issue: 1, Page: C48-C64
2024
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New Findings from Marshall University in the Area of Vesicular Transport Proteins Published (Role of Na/K-ATPase a1 Caveolin-Binding Motif in Adipogenesis)
2024 MAY 21 (NewsRx) -- By a News Reporter-Staff News Editor at Genomics & Genetics Daily -- Investigators publish new report on vesicular transport proteins.
Article Description
Deficiencies in mice and in humans have brought to the fore the importance of the caveolar network in key aspects of adipocyte biology. The conserved N-terminal caveolin-βinding motif (CBM) of the ubiquitous Na/K-ATPase (NKA) a1 isoform, which allows NKA/caveolin-1 (Cav1) interaction, influences NKA signaling and caveolar distribution. It has been shown to be critical for animal development and ontogenesis, as well as lineage-specific differentiation of human induced pluripotent stem cells (hiPSCs). However, its role in postnatal adipogenesis has not been fully examined. Using a genetic approach to alter CBM in hiPSCderived adipocytes (iAdi-mCBM) and in mice (mCBM), we investigated the regulatory function of NKA CBM signaling in adipogenesis. Seahorse XF cell metabolism analyses revealed impaired glycolysis and decreased ATP synthesis-coupled respiration in iAdi-mCBM. These metabolic dysfunctions were accompanied by evidence of extensive remodeling of the extracellular matrix (ECM), including increased collagen staining, overexpression of ECM marker genes, and heightened TGF-β signaling uncovered by RNAseq analysis. Rescue of mCBM by lentiviral delivery of WT NKA a1 or treatment of mCBM hiPSCs with the TGF-β inhibitor SB431542 normalized ECM, suggesting that NKA CBM signaling integrity is required for adequate control of TGF-β signaling and ECM stiffness during adipogenesis. The physiological impact was revealed in mCBM male mice with reduced fat mass accompanied by histological and transcriptional evidence of elevated adipose fibrosis and decreased adipocyte size. Based on these findings, we propose that the genetic alteration of the NKA/Cav1 regulatory path uncovered in human iAdi leads to lipodystrophy in mice.
Bibliographic Details
American Physiological Society
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