TRPV4 modulation affects mitochondrial parameters in adipocytes and its inhibition upregulates lipid accumulation

Life Sci. 2024 Dec 1:358:123130. doi: 10.1016/j.lfs.2024.123130. Epub 2024 Oct 14.

Abstract

Enhanced lipid-droplet formation by adipocytes is a complex process and relevant for obesity. Using knock-out animals, involvement of TRPV4, a thermosensitive ion channel in the obesity has been proposed. However, exact role/s of TRPV4 in adipogenesis and obesity remain unclear and contradictory. Here we used in vitro culture of 3T3L-1 preadipocytes and primary murine-mesenchymal stem cells as model systems, and a series of live-cell-imaging to analyse the direct involvement of TRPV4 exclusively at the adipocytes that are free from other complex signalling as expected in in-vivo condition. Functional TRPV4 is endogenously expressed in pre- and in mature-adipocytes. Pharmacological inhibition of TRPV4 enhances differentiation of preadipocytes to mature adipocytes, increases expression of adipogenic and lipogenic genes, enhances cholesterol, promotes bigger lipid-droplet formation and reduces the lipid droplet temperature. On the other hand, TRPV4 activation enhanced the browning of adipocytes with increased UCP-1 levels. TRPV4 regulates mitochondrial-temperature, Ca2+-load, ATP, superoxides, cardiolipin, membrane potential (ΔΨm), and lipid-mitochondrial contact sites. TRPV4 also regulates the extent of actin fibres, affecting the cells mechanosensing ability. These findings link TRPV4-mediated mitochondrial changes in the context of lipid-droplet formation involved in adipogenesis and confirm the direct involvement of TRPV4 in adipogenesis. These findings may have broad implication in treating adipogenesis and obesity in future.

Keywords: ATP; Adipogenesis; F-actin; Lipid droplet; ROS; TRPV4.

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes* / metabolism
  • Adipogenesis* / physiology
  • Animals
  • Cell Differentiation
  • Cells, Cultured
  • Lipid Metabolism
  • Membrane Potential, Mitochondrial
  • Mesenchymal Stem Cells / drug effects
  • Mesenchymal Stem Cells / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria* / metabolism
  • TRPV Cation Channels* / genetics
  • TRPV Cation Channels* / metabolism
  • Up-Regulation

Substances

  • TRPV Cation Channels
  • Trpv4 protein, mouse