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Cell-cell contacts via N-cadherin induce a regulatory renin secretory phenotype in As4.1 cells

Jai Won Chang1,2, Soohyun Kim1, Eun Young Lee3

  • 1Department of Physiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology
|October 27, 2022
PubMed

Insights

Researchers induced regulated active renin secretion in a cell line by promoting cell-cell contact. This finding reveals myosin light chain phosphorylation regulates active renin secretion via exocytosis.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Lack of a clonal renin-secreting cell line impedes research on renin secretion regulation.
  • Investigating renin secretion mechanisms requires suitable cellular models.

Purpose of the Study:

  • To induce regulated active renin secretion in the As4.1 cell line.
  • To investigate the molecular mechanisms underlying renin secretion regulation.

Main Methods:

  • Phenotypic switching of As4.1 cells by inducing postconfluence and cell-cell contact via N-cadherin.
  • Stimulation of switched cells to assess active renin secretion.
  • Analysis of myosin light chain phosphorylation in regulating renin secretion.

Main Results:

  • Postconfluence and N-cadherin-mediated cell-cell contacts triggered phenotypic switching in As4.1 cells.
  • Switched cells exhibited regulated active renin secretion in response to stimuli.
  • Active renin secretion via exocytosis is regulated by 20 kDa myosin light chain phosphorylation/dephosphorylation.

Conclusions:

  • Phenotypic switching of As4.1 cells provides a model for regulated active renin secretion.
  • Myosin light chain phosphorylation is a key regulator of active renin secretion.
  • This study establishes a novel cellular model for studying renin secretion mechanisms.
Keywords:
MRTF-AMyosin light chainMyosin light chain phosohatase-1Myosin light-chain kinaseN-cadherinPhenotype switching

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