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High-Calcium Microenvironment during the Development of Kidney Calculi Can Promote Phenotypic Transformation of

Li-Sha Li1, Yun-Peng Zhu2, Qi-Dong Xia1

  • 1Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030 Hubei, China.

Biomed Research International
|March 11, 2022
PubMed
Abstract

Insights

Stromal Interaction Molecule-1 (STIM1) promotes NRK-52E cell phenotypic transformation in high-calcium environments. Suppressing STIM1 expression accelerates this transformation, highlighting its critical role in cellular response to calcium.

Area of Science:

  • Cell Biology
  • Renal Physiology
  • Molecular Mechanisms

Background:

  • High calcium environments can induce cellular changes in kidney cells.
  • Stromal Interaction Molecule-1 (STIM1) is a key regulator of calcium homeostasis.
  • The role of STIM1 in renal cell phenotypic transformation under hypercalcemia is not fully understood.

Purpose of the Study:

  • To investigate the role of STIM1 in the phenotypic transformation of NRK-52E cells.
  • To determine if STIM1 expression is altered in a high-calcium microenvironment.
  • To elucidate the functional significance of STIM1 in cellular responses to high calcium.

Main Methods:

  • NRK-52E cells were exposed to high calcium concentrations.
  • Cell viability (CCK-8) and apoptosis (flow cytometry) were assessed.
  • Protein and gene expression of phenotypic markers (E-cadherin, OPN) and calcium channels (STIM1, Orai1) were analyzed (Western blotting, qRT-PCR).
  • STIM1 expression was manipulated using plasmids for upregulation and shRNA for downregulation.
  • Intracellular calcium levels were measured via flow cytometry.

Main Results:

  • High calcium promoted phenotypic transformation and calcium salt adhesion in NRK-52E cells.
  • High calcium suppressed STIM1 protein expression.
  • STIM1 downregulation enhanced phenotypic transformation.
  • STIM1 overexpression and matrix gla protein (MGP) gene silence reversed these effects.

Conclusions:

  • STIM1 plays a significant role in promoting phenotypic transformation of NRK-52E cells.
  • STIM1 acts as a crucial mediator in the cellular response to high-calcium microenvironments.
  • Modulation of STIM1 offers a potential target for managing hypercalcemia-induced cellular changes.

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