KCNK2-mediated regulation of MMP-2/9 by PlGF influences uterine artery function in pregnancy-induced hypertension

BMC Pregnancy Childbirth. 2025 Jun 2;25(1):646. doi: 10.1186/s12884-025-07743-5.

Abstract

Background: Pregnancy induced hypertension (PIH) is characterized by aberrant uterine arterial remodeling, a process tightly associated with an imbalance between placental growth factor (PlGF) and soluble fms like tyrosine kinase 1 (sFlt 1) as well as the down regulation of matrix metalloproteinases 2/9 (MMP 2/9). This study investigated the regulatory effect of PlGF on the two pore domain potassium channel KCNK2 and its downstream targets MMP 2/9, and explored the role of the PlGF KCNK2 MMP 2/9 axis in PIH related uterine arterial dysfunction.

Methods: In vitro, human aortic endothelial cells (HAECs) were assessed for proliferation and migration using CCK 8 and Transwell assays. Nitric oxide (NO) and endothelin 1 (ET 1) levels were quantified by ELISA, while KCNK2 and MMP 2/9 expression was analyzed by Western blotting. In vivo, a Sprague Dawley rat PIH model was established to monitor blood pressure and 24 h urinary protein. Hematoxylin-eosin staining was used to measure uterine arterial intimal thickness; endothelial nitric oxide synthase (eNOS) and ET 1 localization was determined by immunohistochemistry, and KCNK2 as well as MMP 2/9 expression was quantified by immunohistochemistry and Western blotting.

Results: 2,2,2 Trichloroethanol and PlGF significantly enhanced endothelial cell proliferation and migration, increased NO, decreased ET 1, and up regulated KCNK2 and MMP 2/9 expression (P < 0.05); ropivacaine produced opposite effects. PIH rats exhibited markedly elevated blood pressure and urinary protein, intimal thickening, reduced eNOS and elevated ET 1, together with diminished MMP 2/9 expression. Combined treatment with PlGF and 2,2,2 trichloroethanol lowered blood pressure and urinary protein, attenuated intimal thickness, increased eNOS and decreased ET 1, and up regulated KCNK2 and MMP 2/9 (P < 0.05).

Conclusion: 2,2,2 Trichloroethanol activates KCNK2, elevates MMP 2/9, and improves uterine arterial endothelial function, while PlGF synergizes with KCNK2 signaling to potentiate these effects. The PlGF KCNK2 MMP 2/9 axis plays a pivotal regulatory role in the vascular pathology of PIH, highlighting its potential as a therapeutic target for PIH related vascular dysfunction.

Keywords: KCNK2; Matrix metalloproteinases (MMP-2/9); Placental growth factor (PlGF); Pregnancy-induced hypertension (PIH); Uterine artery.

MeSH terms

  • Animals
  • Cell Movement
  • Cell Proliferation
  • Disease Models, Animal
  • Endothelial Cells / metabolism
  • Endothelin-1 / metabolism
  • Female
  • Humans
  • Hypertension, Pregnancy-Induced* / metabolism
  • Hypertension, Pregnancy-Induced* / physiopathology
  • Matrix Metalloproteinase 2* / metabolism
  • Matrix Metalloproteinase 9* / metabolism
  • Nitric Oxide / metabolism
  • Placenta Growth Factor* / metabolism
  • Placenta Growth Factor* / pharmacology
  • Potassium Channels, Tandem Pore Domain* / metabolism
  • Pregnancy
  • Rats
  • Rats, Sprague-Dawley
  • Uterine Artery* / metabolism
  • Uterine Artery* / physiopathology

Substances

  • Placenta Growth Factor
  • Matrix Metalloproteinase 2
  • Matrix Metalloproteinase 9
  • Nitric Oxide
  • Endothelin-1
  • Potassium Channels, Tandem Pore Domain

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