Effect of Gracilaria fisheri sulfated galactan with increased sulfation on cell migration and expression of cell adhesion molecules in sodium oxalate-induced HK-2 cell injury
Issued Date
2025-08-01
Resource Type
ISSN
20499434
eISSN
20499442
Scopus ID
2-s2.0-105008968439
Journal Title
Biomedical Reports
Volume
23
Issue
2
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomedical Reports Vol.23 No.2 (2025)
Suggested Citation
Rudtanatip T., Phanphak J., Somintara S., El-Abid J., Wongprasert K., Kovensky J., Sakaew W. Effect of Gracilaria fisheri sulfated galactan with increased sulfation on cell migration and expression of cell adhesion molecules in sodium oxalate-induced HK-2 cell injury. Biomedical Reports Vol.23 No.2 (2025). doi:10.3892/br.2025.2001 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/111013
Title
Effect of Gracilaria fisheri sulfated galactan with increased sulfation on cell migration and expression of cell adhesion molecules in sodium oxalate-induced HK-2 cell injury
Corresponding Author(s)
Other Contributor(s)
Abstract
Exposure to oxalate crystals causes cellular injury and dysfunction in the renal tubular epithelium. Sulfated galactan with increased sulfation (SGS) from the red seaweed Gracilaria fisheri exhibits anti-urolithiasis effects by inhibiting oxalate crystal formation and preventing sodium oxalate (NaOX)-induced death of renal tubular (HK-2) cells. However, the effects of SGS on wound healing and adhesion molecule expression in NaOX-induced HK-2 cell injury remain unexplored. The present study investigated the effects of SGS on wound healing and the regulation of adhesion molecule expression in NaOX-induced HK-2 cell damage. The findings showed that SGS promoted wound healing in HK-2 cells following a scratch injury under NaOX-induced conditions. NaOX exposure increased the expression of CD44 and vimentin while decreasing the expression of EpCAM, E-cadherin, occludin and ZO-1, as demonstrated by reverse transcription-quantita-tive PCR, western blotting and immunofluorescence analysis. Treatment with SGS restored these adhesion molecule expression levels to near normal. Scanning electron microscopy revealed that SGS also reversed NaOX-induced morphological changes in HK-2 cells. Additionally, SGS reduced the expression of Akt and p38 while upregulating PI3K and Erk1/2 in NaOX-treated HK-2 cells. These results suggested that SGS enhances wound healing and regulates the expression of adhesion molecules, possibly through the PI3K/Akt and MAPK (p38 and Erk1/2) signaling pathways, highlighting the potential of SGS as a promising therapeutic compound for preventing and treating NaOX-induced renal damage.