ArticleDiabetology & metabolic syndrome2025
THBS1 regulates the function and insulin sensitivity of HTR8/SVneo cells treated with high glucose through the RhoA/ROCK1 signaling pathway.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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1 citing paper in PubMed.
- Correction: THBS1 regulates the function and insulin sensitivity of HTR8/SVneo cells treated with high glucose through the RhoA/ROCK1 signaling pathway.Diabetology & metabolic syndrome · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimGestational diabetes mellitus (GDM) increases the risk of maternal and fetal complications and impairs insulin sensitivity and placental function. This study aimed to explore the effect of thrombospondin-1 (THBS1) on HTR8/SVneo cell function and insulin sensitivity in GDM.
methodsPlacental tissues from pregnant women with GDM and normoglycemic pregnant women were collected, and HTR8/SVneo cells were exposed to normal and high glucose conditions. By overexpressing and knocking down THBS1, its effects on cell viability, migration, secretion of inflammatory factors, insulin signaling and glucose uptake were observed. qRT-PCR, Western blot, MTT, scratch test and ELISA were used for detection.
resultsCompared with the normal group, the expression of THBS1 in placenta tissue and HTR8/SVneo cells under high glucose conditions in the GDM group was significantly increased. THBS1 overexpression reduced cell viability and migration ability, increased the secretion of inflammatory factors, inhibited insulin signaling, and reduced glucose uptake; on the contrary, THBS1 knockdown significantly improved these indicators. In addition, the activation of the RhoA/ROCK pathway plays an important regulatory role in the effects of THBS1.
conclusionTHBS1 impairs the function and insulin sensitivity of HTR8/SVneo cells by inhibiting insulin signaling and activating the RhoA/ROCK pathway. This indicates that THBS1 may play an important role in the pathogenesis of GDM and become a potential therapeutic target.
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