MAPK/ERK signal pathway involved expression of COX-2 and VEGF by IL-1β induced in human endometriosis stromal cells in vitro.

Fengying Huang, Jing Cao, Qiuhong Liu, Ying Zou, Hongyun Li, Tuanfang Yin
International journal of clinical and experimental pathology · 2013 · vol. 6(10) , pp. 2129–36 · PMID:24133591 · PMC3796235 · W1945845719
article OA: green CC0 ⤵ 24 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed
⚙ AI-generated summary by claude@2026-06, 2026-06-09 ⓘ

In human endometriosis stromal cells, IL-1β up-regulated COX-2 via the p38 MAPK pathway and increased VEGF release, with COX-2 involvement in the VEGF upregulation.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

OBJECTIVE: Now there are more and more evidences that Cyclooxygenase-2 (COX-2) plays an important role in angiogenesis of endometriosis (EMs). Vascular endothelial growth factor (VEGF) has a potent angiogenic activity. However, it is worth studying about the regulating mechanism of COX-2/COX-1 and VEGF in the development of human endometriosis in vitro. The current study was designed to investigate the effect of 4 cytokines on COX-2/COX-1 expression and the effect of IL-1β on VEGF release in human endometriosis stromal cells (ESC), and to explore the related signaling pathways involved in vitro. METHODS: Isolation, culture and identification of ESC. Cells were treated with 4 cytokines, and the inhibitor mitogen-activated protein-Erk (MEK) and the inhibitor p38 mitogen-activated protein kinase (MAPK) prior to adding cytokine IL-1β. COX-2 protein expression was measured by western blot and VEGF secretion was determined by ELISA. RESULTS: Among four kinds of cytokines, IL-1β treatment increased COX-2 protein expression and VEGF release in three ESC, and TNF-α had the same effect on COX-2 protein level as IL-1β only in ectopic and eutopic ESC, and MCSF had only slight effect on ectopic ESC. In contrast, cytokines had no effect on COX-1 expression. We also demonstrated that MAPK reduced the synthesis of COX-2 by IL-1β induced. COX-2 inhibitor reduced VEGF release by IL-1β induced. CONCLUSIONS: i) In human ESC in vitro, IL-1β up-regulated the COX-2 expression through the activation of p38 MAPK pathway, and not to COX-1. ii) Up-regulation of VEGF level by IL-1β treatment was found in human endometriosis stromal cell and COX-2 inhibitor was involved in this process.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cyclooxygenase 2 Endometriosis Interleukin-1beta MAP Kinase Signaling System Stromal Cells Vascular Endothelial Growth Factor A Adult Cyclooxygenase 2 Endometriosis Endometriosis Endometrium Endometrium Endometrium Endometrium Female Humans Interferon-gamma Interferon-gamma Interleukin-1beta Macrophage Colony-Stimulating Factor

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (31)

Cited by (24)

Source provenance

europepmc
last seen: 2026-07-04T06:08:07.471253+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:18:47.062786+00:00
License: CC0 · commercial use OK