Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression

Alexander Kotlyar, Alexander M Kotlyar, Kotlyar AM, Ramanaiah Mamillapalli, Valerie A. Flores, Hugh S. Taylor
Molecular human reproduction · 2021 · vol. 27(4) · doi:10.1093/molehr/gaab016 · PMID:33693775 · PMC8454207 · W3133957550
Lab / animal OA: bronze CC0 ⤵ 23 in-corpus citations
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Tofacitinib treatment reduced endometriosis lesion size and adhesion burden in mice by inhibiting STAT3 phosphorylation in various cell types.

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Abstract

Endometriosis is a widespread gynecologic condition affecting up to 15% of women of reproductive age. The Janus kinase/signal transducer and activator of transcription (JAK/STAT3) pathway is upregulated in endometriosis and is a therapeutic target. Here we sought to determine the effect of Tofacitinib, a JAK inhibitor in widespread clinical use, on JAK/STAT signaling in endometriosis and lesion growth. Endometriosis was surgically induced in C57BL/6 mice using homologous uterine horn transplantation. Lesions were allowed to form over 4 weeks followed by Tofacitinib (10 mg/kg) or vehicle administered by oral gavage over 4 weeks. Tofacitinib treatment in vivo led to endometriosis lesion regression and reduced adhesion burden compared to vehicle treatment. In vitro studies on Ishikawa cells showed that Tofacitinib reduced hypoxia-inducible factor 1α and vascular endothelial growth factor mRNA levels at 12 and 24 h. Western blot analysis showed that Tofacitinib effectively reduced STAT3 phosphorylation in Ishikawa cells and human primary stromal and epithelial cells from eutopic endometrium of patients with and without endometriosis. This study suggests that the inhibition of JAK/STAT signaling using Tofacitinib may be a viable method for the treatment of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Animals Animals Female Female Humans Humans Mice Mice Mice, Inbred C57BL Mice, Inbred C57BL Piperidines Piperidines Pyrimidines Pyrimidines Pyrimidines

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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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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Cited by (27)

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