The role of nuclear factor-kappa-B p50 subunit in the development of endometriosis

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p50 knockout mice exhibited reduced endometrial implant size, phosphorylated p65, and PKCepsilon expression, indicating p50's role in endometriosis development.

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This paper investigated the role of the NF-kappaB p50 subunit in endometriosis by cross-transplanting endometrial fragments between p50 knockout and wild-type mice (and vice versa) and by autotransplanting within each genotype to induce endometriosis, followed by measuring implant size and assessing immunoreactivity to phosphorylated p65, PKCepsilon, and TRPV1 in ectopic and eutopic endometrium and in vagina. p50 deletion significantly reduced the size of endometrial implants, and reduced p-p65 and PKCepsilon immunoreactivity in both ectopic implants and eutopic endometrium/vagina, while TRPV1 was not affected. The authors also reported that p50 deletion disrupted NF-kappaB activation and PKCepsilon expression in eutopic endometrium and vagina, suggesting a regulatory link involving nociception-related signaling. This paper is centrally about endometriosis — it specifically tests how NF-kappaB p50 influences endometriosis development and associated inflammatory/nociceptive markers.

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Abstract

p50 is a member of the NF-kappaB family known to be involved in endometriosis. To gain insight into the roles of p50 in the development of endometriosis, we cross-transplanted endometrial fragments from p50 knockout mice to wild-type mice and vice versa, and also autotransplanted the fragments within the knockout and wild-type mice, inducing endometriosis. We then evaluated the size of the endometrial implants, and immunoreactivity to phosphorylated p65 (p-p65), PKCepsilon and TRPV1 in ectopic and eutopic endometrium as well as in vagina. We found that p50 deletion significantly reduces the size of endometrial implants. The immunoreactivity to p-p65 and PKCepsilon, but not TRPV1, was reduced in endometrial implants in p50 knockout mice. Deletion of p50 significantly reduced p-p65 and PKCepsilon, but not TRPV1, expression in eutopic endometrium and vagina. It also disrupts NF-kappaB activation and PKCepsilon expression in eutopic and vagina, suggesting the role of NF-kappaB in regulating PKCepsilon, which plays an important role in nociception. These data show that p50 is involved in the development of endometriosis and may be a promising therapeutic target.
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Abstract

p50 is a member of the NF-kappaB family known to be involved in endometriosis. To gain insight into the roles of p50 in the development of endometriosis, we cross-transplanted endometrial fragments from p50 knockout mice to wild-type mice and vice versa, and also autotransplanted the fragments within the knockout and wild-type mice, inducing endometriosis. We then evaluated the size of the endometrial implants, and immunoreactivity to phosphorylated p65 (p-p65), PKCepsilon and TRPV1 in ectopic and eutopic endometrium as well as in vagina. We found that p50 deletion significantly reduces the size of endometrial implants. The immunoreactivity to p-p65 and PKCepsilon, but not TRPV1, was reduced in endometrial implants in p50 knockout mice. Deletion of p50 significantly reduced p-p65 and PKCepsilon, but not TRPV1, expression in eutopic endometrium and vagina. It also disrupts NF-kappaB activation and PKCepsilon expression in eutopic and vagina, suggesting the role of NF-kappaB in regulating PKCepsilon, which plays an important role in nociception. These data show that p50 is involved in the development of endometriosis and may be a promising therapeutic target.

Keywords

- Endometriosis - inflammation - NF- kappaB - p50 - p65 - PKCepsilon - TRPV1

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometrium NF-kappa B p50 Subunit Animals Endometriosis Endometrium Endometrium Female Immunohistochemistry Mice Mice, Knockout NF-kappa B p50 Subunit NF-kappa B p50 Subunit Protein Kinase C-epsilon Protein Kinase C-epsilon Protein Kinase C-epsilon Statistics, Nonparametric Transcription Factor RelA Transcription Factor RelA Transcription Factor RelA

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europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
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