Krüppel-Like Factor 13 Deficiency in Uterine Endometrial Cells Contributes to Defective Steroid Hormone Receptor Signaling but Not Lesion Establishment in a Mouse Model of Endometriosis1

Heard ME, Melissa E. Heard, Velarde MC, Michael C. Velarde, Giudice LC, Linda C. Giudice, Frank A. Simmen, Simmen FA, Rosalia C. M. Simmen, Simmen RC
Biology of reproduction · 2015 · vol. 92(6) , pp. 140 · doi:10.1095/biolreprod.115.130260 · PMID:25904015 · PMC4652611 · W1993345338
article OA: bronze CC0 ⤵ 6 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-11 ⓘ

KLF13 deficiency in mouse endometrial cells alters steroid hormone receptor signaling but does not affect endometriosis lesion establishment or growth.

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

Abstract

Krüppel-like Factor (KLF) 13 and the closely related KLF9 are members of the Sp/KLF family of transcription factors that have collectively emerged as essential regulators of tissue development, differentiation, proliferation, and programmed cell death. Steroid hormone-responsive tissues express multiple KLFs that are linked to progesterone receptor (PGR) and estrogen receptor (ESR) actions either as integrators or as coregulators. Endometriosis is a chronic disease characterized by progesterone resistance and dysregulated estradiol signaling; nevertheless, distinct KLF members' contributions to endometriosis remain largely undefined. We previously demonstrated promotion of ectopic lesion establishment by Klf9 null endometrium in a mouse model of endometriosis. Here we evaluated whether KLF13 loss of expression in endometrial cells may equally contribute to lesion formation. KLF13 transcript levels were lower in the eutopic endometria of women with versus women without endometriosis at menstrual midsecretory phase. In wild-type (WT) mouse recipients intraperitoneally administered WT or Klf13 null endometrial fragments, lesion incidence did not differ with donor genotype. No differences were noted for lesion volume, number, proliferation status, and apoptotic index as well. Klf13 null lesions displayed reduced total PGR and ESR1 (RNA and immunoreactive protein) and altered expression of several PGR and ESR1 target genes, relative to WT lesions. Unlike for Klf9 null lesions, changes in transcript levels for PGR-A, ESR1, and Notch/Hedgehog-associated pathway components were not observed for Klf13 null lesions. Results demonstrate lack of a causative relationship between endometrial KLF13 deficiency and lesion establishment in mice, and they support the broader participation of multiple signaling pathways, besides those mediated by steroid receptors, in the pathology of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Cell Cycle Proteins Endometriosis Endometrium Kruppel-Like Transcription Factors Receptors, Estrogen Receptors, Progesterone Repressor Proteins Signal Transduction Animals Apoptosis Apoptosis Cell Cycle Proteins Cell Cycle Proteins Cell Differentiation Cell Differentiation Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium

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 (50)

Cited by (5)

Source provenance

europepmc
last seen: 2026-09-19T06:15:14.566301+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:17:58.238279+00:00
License: CC0 · commercial use OK