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http://purl.uniprot.org/citations/36453600http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/36453600http://www.w3.org/2000/01/rdf-schema#comment"

Problem

The increased hypothalamic neurokinin B (NKB) level may contribute to the hyperactive LH pulse secretion in Polycystic ovary syndrome (PCOS). However, the expression and role of the neurokinin B-neurokinin 3 receptor (NKB-NK3R) system in the local ovarian tissue of PCOS have not been clarified. We constructed in vivo and in vitro models to elucidate the mechanism of the NKB-NK3R pathway in reproductive endocrine disorders of PCOS.

Method of study

The granulosa cell line-KGN cells were set in palmitic acid (PA) and dihydrotestosterone (DHT) to simulate the PCOS-like conditions. And we used the high-fat/high-glucose diet to build a PCOS-like mice model and neurokinin 3 receptor antagonist (NK3Ra) was administered to half of the mice. The expression of the NKB-NK3R system, mitochondrial functions, hormone levels, and inflammatory state was evaluated.

Results

The PCOS-like stimulations induced the NKB-NK3R system and MAPK-ERK pathway overexpression in KGN cells, in an approximate dose and time-dependent manner. The NKB-NK3R system overactivated the MAPK-ERK pathway to increase NNT overexpression, disturb NADH/NADPH pools, aggravate the oxidation state, and decrease ATP production. With overexpression of the NKB-NK3R system in the local ovarian tissue, ovulatory dysfunction, progesterone deficiency, and pro-inflammatory states were apparent in PCOS-like mice. Antagonizing the receptor, NK3R, reversed the adverse reproductive endocrine phenotypes via improving mitochondrial dysfunction.

Conclusions

In addition to the central regulation, local ovarian overexpression of the NKB-NK3R system participated in the adverse reproductive endocrine phenotypes, supporting the therapeutic implications of NK3Ra for PCOS."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.org/dc/terms/identifier"doi:10.1111/aji.13663"xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/author"Guo F."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/author"Zhu X."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/author"Fernando T."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/name"Am J Reprod Immunol"xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/pages"e13663"xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/title"The overexpression of neurokinin B-neurokinin 3 receptor system exerts direct effects on the ovary under PCOS-like conditions to interfere with mitochondrial function."xsd:string
http://purl.uniprot.org/citations/36453600http://purl.uniprot.org/core/volume"89"xsd:string
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