Evidence map›Paper›PMID 35729637›Full record

ArticleReproductive biology and endocrinology : RB&E2022

Hyperandrogenism induces proportional changes in the expression of Kiss-1, Tac2, and DynA in hypothalamic KNDy neurons.

Hiroe Okada, Haruhiko Kanasaki, Tuvshintugs Tumurbaatar, Zolzaya Tumurgan, Aki Oride, Satoru Kyo

Open access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hiroe OkadaDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan.
Haruhiko KanasakiDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan. kanasaki@med.shimane-u.ac.jp.
Tuvshintugs TumurbaatarDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan.
Zolzaya TumurganDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan.
Aki OrideDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan.
Satoru KyoDepartment of Obstetrics and Gynecology, School of Medicine, Shimane University, 89-1 Enya Cho, Izumo, Shimane, 693-8501, Japan.
Shimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundKisspeptin released from Kiss-1 neurons in the hypothalamus plays an essential role in the control of the hypothalamic-pituitary-gonadal axis by regulating the release of gonadotropin-releasing hormone (GnRH). In this study, we examined how androgen supplementation affects the characteristics of Kiss-1 neurons.

methodsWe used a Kiss-1-expressing mHypoA-55 cell model that originated from the arcuate nucleus (ARC) of the mouse hypothalamus. These cells are KNDy neurons that co-express neurokinin B (NKB) and dynorphin A (DynA). We stimulated these cells with androgens and examined them. We also examined the ARC region of the hypothalamus in ovary-intact female rats after supplementation with androgens.

resultsStimulation of mHypoA-55 cells with 100 nM testosterone significantly increased Kiss-1 gene expression by 3.20 ± 0.44-fold; testosterone also increased kisspeptin protein expression. The expression of Tac3, the gene encoding NKB, was also increased by 2.69 ± 0.64-fold following stimulation of mHypoA-55 cells with 100 nM testosterone. DynA gene expression in these cells was unchanged by testosterone stimulation, but it was significantly reduced at the protein level. Dihydrotestosterone (DHT) had a similar effect to testosterone in mHypoA-55 cells; kisspeptin and NKB protein expression was significantly increased by DHT, whereas it significantly reduced DynA expression. In ovary-intact female rats, DTH administration significantly increased the gene expression of Kiss-1 and Tac3, but not DynA, in the arcuate nucleus. Exogenous NKB and DynA stimulation failed to modulate Kiss-1 gene expression in mHypoA-55 cells. Unlike androgen stimulation, prolactin stimulation did not modulate kisspeptin, NKB, or DynA protein expression in these cells.

conclusionsOur observations imply that hyperandrogenemia affects KNDy neurons and changes their neuronal characteristics by increasing kisspeptin and NKB levels and decreasing DynA levels. These changes might cause dysfunction of the hypothalamic-pituitary-gonadal axis.

Indexed as

DynorphinsHyperandrogenismAndrogensAnimalsFemaleGonadotropin-Releasing HormoneHypothalamusKisspeptinsMiceNeurokinin BNeuronsRatsTachykininsTestosteroneAndrogensDynorphinsGonadotropin-Releasing HormoneKiss1 protein, ratKisspeptinsNeurokinin BTachykininsTestosteroneAndrogenHypothalamusKisspeptinProlactinTestosterone

Identifiers

PMID35729637
PMCPMC9210811
OpenAlexW4283208511

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.