Ask about this productRelated genes to: KiSS1 Blocking Peptide
- Gene:
- KISS1 NIH gene
- Name:
- KiSS-1 metastasis suppressor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-18
- Date modifiied:
- 2018-01-05
Related products to: KiSS1 Blocking Peptide
Related articles to: KiSS1 Blocking Peptide
- Cardiovascular diseases are the leading cause of global mortality and have been associated with alterations in fetal programming. Maternal hypothyroidism (MH) impairs placental function and induces intrauterine growth restriction (IUGR), both of which are risk factors for cardiovascular disease. Kisspeptin-10 (Kp10) has been shown to improve feto-placental development in hypothyroid rats, but its effects on intrauterine cardiac development remain unknown. MH was induced in Wistar rats using propylthiouracil (PTU), and Kp10 administration began on gestational day 8. Offspring hearts were analyzed at fetal day 18 and postnatal days 3 and 21. MH reduced fetal and postnatal body and heart mass, impaired cardiomyocyte proliferation, and dysregulated apoptotic and angiogenic markers. Maternal Kp10 administration enhanced postnatal weight gain, restored cardiomyocyte proliferation and nuclear density, and positively modulated apoptotic (Bax/Bcl2) and angiogenic (Vegf, Ang2, Flk1) pathways. However, it increased redox (8-OHdG) and endoplasmic reticulum (ER) stress (Grp78, Chop) mediators in fetal hearts, while reduced postnatal Chop expression in both sexes. Collectively, these findings demonstrate that maternal hypothyroidism disrupts cardiac development and postnatal cardiac programming, whereas maternal Kp10 administration partially mitigates these effects, highlighting novel mechanisms through which kisspeptin may positively regulate cardiac development. - Source: PubMed
Publication date: 2026/09/11
Barbosa Erikles MacedoRodrigues Natalia PanhocaSantos Bianca ReisDos Anjos Cordeiro Jeane Martinhada Silva Thayna Queiroz MenezesOliveira Cibele LuzSantos Luciano CardosoCunha Maria Clara da Silva GalrãoSerakides RogeriaSilva Juneo Freitas - Pulsatile gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion are essential for reproductive function and are thought to be governed by arcuate nucleus kisspeptin Kiss1 neurons via neurokinin B (NKB) signaling through TacR3. However, discrepancies between ex vivo and in vivo pharmacology limit mechanistic understanding of how TacR3 activation regulates pulsatile hormone release. We developed and synthesized a photoswitchable TacR3 agonist (azo-senktide) and characterized its photochemical and pharmacological properties using UV-Vis spectroscopy, TacR3-expressing HEK293T cells, electrophysiology in mouse hypothalamic slices, and in vivo optofluidic delivery combined with light stimulation to assess LH secretion in freely moving mice. Azo-senktide reversibly photoisomerized between inactive (trans) and more potent (cis) conformations. In cells, light activation enhanced TacR3-mediated Ca signaling. In brain slices, photostimulation depolarized and increased firing of Kiss1 neurons through a mechanism consistent with the established TacR3-TRPC5 signaling pathway. In vivo, optical activation of azo-senktide in the arcuate nucleus elicited a time-locked LH pulse at an intermediate dose, whereas lower or higher doses were ineffective, indicating a nonlinear, dose-dependent response. These findings demonstrate that temporally gated TacR3 activation via photoswitchable azo-senktide evokes an increase in LH, revealing that neurokinin B signaling in the Kiss1 network depends on activation dynamics, reconciles inconsistencies, and establishes photopharmacology as a powerful approach for probing neuroendocrine timing mechanisms. - Source: PubMed
Qiu JianLin YanyanBartram EmilyTobias Janelle MMuñoz AntonioLi Xiao FengHalls Victoria SFrank James AKelly Martin JO'Byrne Kevin T - - Source: PubMed
- Most temperate animals exhibit seasonal rhythms in reproductive physiology and behaviour. Gonadotropin-releasing hormone (GnRH) cells in the preoptic area (POA) and kisspeptin (Kiss) cells in the anteroventral periventricular (AvPv) nucleus are critical for timing photoperiod-induced changes in seasonal reproduction. In response to prolonged exposure to photoperiod cues, many rodents exhibit endogenously generated programmed changes in physiology that reflect a circannual timing mechanism. Here we used transcriptome sequencing coupled with measurements of surface body temperature and testes mass across a simulated circannual interval timer to characterize the molecular changes involved in the seasonal control of reproduction and surface body temperature. Adult male Djungarian hamsters were collected after exposure to short photoperiod on 4-week intervals from 4 to 32 weeks. The POA and AvPv transcriptomes from short-photoperiod hamsters were compared to a long photoperiod reference group. Our analyses confirmed robust photoperiodic regulation of Kiss1 mRNA expression in the AvPv. Weighted gene co-expression network analyses (WGCNAs) identified hundreds (POA: 211, AvPv: 415) of transcripts that were associated with testes mass. Gene set enrichment analysis (GSEA) identified 'gonadotropin secretion' and 'glial cell proliferation' as the primary pathways associated with circannual interval timing. Vimentin had a strong negative association with testes mass, indicating AvPv glial morphology may increase during gonadal involution. In the POA, pathways associated with 'regulation at synapse' and 'regulation of synaptic plasticity' were highly enriched and transcripts positively associated with gonadal involution indicated that ribosomal plasticity and intracellular calcium signalling are key mechanisms involved in seasonal reproduction. WGCNAs identified 567 transcripts in the POA that were significantly associated with surface body temperature. GSEA discovered thyrotrophin-releasing hormone was significantly negatively associated with surface body temperature. Overall, the POA and AvPv transcriptome datasets provide the foundation to expand our understanding of the molecular representation of seasonal time in the mammalian hypothalamus. - Source: PubMed
Stewart CalumMarshall ChristopherStevenson Tyler J - Modern lifestyle changes have contributed to a marked increase in myopia and visual impairments in recent decades. However, the systemic biological effects and underlying mechanisms of prolonged exposure to different artificial light sources remain poorly understood. To address this gap, two-week-old female guinea pigs were randomly assigned to three groups: an indoor natural light (IN) control group, a light-emitting diode (LED) group, and a screen video (SV) group. Animals were maintained under a 12:12-h light-dark cycle (lights on 08:00 h, lights off 20:00 h) for 12 weeks. Ocular axial length, peripheral hormone profiles, and systemic glucose-lipid metabolism were evaluated across the three lighting environments. Compared with the IN group, both the LED and SV groups exhibited significant ocular axial elongation, dysregulated lipid metabolism, and altered endocrine profiles. Retinal expression of melanopsin - the photopigment in intrinsically photosensitive retinal ganglion cells (ipRGCs) that regulates non-image-forming visual functions and circadian photoentrainment - was significantly upregulated in the artificial light groups. Molecular analyses further revealed downregulation of key reproductive and metabolic genes (, , and ) alongside upregulation of hypothalamic circadian clock genes and . These findings suggest that artificial light spectra elevate retinal melanopsin expression, which, combined with altered hypothalamic clock gene activity, disrupts reproductive, and metabolic homeostasis. This work highlights a potential role for melanopsin-mediated non-image-forming pathways in light-induced endocrine and metabolic disorders, warranting further mechanistic investigation. - Source: PubMed
Publication date: 2026/09/02
Fan YiLi LinfangYuan JianbaoPeng MinDeng ZhengtaoWang Yuliang