Publications by authors named "L Adriana Esparza"
Article Synopsis
- Puberty marks a key transition to reproductive capability and is driven by the activation of gonadotropin-releasing hormone (GnRH) neurons, with kisspeptin neurons likely playing a role in this activation.
- Researchers selectively removed arcuate kisspeptin neurons (KNDy neurons) in juvenile mice to study their influence on the timing of puberty, finding that their absence led to delayed puberty and lower hormone levels.
- The study concluded that while most KNDy neurons are critical for the timing of puberty onset, a smaller subset is sufficient for normal GnRH pulse timing, and full KNDy neuron functionality is not necessary for generating the LH surge in females.
Background: Black women in the United States report moderate to high levels of perceived stress during pregnancy. Though lower levels of involvement and support from father of the baby (FOB) and higher levels of conflict have been associated with higher levels of maternal perceived stress, it is not clear how Black pregnant women experience the mother-father relationship and its influence on perceived stress.
Purpose: To examine and describe the mother-father relationship and its role in experiences of perceived stress from the perspective of Black pregnant women.
Study Question: Do hyperactive kisspeptin neurons contribute to abnormally high LH secretion and downstream hyperandrogenemia in polycystic ovary syndrome (PCOS)-like conditions and can inhibition of kisspeptin neurons rescue such endocrine impairments?
Summary Answer: Targeted inhibition of endogenous kisspeptin neuron activity in a mouse model of PCOS reduced the abnormally hyperactive LH pulse secretion and hyperandrogenemia to healthy control levels.
What Is Known Already: PCOS is a reproductive disorder characterized by hyperandrogenemia, anovulation, and/or polycystic ovaries, along with a hallmark feature of abnormal LH hyper-pulsatility, but the mechanisms underlying the endocrine impairments remain unclear. A chronic letrozole (LET; aromatase inhibitor) mouse model recapitulates PCOS phenotypes, including polycystic ovaries, anovulation, high testosterone, and hyperactive LH pulses.
Background: Cardiovascular diseases (CVDs) prevalence has significantly increased in the last decade and atherosclerosis development is the main trigger. MicroRNAs (miRNAs) are non-coding RNAs that negatively regulate gene expression of their target and their levels are frequently altered in CVDs.
Methods: By RT-qPCR, we analysed miR-9-5p, miR-15a-5p, miR-16-5p and miR-199a-3p levels in aorta from apolipoprotein knockout (ApoE ) mice, an experimental model of hyperlipidemia-induced atherosclerosis, and in human aortic and carotid atherosclerotic samples.
Classic pharmacological studies suggested that endogenous dynorphin-KOR signaling is important for reproductive neuroendocrine regulation. With the seminal discovery of an interconnected network of hypothalamic arcuate neurons co-expressing kisspeptin, neurokinin B, and dynorphin (KNDy neurons), the KNDy hypothesis was developed to explain how gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) pulses are generated. Key to this hypothesis is dynorphin released from KNDy neurons acting in a paracrine manner on other KNDy neurons via kappa opioid receptor (KOR) signaling to terminate neural "pulse" events.
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