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The inherited basis of hypergonadotropic hypogonadism
Published in Philip E. Harris, Pierre-Marc G. Bouloux, Endocrinology in Clinical Practice, 2014
The fully developed GnRH system consists between 1500 and 2000 neurons scattered in the anterior septopreoptic area of the hypothalamus, whose axons converge onto the median eminence portal capillaries where neurosecretion occurs. This full developmental sequence, completed by the eighth to ninth week of embryonic development, can therefore be compartmentalized into several discrete but well-coordinated events, starting with (1) fate specification of GnRH neurons; (2) expansion of cell numbers (mitosis and apoptosis); (3) cell migration (a mixture of chemore-pulsive and chemorepellent events); (4) coalescence of individual GnRH neurons into a responsive, secreting, and coordinating network functioning in an integrated manner; and (5) the development of a capacity to incorporate and integrate internal and external feedback signals into the final feedback control mechanisms that modulate GnRH release. Mutations in the genes whose actions determine any one or more of these pathways could theoretically underpin congenital forms of hypogonadotropic hypogonadism. Postnatally, a further tier of regulation of these neurosecretory events involves the reversible detachment of these nerve endings onto the capillary loops of the median eminence.19
Interaction of bone and brain: osteocalcin and cognition
Published in International Journal of Neuroscience, 2021
Misa Nakamura, Masakazu Imaoka, Masatoshi Takeda
In addition to the autonomic nerves, the involvement of sensory nerves has also been reported. Semaphorin-3A (Sema3A), a known chemorepellent, is a molecule belonging to the semaphorin family that is secreted from neurons and determines the directionality of axonal outgrowth in developmental processes [31]. Fukuda et al. reported that in systemic and nerve-specific Sema3A-deficient mice, a decrease in bone mass was observed as bone formation decreased. In addition, in nerve-specific Sema3A-deficient mice, in addition to the fact that the projection of the sensory nervous system was not only physically reduced, functional sensory nerve abnormalities were revealed [32]. In other words, it has been suggested that the sensory nerves in bone not only function as sensory receptors, but also play an important role in bone mass regulation [33] (see Figure 1).
Pinocembrin ameliorates arrhythmias in rats with chronic ischaemic heart failure
Published in Annals of Medicine, 2021
Yan Guo, Cui Zhang, Tianxin Ye, Xiuhuan Chen, Xin Liu, Xiaoli Chen, Yazhou Sun, Chuan Qu, Jinjun Liang, Shaobo Shi, Bo Yang
Autonomic nervous system (ANS) is a crucial role in the pathogenesis of VAs in CIHF. On the one hand, increased sympathetic activation can lead to increased automaticity of the ventricular pacemaker cells. On the other hand, ANS also regulates early afterdepolarization (EADs) and delayed afterdepolarization (DADs) [23]. Previous studies have shown that the density of sympathetic nervous in myocardial infarction area of spontaneous VAs patients was higher than that of non-spontaneous VAs patients [24]. It is reported that the density of nervous in left stellate ganglion increased significantly after myocardial infarction caused by coronary artery balloon occlusion [25]. Moreover, sympathetic activation reduces ERP and QTc, which could be a prerequisite for circus-type re-entry [26]. Furthermore, sympathetic neurotransmitters increase excitation and conduction heterogeneity and lead to susceptibility to VAs by interacting with cardiac ion channels. Sustained sympathetic activation inhibits Kv4.3, depolarizes L-type calcium channels, and resulting in APD shortening [27, 28]. Our electrophysiological data support these published findings. At the molecular level, autonomic nerves not only acted on ion channels, but also interacted with connexin proteins extensively. Yang et al. found that the neural chemorepellent semaphoring 3a inhibits neural remodelling, reducing the accumulation of dephosphorylated Cx43, and improving the inductivity of VAs [29]. These findings are consistent with our observation that up-regulated Cx43 were parallel with the reduced incidence of VTs following pinocembrin treatment.
Semaphorin-3A and Netrin-1 predict the development of kidney injury in children with congenital hydronephrosis
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Xiaobing Li, Xianghua Liu, Ji Li, ELi Song, Ning Sun, Wen Liu, Tian Wang, Jinchang Yang, Zhenzhen Li
Semaphorins are secreted or membrane-associated glycoproteins found in eight classes based upon their structure elements and amino acid sequences. Class 3 semaphorins are secreted, classes 4 through 6 are transmembrane proteins and class 7 are membrane associated via glycosylphosphatidylinositol (GPI) linkage. They are characterized structurally by a conserved ∼400 amino acid sema domain [6]. Semaphorins are classically described as collapsing factors and mediators of axon repulsion, although they may also act as context-dependent chemoattractants. Semaphorin-3A (SEMA-3A) is a chemorepellent with multiple guidance functions, including axon pathfinding, cardiac and peripheral vascular patterning, and branching morphogenesis [7]. Semaphorin-3A expression persists in adult podocytes and collecting tubules [8,9], and is highly induced after an acute tubular injury, leading to increased excretion of SEMA-3A in urine in both mice and humans [10–12]. Urinary SEMA-3A (uSEMA-3A) is a very early and sensitive biomarker of kidney injury, and various studies have reported that uSEMA-3A levels are significantly increased in AKI, diabetic nephropathy and non-diabetic hypertensive patients with CKD [10,13].