Transient receptor potential (TRP) channel function in the reproductive axis

TRPC channels: Structure, function, regulation and recent advances in small molecular probes

“…Numerous studies have provided very rich information concerning the physiological significance and pathophysiological roles of individual TRPC isoforms. Many of these studies have been included in recent comprehensive review articles and book chapters that focus on specific organ/tissue system or disease, including cardiovascular system (Yue et al, 2015;Alonso-Carbajo et al, 2017;Xiao, Liu, Shen, Cao, & Li, 2017;Avila-Medina et al, 2018), with emphasis on vascular endothelial and smooth muscle cells (Beech, 2013;Earley & Brayden, 2015;Ampem et al, 2016;Grayson, Murphy, & Sandow, 2017), cardiac remodeling (Falcon et al, 2019), cardiac fibrosis (Numaga-Tomita et al, 2017), atrial fibrillation (Han & Li, 2018) and therapeutic angiogenesis (Moccia, Lucariello, & Guerra, 2018); skeletal muscles (Numaga-Tomita et al, 2019;Sauc & Frieden, 2017); lung and lung diseases (Smith, Ayon, Tang, Makino, & Yuan, 2016;Malczyk et al, 2017;Dietrich, Steinritz, & Gudermann, 2017); kidney and kidney diseases (Schlondorff, 2017;Staruschenko, Spires, & Palygin, 2019;Zhou & Greka, 2016); salivary gland physiology and dysfunction (Ambudkar, 2016), reproduction and sperm function (Götz, Qiao, Beck, & Boehm, 2017;Kumar et al, 2018); immune system and inflammation (Ramirez et al, 2018); and many different aspects of nervous systems and neurological diseases, e. g. neurological functions (Sun et al, 2014); neurotransmission and hormone sensing as well as glucose sensing (Fioramonti, Chrétien, Leloup, & Pénicaud, 2017) in the hypothalamus, neural development (Feng, He, Li, & Wang, 2015;Tai & Jia, 2017), neurological diseases especially neurodegeneration (Pchitskaya, Popugaeva, & Bezprozvanny, 2018;Secondo, Bagetta, & Amantea, 2018;Wang et al, 2017), Alzheimer's disease…”

TRPCing around the hypothalamus

“…Therefore, cSrc kinase appears to be a key signaling molecule in the kisspeptin-mediated activation of TRPC 4 channels in GnRH neurons, and Kiss1R activation of TRPC 4 channels appears to be a major cellular mechanism by which kisspeptin causes a robust, sustained depolarization of GnRH neurons to generate a surge for maintaining reproductive function (d’Anglemont de Tassigny and Colledge, 2010). TRPC 5 channels are also expressed in the pituitary gonadotropes and mediate, at least in part, the depolarizing effects of GnRH (Götz et al, 2017).…”

PTPN5 promotes follicle‐stimulating hormone secretion through regulating intracellular calcium homeostasis

“…levels in gonadotropes. [22][23][24] To evaluate the cellular function of PTPN5 in gonadotropes, we tested whether blocking of PTPN5 had effect on the intracellular calcium increase induced by GnRH in gonadotropes.…”