Physiological Functions of Potassium and Chloride Channels through Non-Classical Hormone Signal Transduction in Sertoli Cells: Clinical Significance

2021 ◽  
Author(s):  
Danusa Menegaz ◽  
Ana Karla Bittencourt Mendes ◽  
Fátima Regina Mena Barreto Silva
Keyword(s):  
Signal Transduction ◽  
Clinical Significance ◽  
Sertoli Cells ◽  
Chloride Channels ◽  
Physiological Functions

INTRACELLULAR SIGNAL TRANSDUCTION IN EOSINOPHILS AND ITS CLINICAL SIGNIFICANCE

2002 ◽  
Vol 24 (2) ◽  
pp. 165-186 ◽  
Author(s):  
Chun Kwok Wong ◽  
Jiping Zhang ◽  
Wai Ki Ip ◽  
Christopher Wai Kei Lam
Keyword(s):  
Signal Transduction ◽  
Clinical Significance ◽  
Intracellular Signal Transduction ◽  
Intracellular Signal

A Supramolecular Host for Phosphatidylglycerol (PG) Lipids with Antibacterial Activity

2022 ◽  
Author(s):  
Elliot S Williams ◽  
Hassan Gneid ◽  
Sarah Ruth Marshall ◽  
Mario J González ◽  
Jorgi A Mandelbaum ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Antibacterial Activity ◽  
Energy Storage ◽  
Physiological Functions ◽  
Hydrophobic Barrier

Lipids fulfill a variety of important physiological functions, such as energy storage, providing a hydrophobic barrier, and signal transduction. Despite this plethora of biological roles, lipids are rarely considered a...

Signal transduction pathways in FSH regulation of rat Sertoli cell proliferation

2012 ◽  
Vol 302 (8) ◽  
pp. E914-E923 ◽  
Author(s):  
María F. Riera ◽  
Mariana Regueira ◽  
María N. Galardo ◽  
Eliana H. Pellizzari ◽  
Silvina B. Meroni ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Cell Proliferation ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Kinase Inhibitors ◽  
Production Capacity ◽  
Signal Transduction Pathways ◽  
Mtorc1 Signaling ◽  
Mtorc1 Pathway ◽  
Cell Mitogen

The final number of Sertoli cells reached during the proliferative periods determines sperm production capacity in adulthood. It is well known that FSH is the major Sertoli cell mitogen; however, little is known about the signal transduction pathways that regulate the proliferation of Sertoli cells. The hypothesis of this investigation was that FSH regulates proliferation through a PI3K/Akt/mTORC1 pathway, and additionally, AMPK-dependent mechanisms counteract FSH proliferative effects. The present study was performed in 8-day-old rat Sertoli cell cultures. The results presented herein show that FSH, in addition to increasing p-Akt, p-mTOR, and p-p70S6K levels, increases p-PRAS40 levels, probably contributing to improving mTORC1 signaling. Furthermore, the decrease in FSH-stimulated p-Akt, p-mTOR, p-p70S6K, and p-PRAS40 levels in the presence of wortmannin emphasizes the participation of PI3K in FSH signaling. Additionally, the inhibition of FSH-stimulated Sertoli cell proliferation by the effect of wortmannin and rapamycin point to the relevance of the PI3K/Akt/mTORC1 signaling pathway in the mitotic activity of FSH. On the other hand, by activating AMPK, several interesting observations were made. Activation of AMPK produced an increase in Raptor phosphorylation, a decrease in p70S6K phosphorylation, and a decrease in FSH-stimulated Sertoli cell proliferation. The decrease in FSH-stimulated cell proliferation was accompanied by an increased expression of the cyclin-dependent kinase inhibitors (CDKIs) p19INK4d, p21Cip1, and p27Kip1. In summary, it is concluded that FSH regulates Sertoli cell proliferation with the participation of a PI3K/Akt/mTORC1 pathway and that AMPK activation may be involved in the detention of proliferation by, at least in part, a decrease in mTORC1 signaling and an increase in CDKI expression.

scholarly journals Pharmacological profile of inhibition of the chloride channels activated by extracellular acid in cultured rat Sertoli cells

2006 ◽  
Vol 46 (3) ◽  
pp. 241-255 ◽  
Author(s):  
Céline Auzanneau ◽  
Caroline Norez ◽  
Sabrina Noël ◽  
Chantal Jougla ◽  
Frédéric Becq ◽  
...  
Keyword(s):  
Sertoli Cells ◽  
Chloride Channels ◽  
Pharmacological Profile

scholarly journals Stress-Induced Hyperprolactinemia: Pathophysiology and Clinical Approach

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Samara Levine ◽  
Ozgul Muneyyirci-Delale
Keyword(s):  
Chest Wall ◽  
Clinical Significance ◽  
Prolactin Secretion ◽  
Clinical Approach ◽  
Physiological Functions ◽  
Trauma Stress

While prolactin is most well known for its role in lactation and suppression of reproduction, its physiological functions are quite diverse. There are many etiologies of hyperprolactinemia, including physiologic as well as pathologic causes. Physiologic causes include pregnancy, lactation, sleep-associated, nipple stimulation and sexual orgasm, chest wall stimulation, or trauma. Stress is also an important physiologic cause of hyperprolactinemia, and its clinical significance is still being explored. This review will provide an overview of prolactin physiology, the role of stress in prolactin secretion, as well as the general clinical approach to hyperprolactinemia.

scholarly journals Electrophysiological and Molecular Mechanisms of Sinoatrial Node Mechanosensitivity

2021 ◽  
Vol 8 ◽  
Author(s):  
Daniel Turner ◽  
Chen Kang ◽  
Pietro Mesirca ◽  
Juan Hong ◽  
Matteo E. Mangoni ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Ion Channels ◽  
Chloride Channels ◽  
Molecular Mechanisms ◽  
Transient Receptor Potential ◽  
Sinoatrial Node ◽  
Receptor Potential ◽  
Past Century ◽  
Transient Receptor

The understanding of the electrophysiological mechanisms that underlie mechanosensitivity of the sinoatrial node (SAN), the primary pacemaker of the heart, has been evolving over the past century. The heart is constantly exposed to a dynamic mechanical environment; as such, the SAN has numerous canonical and emerging mechanosensitive ion channels and signaling pathways that govern its ability to respond to both fast (within second or on beat-to-beat manner) and slow (minutes) timescales. This review summarizes the effects of mechanical loading on the SAN activity and reviews putative candidates, including fast mechanoactivated channels (Piezo, TREK, and BK) and slow mechanoresponsive ion channels [including volume-regulated chloride channels and transient receptor potential (TRP)], as well as the components of mechanochemical signal transduction, which may contribute to SAN mechanosensitivity. Furthermore, we examine the structural foundation for both mechano-electrical and mechanochemical signal transduction and discuss the role of specialized membrane nanodomains, namely, caveolae, in mechanical regulation of both membrane and calcium clock components of the so-called coupled-clock pacemaker system responsible for SAN automaticity. Finally, we emphasize how these mechanically activated changes contribute to the pathophysiology of SAN dysfunction and discuss controversial areas necessitating future investigations. Though the exact mechanisms of SAN mechanosensitivity are currently unknown, identification of such components, their impact into SAN pacemaking, and pathological remodeling may provide new therapeutic targets for the treatment of SAN dysfunction and associated rhythm abnormalities.

scholarly journals Clinical significance of RAS pathway alterations in pediatric acute myeloid leukemia

Haematologica ◽  
2021 ◽  
Author(s):  
Taeko Kaburagi ◽  
Genki Yamato ◽  
Norio Shiba ◽  
Kenichi Yoshida ◽  
Yusuke Hara ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Acute Myeloid Leukemia ◽  
Multivariate Analysis ◽  
Clinical Significance ◽  
Myeloid Leukemia ◽  
De Novo ◽  
Kit Mutation ◽  
Pediatric Acute Myeloid Leukemia ◽  
Ras Pathway ◽  
Acute Myeloid

RAS pathway alterations have been implicated in the pathogenesis of various hematological malignancies. However, their clinical relevance in pediatric acute myeloid leukemia (AML) is not well characterized. We analyzed the frequency, clinical significance, and prognostic relevance of RAS pathway alterations in 328 pediatric patients with de novo AML. RAS pathway alterations were detected in 80 (24.4%) out of 328 patients: NF1 (n = 7, 2.1%), PTPN11 (n = 15, 4.6%), CBL (n = 6, 1.8%), NRAS (n = 44, 13.4%), KRAS (n = 12, 3.7%). Most of these alterations were mutually exclusive and were also mutually exclusive with other aberrations of signal transduction pathways such as FLT3-ITD (p = 0.001) and KIT mutation (p = 0.004). NF1 alterations were frequently detected in patients with complex karyotype (p = 0.031) and were found to be independent predictors of poor overall survival (OS) in multivariate analysis (p = 0.007). At least four of seven patients with NF1 alterations had bi-allelic inactivation. NRAS mutations were frequently observed in patients with CBFB-MYH11 and were independent predictors of favorable outcomes in multivariate analysis [OS, p = 0.023; event-free survival (EFS), p = 0.037]. Patients with PTPN11 mutations more frequently received stem cell transplantation (p = 0.035) and showed poor EFS than patients without PTPN11 mutations (p = 0.013). Detailed analysis of RAS pathway alterations may enable a more accurate prognostic stratification of pediatric AML and may provide novel therapeutic molecular targets related to this signal transduction pathway.

scholarly journals DTA expression in mTas1r3+ cells lead to male infertility

2020 ◽  
Author(s):  
Feng Li ◽  
Bowen Niu ◽  
Lingling Liu
Keyword(s):  
Signal Transduction ◽  
Male Infertility ◽  
Sertoli Cells ◽  
Critical Role ◽  
Seminiferous Epithelium ◽  
Taste Receptors ◽  
Transgenic Mouse Models ◽  
Signal Transduction Cascade ◽  
Conditional Deletion ◽  
Sperm Development

AbstractTAS1R taste receptors and their associated heterotrimeric G protein gustducin are strongly expressed in testis and sperm, but their functions and distribution in these tissues were unknown. Using transgenic mouse models, we show that taste signal transduction cascades (mTas1r3-Gnat3-Trmp5) are observed in testis form GFP transgenic mice. It is mTas1rs and mTas2rs, not Gnat3, that was expressed in leydig and sertoli cells. The pattern of mTas1r3 expression was different from that of mTas2r105 expression in seminiferous epithelium. Analysis of the seminiferous epithelium cycle show that both mTas1r3 and mTas2r105 is expressed in the spermatid stage, but mTas2r5 expression is found in spermatocyte stage. Conditional deletion of mTas1r3+ cells leads to male infertility, but do not affect the expression of taste signal transduction cascade during the spermatogenesis. The current results indicate a critical role for mTas1r3+ cell in sperm development and maturation.

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