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Interleukin-6 and the Lung
Published in Jason Kelley, Cytokines of the Lung, 2022
Ralph J. Zitnik, Jack A. Elias
The biological effects of IL-6 are protean, and newly discovered activities continue to be described. These include the ability to stimulate hepatic acute-phase protein production and fever; growth enhancement of hematopoietic precursors as well as plasmacytomas and hybridomas; induction of B-cell maturation; activation of T cells and CTL cells; and the regulation of cutaneous and neural tissue function. Physiologically, IL-6 acts both as a systemically active “hormone,” and as an autocrine or paracrine regulator of cellular function.
Caffeine
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
Adenosine acts as a major autocrine and paracrine regulator of tissue function (21). It initiates its biological effects via four receptor subtypes, namely the A1, A2A, A2B and A3 adenosine receptors (87). A2B and A3 receptors have a low affinity for adenosine and are likely only activated under conditions of severe cellular stress (e.g., ischemia) (34). In contrast, A1 and A2A receptors are considered high-affinity receptors and are responsible for the tonic actions of endogenous adenosine (79). The A1 receptor is the most abundant receptor in the body (22) and has the highest affinity for adenosine. A1 receptors are expressed at high levels throughout the brain, particularly in the cortex, hippocampus and cerebellum (77). A2A receptors on the other hand, have a slightly lower affinity for adenosine compared to the A1 receptor and are expressed most strongly in the striatum (85) with intermediate expression in the sarcolemma and cytosol of skeletal muscle cells (63). Both receptors are expressed in the basal ganglia, which is a group of structures involved in various aspects of motor control (31).
The Metabolic Syndrome in Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Josep Redon, Fernando Martinez, Gernot Pichler
Altered function of adipose tissue, mainly in visceral fat, has been identified as a key driver, which precludes the development of the other features of MS, including impaired glucose homeostasis (72–74). The first structural event which follows from fat tissue increase is the infiltration of adipose tissue by bone marrow—derived macrophages in response to as-yet unknown signals (5,6,75,76). This is both a paracrine regulator of adipocyte function influencing free fatty acid (FFA) liberation and hormone secretion of leptin and adiponectin, as well as a source of the inflammatory mediators interleukin (IL)-6 and tumour-necrosis factor (TNF)-α released by adipose tissue. In addition to the structural changes, various functional abnormalities of adipose tissue—derived products have been described. These include an increase in FFA, leptin and cytokine release, and a reduction in adiponectin secretion. Age can also have a role in adipocyte dysfunction, and several genes associated with longevity such as IGF-1 and mTOR could influence the adipocyte function (73,77).
COVID-19 during Pregnancy and Postpartum:
Published in Journal of Dietary Supplements, 2022
Sreus A. G. Naidu, Roger A. Clemens, Peter Pressman, Mehreen Zaigham, Kelvin J. A. Davies, A. Satyanarayan Naidu
During normal pregnancy, the renin-angiotensin system (RAS) is activated. Estrogen and progesterone upregulate angiotensinogen and renin, which results in the rise of angiotensin (ANG) II levels in the cell surface of lungs, arteries, heart, kidney, and intestines. ACE2 lowers blood pressure by converting the ANG-II into ANG-(1-7), a vasodilator (Figure 3) (Donoghue et al. 2000). In human ovaries, ACE2 is found in primordial, primary/secondary/antral follicles, stroma, and corpora lutea (Reis et al. 2011). ACE2 plays a regulatory role in oocyte maturation, steroidogenesis, ovulation, and atresia (Honorato-Sampaio et al. 2012). ACE2 expression is also upregulated during follicular development and after gonadotrophin stimulation (Pereira et al. 2009). ACE2 may act as a local autocrine/paracrine regulator throughout pregnancy, participating in the early (angiogenesis, apoptosis, and growth) and late (utero-placental blood flow) events of pregnancy (Neves et al. 2008). During pregnancy, the placenta and the uterus constitute an important source of ACE2 (Levy et al. 2008).
Genetic polymorphism of glial cell-derived neurotrophic factor (GDNF) in male infertility
Published in British Journal of Biomedical Science, 2019
S Shabani, F Mashayekhi, SS Shahangian, Z Salehi
We hypothesised an association between a SNP (rs2075680) located in GDNF and the risk of male infertility by a case-control approach. Our results showed that A allele of rs2075680 could confer a genetic predisposition male infertility. Moreover, AA genotype carriers have an increased risk of infertility of about two times higher than those with the CC genotype. We also found the AA genotype to be associated with azoospermia. In the literature, few studies have been conducted regarding association between GDNF SNPs and different diseases. A case-control study conducted by Fernandez et al. did not find any association between gene variants of GDNF (rs2075680, rs2910797 and rs11111) and Hirschsprung disease [9]. A study of 930 young adults reported that GDNF rs3096140 might be involved in the genetic background of smoking, independent of anxiety characteristics [10]. In the adult mouse, GDNF is a pivotal paracrine regulator of the numbers, replication and differentiation of SSCs and progenitor spermatogonia. Inhibition of GDNF signalling reduces the replication of SSCs, and promotes their differentiation [7]. An in vitro and in vivo study has elucidated the expression of GDNF in normal and Sertoli cell-only (SCO) testes. It has been shown that the Sertoli cells are the primary source of GDNF in the human testis and in the SCO testis these cells produce substantially less GDNF compare to normal testis [6].
Glial-derived neurotrophic factor is essential for blood-nerve barrier functional recovery in an experimental murine model of traumatic peripheral neuropathy
Published in Tissue Barriers, 2018
Chaoling Dong, E. Scott Helton, Ping Zhou, Xuan Ouyang, Xavier d‘Anglemont de Tassigny, Alberto Pascual, José López-Barneo, Eroboghene E. Ubogu
Primary human endoneurial endothelial cells that form the BNB express GFRα1 in vitro and in situ.46-49 Our prior work demonstrated that GDNF is a sufficient paracrine regulator of the human BNB in vitro following diffuse injury mediated by serum withdrawal (which causes endothelial cell detachment in vitro). GDNF (in a dose-dependent manner) restored human BNB biophysical properties dependent on RET-Tyrosine kinase signaling pathways. There was observable cytoskeletal reorganization (translocation of F-actin filaments from the cytoplasm to cell membranes) that resulted in more continuous intercellular junctions, without significantly enhancing known adherens and tight junction associated protein expression, or modulating claudin-5 phosphorylation in vitro.47 A role for GDNF in regulating microvascular endothelial and epithelial tight junction barrier function had also been described in mammalian blood-brain, blood-retina, blood-testis and intestinal barriers in vitro or in vivo,49-56 in addition to the in vitro BNB. In order to ascertain whether GDNF regulates mammalian BNB function in vivo, we performed macromolecular permeability assessments of endoneurial microvessels using a validated conditional knockout murine model following non-transecting sciatic nerve crush injury, with appropriate controls. We also sought to determine whether changes in VE-Cadherin and claudin-5 expression by endoneurial microvessels (as markers of adherens and tight junctions respectively) were associated with GDNF-mediated BNB macromolecular permeability regulation following sciatic nerve crush injury.