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Neuronal Regulation of the Immune System in Cardiovascular Diseases
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Daniela Carnevale, Giuseppe Lembo, Marialuisa Perrotta, Lorenzo Carnevale
High-fat diet induced obesity is one of the most common causes of the onset of T2D. Similar to what was observed for T1D, T2D also has profound implications for dysregulation in neural and immune homeostasis. During obesity, the accumulation of macrophages in fat tissue propagates the chronic inflammation and insulin resistance typically associated with T2D. In this regard, fat tissue is critically regulated by neural signals and by immune cells. An interesting study investigated the role of a purely neural signal – netrin-1 – in regulating immune activation in fat tissue. Netrin-1 has been known as a neuroimmune guidance cue that orients axonal growth cones by balancing chemoattractive and chemorepulsive impulses. Interestingly, it was discovered that netrin-1 is also expressed in the adipose tissue of obese mice and humans. This observation led researchers to hypothesize that chemoattractive and chemorepulsive signals might also be relevant for the regulation of immune cell infiltration in fat tissue. In a model of high-fat diet induced obesity, it was found that the expression of netrin-1 controls macrophage infiltration and retention in the adi-pose tissue, in turn modulating insulin resistance (Ramkhelawon et al., 2014).
Pharmacological Management of Amyotrophic Lateral Sclerosis
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Shalini Mani, Chahat Kubba, Tanya Sharma, Manisha Singh
Neurons lengthen their axons in excess of extensive distances during developing connections with other synaptic neurons. Proteins involved in guiding the axon may control the progression of axon guidance. These proteins can play a function in attracting or repelling axons thus guide them to a definite area or stopping them from rising into unsuitable regions, correspondingly. Recently several report sustain the testing theory that abnormal expression or function of axon guiding proteins such as ephrins, semaphorins, slits, and netrins usually implicated in curating and maintaining circuits of motor neuron may bring on pathological variations in circuits of motor neuron (Hollis, 2015). Interestingly, pathological variations occurring in nerve terminals and motor axons are found to lead degeneration of motor neurons and associated clinical abnormalities (Fischer et al., 2004). It can be inferred from this discovery that the disease development may begin at the nerve endings and ultimately grow toward the body of the neuronal cell. Numerous diverse molecules responsible for guiding the axons changed expressions in patients of ALS. Thus single-nucleotide polymorphisms (SNPs) in genes expressing proteins for axon guidance may important for diagnosis of ALS (Lesnick et al., 2008). After realizing the importance of these proteins, recently the cell replacement strategies have been designed for corrections of the degenerating motor system of these patients (Silva and Yu, 2008).
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Macrophage flux involves monocyte migration across the endothelium, monocyte differentiation to macrophages, macrophage retention in the atheromata, exit, or death. The preferential accumulation of Ly-6Chigh monocytes in the growing atheromata relies on chemokine-dependent signaling through CCR2-CCL2, CX3CR1-CX3CL1, and CCR5-CCL5,252 and neutralizing these axes in mice almost abolishes atherosclerosis.253,254 Upon accumulation and lipid ingestion, macrophages release netrin-1, a guidance molecule that binds to UNC5b on the plasma membrane and blocks the directed migration of macrophages out of the lesion.255 In the absence of netrin-1, lesions are smaller. Lesions with large necrotic cores are most vulnerable. When one surveys, the peripheral blood counts differential in the chemically sensitive monocytes are usually decreased. This suggests that they are converting to macrophages in the tissue areas containing toxics.
Relationship between circulating netrin-1 levels, obesity, prediabetes and newly diagnosed type 2 diabetes
Published in Archives of Physiology and Biochemistry, 2022
Iveta Nedeva, Antoaneta Gateva, Yavor Assyov, Vera Karamfilova, Tsvetelina Velikova, Zdravko Kamenov
The above-mentioned findings are consistent with some of the features attributed to netrin-1. De Breuck et al. (2003) reported that it is expressed and secreted in the pancreas where it plays a major role in pancreatic morphogenesis in the regenerating pancreas. In patients with newly diagnosed T2DM, secretion of netrin-1 in the injured and apoptotic β-cells is significantly reduced, which implies that netrin-1 could possibly have a protective role for the β-cell. In order to prove this hypothesis, they followed-up for 30 days the continuous administration of netrin-1 to HFD (high-fat diet)/STZ induced diabetic mice. Its stimulatory effect on the insulin release from β-cells was noted via promotion of Ca2+ influx and the cAMP signalling pathway, which is similar to neuronal axon growth/guidance cone response. A hypoglycaemic asset of Netrin-1 was also verified, which is possibly attributed to enhancing β-cell function, presented as amplifying the levels of insulin and pre-proinsulin mRNA expression. Besides, intensified islet vascularisation and diminished islet macrophage infiltration were detected (Gao et al. 2016).
Serum netrin-1 levels at presentation and delayed neurological sequelae in unintentional carbon monoxide poisoning
Published in Clinical Toxicology, 2020
Kamil Kokulu, Hüseyin Mutlu, Ekrem Taha Sert
The use of biochemical markers to identify neuronal damage in the early stage of CO poisoning can provide objective data that can help predict the development of DNS. Netrin-1 is a protein that regulates angiogenesis and the migration of neuron cells to damaged regions of the central nervous system [10,11]. Netrin-1 is also involved in the regulation of the blood-brain barrier, has anti-inflammatory effects, and has been reported to inhibit the apoptosis of neuron cells [12–14]. This protein and its receptor have been reported to be associated with psychiatric diseases, such as depression and schizophrenia [15]. Serum netrin-1 levels have been extensively investigated as a predictive marker of neurological sequelae following ischemic stroke, hemorrhagic stroke, and subarachnoid hemorrhage [16–18]. However, to date, no studies have been conducted on the utility of serum netrin-1 in the prediction of DNS in patients with acute CO poisoning.
Netrin-1 plays a critical role in regulating capacities of epidermal stem cells upon ultraviolet-B (UV-B) irradiation
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Peng Wu, Yongqian Cao, Ran Zhao, Yibing Wang
Netrin-1, an important member of the netrins family, was originally identified as an axonal guidance protein involved in the process of embryonic development [9]. Diverse biological functions of netrin-1 have been reported in previous studies. For example, netrin-1 plays an important role in angiogenic processes by interacting with specific receptors on the surface of the endothelium, such as UNC-5 homolog B (UNC5b) [10]. UNC5b is recognized as a dependence receptor of netrin-1, playing an important role in mediating the intracellular biological functions of netrin-1. Activation of UNC5b has been implicated in several physiological processes, including neural development, angiogenesis, inflammatory responses and tumorigenesis [11]. Interestingly, netrin-1 has been recently reported to improve the tissue-regeneration capacity of stem cells [12]. However, less about the physiological role of netrin-1 and UNC5b in UV-B exposure-induced impairment of the capacities of ESCs has been characterized. In this study, we report a new function of netrin-1 and UNC5b by showing that netrin-1 treatment attenuated UVB-induced impairment of the capacities of ESCs, dependent on UNC5b.