Author Login

Correspondence to Author: Ashok Chakraborty, 

Ashok Chakraborty All Excel, Inc, CT,USA.

Abstract:

For Parkinson’s disease cell replacement therapy, dopaminergic neural cells can be employed (PD). When neural cell death in the brain causes a decrease in dopamine release, PD is the result. Therefore, it is thought that replacing neural cells in the brain from the outside may increase dopamine levels, which will help to reduce the symptoms of Parkinson’s disease. According to a recent analysis by Chakraborty and Diwan, neural stem cells (NSCs) are a better option than many other cells that can be considered for the same reasons. These hNSC cells also prevent any future dopamine-related issues, including as dyskinesia and motor neuron defects in the person, thanks to their mechanisms for maintaining the controlled level of dopamine. NSCs, however, senescence occurs after very sluggish growth few passes, hence it might not be possible to collect a large number of cells for the treatment of several PD patients. Here, we’ll talk about a potential way to alter cells to improve their capacity for dopamine production, growth, and survival. Cell-Cell interactions are frequently known to change the cells and can be taken into account for the aforementioned goal.

Keywords:Human Neural Stem Cells. Melanocytes. Cell-cell Interaction. Dopamine.Parkinson’s Disease

Introduction: Dopaminergic Parkinson’s disease (PD) is ultimately brought on by the death of neurons in the Substantia Nigra (SN) area of the brain [1,2]. The number of PD cases worldwide is significantly rising [3]. There are now no such curative treatments available, only some palliative ones such supplementing with DOPA, a precursor to dopamine [4]. Long-term DOPA supplement use, however, may result in dyskinesia, motor neuron damage, etc. [5]. The use of neural stem cells (NSCs), induced pluripotent stem cells (iPSCs), and other DOPA-producing cells including melanocytes as a cell therapy regiment for PD treatment has recently come under consideration [6,7]. However, hNSCs for PD cell treatment have been supported by a number of evidences in a recent study by Chakraborty and Diwan (2019) [8].In short, hNSCs can effectively regulate the physiologic level of that neurotransmitter since they are endowed with both Tyrosine hydroxylase, a critical rate-limiting enzyme for Dopamine synthesis, and its scavenging enzymes (DAT and MAO-B) [9]. As a result, cell therapy for Parkinson’s disease using human neural stem cells (hNSCs) should be preferable to levodopa therapy itself since it eliminates the risk of developing dyskinesia or a motor neuron deficiency in the long term. Additionally, hNSCs have the capacity to create glial-cell derived neural factors (GDNF) and brain-derived neural factors (BDNF), which can have an autocrine effect on hNSC development and dopamine production[10–12]. However, hNSCs have a poor rate of growth and enter senescence after a few passages, leaving little cell supply for therapeutic purposes [13].Mobility, endocrine control, heart health, and so forth. Dopamine serves as the main precursor of the sympathetic nervous system’s adrenaline neurotransmitter in the periphery, while noradrenaline serves as the adrenomedullary hormone. Tyrosine hydroxylase (TH) in dopamine-producing cells converts tyrosine to dihydroxyphenylalanine (DOPA), which is then decarboxylated to produce dopamine. Five different dopamine receptor types, D1 and D5, form couples with the Gs class of G proteins, which can stimulate cAMP formation, while D2, D3, and D4 form couples with the Gi class of G proteins, which can cause a decrease in intracellular cAMP formation [36, 37]. Additionally, TH is activated by cAMP [36, 37]. Dopamine, which is released by leukocytes and has both autocrine and paracrine immune modulatory effects. Forskolin, a cAMP inducer, has been shown to increase dopamine synthesis and storage in monocyte-derived dendritic cells (Mo-DCs) [38]. Dopamine also promotes T-cell differentiation to Th2 and increases cAMP levels in naive CD41 T cells via D1-receptors.DARPP32kDa, a dopamine- and cAMPregulated phosphoprotein, is phosphorylated at a higher level in the lesioned striatum in the hemi Parkinsonian rat model. DARPP-32, a key player in dopamine signalling, prevents PKA-targeted proteins from being dephosphorylated while sustaining D1DR-mediated signalling [39,40].

DiscussionMore than 200 different types of cells are thought to make up the human body. Specialized cells coordinate their behaviourthrough communication with other cells to form functional units including organs (brain, heart, liver, etc.), skin, bone, blood, and muscle. A single cell can connect with many other cells by physical contact, surface receptor-ligand interaction, cellular junctions, and secretory stimulation from nearby cells or those of distant organs. Cell-cell interaction is a complex process. Extensive research has been done on interactions involving factors that are secreted, such as growth factors and cytokines that are protein- or peptide-based, small molecules, and metabolites. Extracellular vesicle contacts have recently become another type of interaction. Additionally, the physiological surroundings of cells, including the extracellular matrix’s physical characteristics and its biochemical characteristics, such as oxygen levels (hypoxia) or nutrition, have an impact on how cells interact with one another (energy deprivation). Lipoxin (LX) biosynthesis is an illustration of LO-LO (lipoxygenases) interactions via transcellular circuits in people and other mammalian systems. Because LXs are a distinct type of local mediators made from arachidonic acid, they have unique and powerful biological functions [31]. Together, it seems that cell-cell interaction can support complicated biological processes in tissues, such as neurotransmission, embryonic development, wound healing, inflammation, etc., as well as coordinated cellular behaviour. Parkinson’s disease (PD) is a neurological condition that affects older adults and is characterised by tremor that appears gradually, delayed mobility, and cognitive decline. Parkinson’s disease is sporadic and has no known cause. Its molecular hallmarks include the death of neuronal cells in the subatantia nigra (SN) region of the brain. It is anticipated that a modified neural cells transplant in the brain will be a curative method.

ConclusionTogether, it appears that cell-cell interaction can enable coordinated cellular behaviour as well as complex biological processes in tissues like neurotransmission, embryonic development, wound healing, and inflammation. Parkinson’s disease (PD) is a neurological disorder that mostly affects older persons. It is characterised by gradual tremor development, delayed movement, and cognitive impairment. There is no known aetiology for Parkinson’s disease, which is sporadic. The death of neuronal cells in the subatantia nigra (SN) area of the brain is one of its chemical characteristics. A modified neural cell transplant in the brain is expected to be a curative procedure.

References1. Cheng HC, et al. Clinical progression in Parkinson’ s disease and the neurobiology of axons. Ann Neurol. 67.6 (2010): 715-725. 2. Patrick PM, et al. Understanding Dopaminergic Cell Death Pathways in Parkinson Disease. Neuron 90.18 (2016): 675-691. 3. Dorsey ER, et al. The Emerging Evidence of the Parkinson Pandemic. J Parkinson’s Dis 8.1 (2018): S3- S8. 4. Dorszewska J, et al. Molecular Effects of L-dopa Therapy in Parkinson’s Disease. Curr Genomics 15.1(2014):11-17. 5. Thanvi B, et al. Levodopa-induced dyskinesia in Parkinson’s disease: clinical features, pathogenesis, prevention and treatment. Postgrad Med J 83.2 (2007): 384-388. 6. Han F, et al. Development of stem cell-based therapy for Parkinson’s disease. Transl Neurodegener 4.16 (2015): 38-39. 7. Mull AN, et al. Understanding Melanocyte Stem Cells for Disease Modeling and Regenerative Medicine Applications. Int J Mol Sci 16.12 (2015): 30458-30469. 8. Chakraborty A, et al. Selection of Cells for Parkinson’s Disease Cell-Therapy.Int J Stem Cell Res Ther 6.2 (2019): 63. 9. Meiser J, et al. Complexity of dopamine metabolism. Cell Commun Signal.11.1 (2013): 34. 10. Erickson JT, et al. Brain-derived neurotrophic factor and glial cell linederived neurotrophic factor are required simultaneously for survival of dopaminergic primary sensory neurons in vivo. Exp Neurol 183.2 (2003):610-619. 11. Boyd JG, et al. Glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor sustain the axonal regeneration of chronically axotomized motoneurons in vivo. J Neurosci 21.2 (2001): 581-589. 12. Chakraborty A, et al. Autocrine and paracrine stimulation of dopamine secretion by human neural stemcells:RoleBDNF andGDNF.Neurol Neurosci 3.2 (2020): 1-6. 13. De Filippis L, et al. Immortalization of Human NeuralStem Cells with the cMyc Mutant T58A. PLoS ONE 3.10 (2008): e3310. 14. Balkwill FR, et al. The tumor microenvironment at a glance. J Cell Sci 125.4 (2012): 5591-5596. 15. Quail DF, et al. Microenvironmental regulation of tumor progression and metastasis. Nat Med 19.1 (2013):1423-1437. 16. Egeblad M, et al. Tumors as organs: complex tissues that interface with the entire organism. Dev Cell 18.1 (2010): 884-901. 17. Gajewski TF, et al. Innate and adaptive immune cells in the tumor microenvironment. Nat Immunol. 14.2 (2013):1014-1022. 18. Noy R, Pollard JW. Tumor-associated macrophages: from mechanisms to therapy. Immunity. 41.1 (2014):49-61. 19. Mantovani A, Sozzani S, Locati M, Allavena P, Sica A. Macrophage polarization: tumor-associated macrophages as a paradigm for polarized M2 mononuclear phagocytes. Trends Immunol 23.4 (2002): 549-555. 20. Binnewies M, et al. Understanding the tumor immune microenvironment (TIME) for effective therapy. Nat Med 24.2 (2018): 541-550. 21. Nao Nishida-Aoki, et al. Emerging approaches to study cell–cell interactions in tumor microenvironment. Oncotarget 10.7 (2019): 785-797. 22. Pawelek JM, et al. Fusion of tumour cells with bone marrow-derived cells: a unifying explanation for metastasis. Nat Rev Cancer. 8.5 ((2008): 377-386. 23. Xing F, et al. Cancer associated fibroblasts (CAFs) in tumor microenvironment. Front Biosci 15.2 (2010):166-179. 24. Rivera LB, et al. Tumor angiogenesis, from foe to friend. Science 349.1 (2016): 694-695. 25. Semenza GL. The hypoxic tumor microenvironment: A driving force for breast cancer progression. Biochim Biophys Acta 1863.3 (2016): 382-391. 26. Dustin M, et al. The immunological synapse and the actin cytoskeleton: molecular hardware for T cell signaling. Nat Immunol 23.1 (2000): 4-7. 27. O’Connell, et al. A novel form of immune signaling revealed by transmission of the inflammatory mediator serotonin between dendritic cells and T cells. Blood 107.2 (2006): 1010-1014. 28. Pacheco R, et al. Glutamate released by dendritic cells as a novel modulator of T cell activation. J Immunol. 177.10 (2006): 6695-6704. 29. Eming SA, et al. Wound repair and regeneration: mechanisms, signaling, and translation. Sci Transl Med 6.1 (2014): 265. 30. Zou Y. Does planar cell polarity signaling steer growth cones? Curr Top Dev Biol. 101.4 (2012): 141-160. 31. Cardona AE, et al. Control of microglial neurotoxicity by the fractalkine receptor. Nat Neurosci 9.7 (2006):917- 924. 32. Zhang RL, et al. Ischemic stroke and Neurogenesis in the Subventricular Zone. Neuropharmacol. 55.3 (2008): 345-352. 33. Hayakawa K, Qiu I, Lo EH. Biphasic actions of HMGB1 signaling in inflammation and recovery after stroke. Ann NY Acad Sci 12.7 (2010): 50-57. 34. Morrison BM, et al. Oligodendroglia: metabolic supporters of axons. Trends Cell Biol 23.7 (2013):644- 651. 35. Kang SH, et al. NG2+ CNS glial progenitors remain committed to the oligodendrocyte lineage in postnatal life and following neurodegeneration. Neuron 68.4 (2010): 668-681. 36. Roskoski, et al. Activation of tyrosine hydroxylase in PC12 cells by the cyclic GMP and cyclic AMP second messenger systems. J Neurochem 48.2 (1987):236. 37. Missale C, et al. Dopamine receptors: from structure to function. Physiol Rev 78.3 (1998): 189.38. Nakano K, et al. Dopamine released by dendritic cells polarizes Th2 differentiation. International Immunol 21.6 (2009):645-654. 39. Fienberg AA, et al. DARPP-32: regulator of the efficacy of dopaminergic neurotransmission. Science 281.2 (1998): 838-842. 40. Flores-HJ, et al. Dopamine enhancement of NMDA currents in dissociated medium-sized striatal neurons: role of D1 receptors and DARPP-32. J Neurophysiol 88.6 (2002): 3010-3020. 41. Norcross MA, et al. Membrane Ia expression and antigen-presenting accessory cell function of L cells transfected with class II major histocompatibility complex genes. J Exp Med. 160.2 (1984): 1316. 42. Lu P, et al. The extracellular matrix: a dynamic niche in cancer progression. J Cell Biol 196.2 (2012): 395-406.

Citation:

Ashok Chakraborty. Cell-Cell Interaction: A Technique To Improve The Function Of The Neural Cells. Clinics of Neurology 2024.