Morphological differentiation of human SH-SY5Y neuroblastoma cells inhibits human immunodeficiency virus type 1 infection

Vesanen, Mika; Salminen, Mika; Wessman, Maija; Lankinen, Hilkka; Sistonen, Pertti; Vaheri, Antti

doi:10.1099/0022-1317-75-1-201

Cited by 15 publications

(6 citation statements)

References 23 publications

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“…1), which are in agreement with previous reports (18,19). We next studied the effect of morphine on MOR-1 mRNA levels in the differentiated cells.…”

Section: Discussionsupporting

confidence: 93%

Regulation of mammalian MOR-1 gene expression after chronic treatment with morphine

Prenus

Luscar

Zhu

et al. 2012

International Journal of Molecular Medicine

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Morphine is an effective analgesic that acts by binding to the μ-opioid receptor (MOR) coded in the human by the OPRM1 gene. In the present study, we investigated the regulation of μ-opioid receptor (MOR-1) mRNA levels in all-trans-retinoic acid-differentiated SH-SY5Y human neuroblastoma cells under in vitro conditions with 10 μM morphine treatment for 24 h. In addition, we measured the MOR-1 levels in recombinant Chinese hamster ovary (CHO) cells, transfected with human μ-opioid receptor gene (hMOR) with 10 μM morphine treatment for 24 h. The isolated mRNA from these cells was subjected to real-time quantitative RT-PCR analysis to determine the regulation of μ-opioid receptor gene expression. It was observed that morphine treatment did not alter MOR-1 levels in undifferentiated SH-SY5Y cells compared to undifferentiated control cells. However, the MOR-1 levels in all-trans-retinoic acid-differentiated cells were significantly higher compared to the undifferentiated cells. Morphine treatment in differentiated SH-SY5Y cells caused significant downregulation of MOR-1 expression compared to the control cells. In the morphine-treated CHO cells, the hMOR-1 mRNA levels remained the same as the untreated control. Finally, pretreatment of SH-SY5Y cells with 10 μM naloxone, the antagonist of μ-opioid receptor, for 1 h significantly blocked the downregulation of MOR-1 mRNA levels with morphine treatment. These findings suggest that regulation of MOR-1 gene expression is cell-type specific after chronic morphine treatment and provide some evidence in the understanding of morphine tolerance.

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“…1), which are in agreement with previous reports (18,19). We next studied the effect of morphine on MOR-1 mRNA levels in the differentiated cells.…”

Section: Discussionsupporting

confidence: 93%

Regulation of mammalian MOR-1 gene expression after chronic treatment with morphine

Prenus

Luscar

Zhu

et al. 2012

International Journal of Molecular Medicine

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“…2b). As observed in PC12 cells, progesterone significantly promoted neurite outgrowth in NGF-induced differentiated SH-SY5Y cells 26 (Fig. 2c).…”

Section: Resultssupporting

confidence: 79%

Membrane progesterone receptor beta (mPRβ/Paqr8) promotes progesterone-dependent neurite outgrowth in PC12 neuronal cells via non-G protein-coupled receptor (GPCR) signaling

Kasubuchi

Watanabe

Hirano

et al. 2017

Sci Rep

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Recently, sex steroid membrane receptors garnered world-wide attention because they may be related to sex hormone-mediated unknown rapid non-genomic action that cannot be currently explained by their genomic action via nuclear receptors. Progesterone affects cell proliferation and survival via nongenomic effects. In this process, membrane progesterone receptors (mPRα, mPRβ, mPRγ, mPRδ, and mPRε) were identified as putative G protein-coupled receptors (GPCRs) for progesterone. However, the structure, intracellular signaling, and physiological functions of these progesterone receptors are still unclear. Here, we identify a molecular mechanism by which progesterone promotes neurite outgrowth through mPRβ (Paqr8) activation. Mouse mPRβ mRNA was specifically expressed in the central nervous system. It has an incomplete GPCR topology, presenting 6 transmembrane domains and did not exhibit typical GPCR signaling. Progesterone-dependent neurite outgrowth was exhibited by the promotion of ERK phosphorylation via mPRβ, but not via other progesterone receptors such as progesterone membrane receptor 1 (PGRMC-1) and nuclear progesterone receptor in nerve growth factor-induced neuronal PC12 cells. These findings provide new insights of regarding the non-genomic action of progesterone in the central nervous system. Steroid hormones such as corticosterone, progesterone, testosterone, and estrogen are known to exhibit their physiological effects via their specific nuclear receptors 1 . Steroid hormones regulate gene transcription through nuclear receptors, which act as ligand-dependent transcription factors. These effects are known as "genomic" actions of steroid hormones, which generally take few hours to days to fully manifest. However, in various tissues, including the central nervous system (CNS), steroid hormones present a rapid action on the targeted cells within minutes. These "non-genomic" actions can be partially explained by membrane transport via nuclear receptors 2, 3 . However, other "non-genomic" actions are nuclear receptor-independent responses caused by insensitivity to the receptor antagonist and have been observed in knockout mice 4 . This suggests the possible involvement of unidentified receptors in the rapid non-genomic actions of steroid hormones 5 . The putative receptors for these actions have not yet been identified.

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“…Therefore, this specific geometry mimics the environment required for dopaminergic neuronal cells, which show similar changes as those obtained with RA routinely utilized to obtain cell differentiation in 2D cell cultures. 28,30,31,45,46 Perhaps not surprisingly, a completely different geometric nanoporous surface nurtured primary rodent and human podocytes, on which arborized cell processes were formed similarly to those traditionally obtained by collagen coating. In this sense, podocytes, despite the presence of numerous ramifications, display a similar behavior to that of other epithelial cell types whose attachment and spreading seem to be discouraged by rough surfaces 47,48 and facilitated instead by nanoporous materials.…”

mentioning

confidence: 99%

A nanoporous surface is essential for glomerular podocyte differentiation in three-dimensional culture

Zennaro¹,

Rastaldi²,

Bakeine³

et al. 2016

IJN

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Although it is well recognized that cell–matrix interactions are based on both molecular and geometrical characteristics, the relationship between specific cell types and the three-dimensional morphology of the surface to which they are attached is poorly understood. This is particularly true for glomerular podocytes – the gatekeepers of glomerular filtration – which completely enwrap the glomerular basement membrane with their primary and secondary ramifications. Nanotechnologies produce biocompatible materials which offer the possibility to build substrates which differ only by topology in order to mimic the spatial organization of diverse basement membranes. With this in mind, we produced and utilized rough and porous surfaces obtained from silicon to analyze the behavior of two diverse ramified cells: glomerular podocytes and a neuronal cell line used as a control. Proper differentiation and development of ramifications of both cell types was largely influenced by topographical characteristics. Confirming previous data, the neuronal cell line acquired features of maturation on rough nanosurfaces. In contrast, podocytes developed and matured preferentially on nanoporous surfaces provided with grooves, as shown by the organization of the actin cytoskeleton stress fibers and the proper development of vinculin-positive focal adhesions. On the basis of these findings, we suggest that in vitro studies regarding podocyte attachment to the glomerular basement membrane should take into account the geometrical properties of the surface on which the tests are conducted because physiological cellular activity depends on the three-dimensional microenvironment.

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Morphological differentiation of human SH-SY5Y neuroblastoma cells inhibits human immunodeficiency virus type 1 infection

Cited by 15 publications

References 23 publications

Regulation of mammalian MOR-1 gene expression after chronic treatment with morphine

Regulation of mammalian MOR-1 gene expression after chronic treatment with morphine

Membrane progesterone receptor beta (mPRβ/Paqr8) promotes progesterone-dependent neurite outgrowth in PC12 neuronal cells via non-G protein-coupled receptor (GPCR) signaling

A nanoporous surface is essential for glomerular podocyte differentiation in three-dimensional culture

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