The role of TNF-alpha and its receptors in the production of NGF and GDNF by astrocytes

Kuno, Reiko; Yoshida, Yusuke; Nitta, Atsumi; Nabeshima, Toshitaka; Wang, Jinyan; Sonobe, Yoshifumi; Koyama, Jun; Takeuchi, Hideyuki; Mizuno, Tetsuya; Suzumura, Akio

doi:10.1016/j.brainres.2006.07.120

Cited by 107 publications

(82 citation statements)

References 32 publications

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“…31,74 In addition, TNFa is produced by astrocytes and ependymal cells. 32 In the present study, we did not find a change of TNFa or IL1b in mRNA levels in the PVN in depressed patients.…”

Section: Cytokinesmentioning

confidence: 46%

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

et al. 2008

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Hyperactivity of corticotropin-releasing factor (CRF) neurons in the paraventricular nucleus (PVN) of the hypothalamus is a prominent feature in depression and may be important in the etiology of this disease. The activity of the CRF neurons in the stress response is modulated by a number of factors that stimulate or inhibit CRF expression, including (1) corticosteroid receptors and their chaperones, heat shock proteins 70 and 90, (2) sex hormone receptors, (3) CRF receptors 1 (CRFR1) and 2, (4) cytokines interleukin 1-b and tumor necrosis factor-a, (5) neuropeptides and receptors, vasopressin (AVP), AVP receptor 1a (AVPR1A) and oxytocin and (6) transcription factor cAMP-response element-binding protein. We hypothesized that, in depression, the transcript levels of those genes that are involved in the activation of the hypothalamo-pituitary-adrenal (HPA) axis are upregulated, whereas the transcript levels of the genes involved in the inhibition of the HPA axis are downregulated. We performed laser microdissection and real-time PCR in the PVN and as a control in the supraoptic nucleus. Snap-frozen post-mortem hypothalami of seven depressed and seven matched controls were used. We found significantly increased CRF mRNA levels in the PVN of the depressed patients. This was accompanied by a significantly increased expression of four genes that are involved in the activation of CRF neurons, that is, CRFR1, estrogen receptor-a, AVPR1A and mineralocorticoid receptor, while the expression of the androgen receptor mRNA involved in the inhibition of CRF neurons was decreased significantly. These findings raise the possibility that a disturbed balance in the production of receptors may contribute to the activation of the HPA axis in depression.

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“…31,74 In addition, TNFa is produced by astrocytes and ependymal cells. 32 In the present study, we did not find a change of TNFa or IL1b in mRNA levels in the PVN in depressed patients.…”

Section: Cytokinesmentioning

confidence: 46%

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

et al. 2008

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“…Indeed, elevated GDNF expression is observed in response to lipopolysaccharide (LPS) and to the proinflammatory cytokines IL-1b, IL-6, tumor necrosis factor (TNF)-a and TNF-b in C6 cells (Appel et al, 1997;Verity et al, 1998) and in U-87MG glioblastoma cells . In cultured astrocytes both exogenous TNF-a, via TNF receptors, and endogenously produced TNF-a induce GDNF expression, suggesting that an autocrine loop contributes to the production of neurotrophic factors in response to inflammation (Kuno et al, 2006). LPS also increases GDNF mRNA expression in rodent primary astrocyte cultures Kuno et al, 2006) as well as GDNF secretion (McNaught and Jenner, 2000).…”

Section: Inflammatory Signals and Gdnf Expressionmentioning

confidence: 99%

“…In cultured astrocytes both exogenous TNF-a, via TNF receptors, and endogenously produced TNF-a induce GDNF expression, suggesting that an autocrine loop contributes to the production of neurotrophic factors in response to inflammation (Kuno et al, 2006). LPS also increases GDNF mRNA expression in rodent primary astrocyte cultures Kuno et al, 2006) as well as GDNF secretion (McNaught and Jenner, 2000). However, both LPS and TNF-a trigger a significant decrease in the mRNA level of GFRa1 .…”

Section: Inflammatory Signals and Gdnf Expressionmentioning

confidence: 99%

Driving GDNF expression: The green and the red traffic lights

Saavedra

Baltazar

Duarte

2008

Progress in Neurobiology

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“…Glial cell line-derived neurotrophic factor (GDNF), a growth factor in the TGF-β family is produced and secreted from astrocytes [59] and regulates the permeability of the BBB [60] and the BRB [17]. GDNF acts by a two-component receptor complex; 1) glycosylphospatidylinositol-linked cell surface molecule, the GDNF receptor GFRα-1, which acts as a ligand-binding domain, and 2) the receptor protein tyrosine kinase Ret, which acts as the signal transducing domain [61].…”

Section: Barrier Regulationmentioning

confidence: 99%

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

Rönnbäck¹

2017

IJOAO

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The blood-brain barrier (BBB), the blood-retinal barrier (BRB), and the blood-nerve barrier (BNB) may have similarities in systemic chronic inflammation, as seen in a variety of diseases. A disturbance of the barriers lead to a disruption of the cells coupled with gap junctions in syncytium. The network coupling may be principal to understand the homeostatic imbalance in systemic inflammation. This review high-lightens the role of gap junction network coupled cells in inducing and maintaining barrier properties under physiological conditions as well as their involvement in inflammatory pathologies. Rigshospitalet, 2600 Glostrup, Denmark, Tel. +45 3863 4820, Fax +45 3863 4834; E-mail elisabeth.cecilia.roennbaeck@regionh.dk and waste products between the vascular lumen and the neural retina and is formed by the interaction of retinal glia and pericytes with the endothelium. The blood-nerve barrier (BNB) consists of blood vessels and sensory nerves but gap junction coupled cells in networks, such as the articular cartilage in joints, might be involved in these cell interactions [3]. KeywordsFuture studies elucidating barrier induction and maintenance will provide a framework for rational therapies in several diseases, to restore the barriers with influence of gap junction syncytium coupled cells on the barrier functions.

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The role of TNF-alpha and its receptors in the production of NGF and GDNF by astrocytes

Cited by 107 publications

References 32 publications

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

Gene expression analysis in the human hypothalamus in depression by laser microdissection and real-time PCR: the presence of multiple receptor imbalances

Driving GDNF expression: The green and the red traffic lights

Gap Junction Coupled Cells, Barriers and Systemic Inflammation

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