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Different in vitro response to rIL-1β of newborn and adult rat astroglia
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International Journal of Developmental Neuroscience
Volume 9, Issue 5, 1991, Pages 501-507
Different in vitro response to rIL-1β of newborn and adult rat astroglia (Article)
Colasanti, M.a,
Ramacci, M.T.b,
Foresta, P.c,
Lauro, G.M.a
a Dipartimento di Biologia Cellulare e dello Sviluppo, Università La Sapienza, Via degli Apuli, 1-00185 Roma, Italy
b Istituto per la Ricerca sulla Senescenza. SIGMA-TAU, Pomezia, Italy
View references (17)
Abstract
In recent literature, lymphokines have been reported to be able to promote both proliferation and maturation of some glial populations. In this paper, we compare the effect of rIL-1 on newborn and adult rat astroglial cells in vitro. In newborn, but not in adult astrocytes, 100 U/ml of rIL-1β increase [3H]thymidine incorporation with a maximal response by 3 days as compared to the control untreated culture. In contrast, rIL-1β induces an increase of GFAP immunoreactivity both in newborn and in adult astrocytes, as compared to the control untreated cells. These data indicate that, while both newborn and adult astroglial cells are capable of responding to rIL-1β, only newborn astrocytes can respond to this lymphokine with proliferation. Thus, it appears likely that different factors, other than rIL-1β, are needed by adult astrocytes to proliferate
Amyloid-β 25-35 induces neurotoxicity through the up-regulation of astrocytic system xc −
No full textAmyloid-β (Aβ) deposition, a hallmark of Alzheimer’s disease, is known to induce free radical production and oxidative stress, leading to neuronal damage. During oxidative stress, several cell types (including astrocytes) can activate the nuclear factor erythroid 2-related factor 2 (Nrf2), a regulator of several phase II detoxifying and antioxidant genes, such as the System Xc− subunit xCT. Here, we studied (i) the effect of the Aβ fragment 25-35 (Aβ25-35 ) on Nrf2-dependent System Xc − expression in U373 human astroglial cells and (ii) the effect of Aβ25-35-induced astrocytic response on neuronal cell viability using an in vitro co-culture system. We found that Aβ25-35 was able to activate an antioxidant response in astrocytes, by inducing both Nrf2 activation and System Xc− up-regulation. However, this astrocytic response caused an enhanced cell mortality of co-cultured SH-SY5Y cells, taken as a neuronal model. Consistently, the specific System Xc− inhibitor sulfasalazine prevented the increase of both neuronal mortality and extracellular glutamate levels, thus indicating that the neurotoxic effect was due to an augmented release of glutamate through the transporter. The involvement of NMDA receptor activation in this pathway was also demonstrated using the specific inhibitor MK801 that completely restored neuronal viability at the control levels. The present study sheds light on the Nrf2/system Xc− pathway in the toxicity induced by Aβ25-35 and may help to better understand the involvement of astrocytes in neuronal death during Alzheimer’s disease
Inhibition of inducible nitric oxide synthase mRNA expression by basic fibroblast growth factor in human microglial cells
No full textInhibition of nitric-oxide synthase-I (NOS-I)-dependent nitric oxide production by lipopolysaccharide plus interferon-gamma is mediated by arachidonic acid. Effects on NFkappaB activation and late inducible NOS expression.
No full textPrevious results have indicated that lipopolysaccharide (LPS) plus interferon-gamma (IFNgamma) inhibits nitric-oxide synthase (NOS)-I activity in glial cells. We report here that arachidonic acid ( AA) plays a pivotal role in this response, which was consistently reproduced in different glial cell lines and in primary rat astrocytes. This notion was established using pharmacological inhibitors of phospholipase A(2) (PLA(2)), cytosolic PLA(2) (cPLA(2)) antisense oligonucleotides, and AA add-back experiments. This approach not only allowed the demonstration that AA promotes inhibition of NOS-I activity but also produced novel experimental evidence that LPS/IFNgamma itself is a potential stimulus for NOS-I. Indeed, LPS/IFNgamma fails to generate nitric oxide (NO) via NOS-I activation simply because it activates the AA-dependent signal that impedes NOS-I activity. Otherwise, LPS/IFNgamma promotes NO formation, sensitive to exogenous AA, in cells in which cPLA(2) is pharmacologically inhibited or genetically depleted. Because NO suppresses the NFkappaB-dependent NOS-II expression, inactivation of NOS-I by the LPS/IFNgamma-induced AA pathway provides optimal conditions for NFkappaB activation and subsequent NOS-II expression. Inhibition of cPLA(2) activity, while reducing the availability of AA, consistently inhibited NFkappaB activation and NOS-II mRNA induction and delayed NO formation. These responses were promptly re-established by addition of exogenous AA. Finally, we have demonstrated that the LPS/IFNgamma-dependent tyrosine phosphorylation of NOS-I and inhibition of its activity are mediated by endogenous AA
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
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