Transforming growth factor-β1 differentially regulates proliferation and MHC class-II antigen expression in forebrain and brainstem astrocyte primary cultures

Johns, Lennart D.; Babcock, Gerald T.; Green, Damian; Freedman, Mark S.; Subramaniam, Sriram; Ransohoff, Richard M.

doi:10.1016/0006-8993(92)91211-v

Cited by 47 publications

(22 citation statements)

References 26 publications

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“…A sharp inhibitory effect on astrocyte proliferation induced by mitogens is documented for TGFb [34,39]. Responses of astrocytes to TGFb are region-specific, as this factor stimulates proliferation of brainstem, but not of forebrain rat astrocytes [40]. This is consistent with the present data, as our astrocyte cultures were prepared from rat neocortex.…”

Section: Discussionsupporting

confidence: 86%

Astroglial-Conditioned Media and Growth Factors Modulate Proliferation and Differentiation of Astrocytes in Primary Culture

et al. 2006

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Astroglial conditioned media (ACM) influence the development and maturation of cultured nerve cells and modulate neuron-glia interaction. To clarify mechanisms of astroglial cell proliferation/differentiation in culture, incorporation of [methyl-3H]-thymidine or [5,6-3H]-uridine in cultured astrocytes was assessed. Cultures were pre-treated with epidermal growth factor (EGF), insulin (INS), insulin-like growth factor-I (IGF-I), and basic fibroblast growth factor (bFGF) and subsequently with ACM. DNA labeling revealed a marked stimulatory effect of ACM from 15 days in vitro (DIV) cultures in 30 DIV astrocytes after 12 h pre-treatment with growth factors. The main effects were found after INS or EGF pre-treatment in 30 DIV cultures. ACM collected from 15 or 60 or 90 DIV increased RNA labeling of 15 and 30 DIV astrocyte cultures, being the highest value that of 30 DIV cultures added with ACM from 90 DIV. The findings of increased DNA labeling after EGF or INS pre-treatment in 30 DIV cultures, followed by addition of ACM from 15 DIV cultures, suggest that these phenomena may depend by extra cellular signal-regulated kinase 1 (ERK1) activation.

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Section: Discussionsupporting

confidence: 86%

Astroglial-Conditioned Media and Growth Factors Modulate Proliferation and Differentiation of Astrocytes in Primary Culture

et al. 2006

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“…The first CNS cell types in which TGF-beta was associated with an anti-proliferative activity, were astrocytes in culture (Johns et al 1992;Lindholm et al 1992;Morganti-Kossmann et al 1992;Baghdassarian et al 1993;Rich et al 1999). In these experiments, TGF-beta1 either had a direct influence on the division rate or acted as an antagonist to other growth Fig.…”

Section: Tgf-beta1 As a Cytostatic Factor Of Neural Stem Cells And Inmentioning

confidence: 98%

TGF-beta in neural stem cells and in tumors of the central nervous system

Aigner

Bogdahn

2007

Cell Tissue Res

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Mechanisms that regulate neural stem cell activity in the adult brain are tightly coordinated. They provide new neurons and glia in regions associated with high cellular and functional plasticity, after injury, or during neurodegeneration. Because of the proliferative and plastic potential of neural stem cells, they are currently thought to escape their physiological control mechanisms and transform to cancer stem cells. Signals provided by proteins of the transforming growth factor (TGF)-beta family might represent a system by which neural stem cells are controlled under physiological conditions but released from this control after transformation to cancer stem cells. TGF-beta is a multifunctional cytokine involved in various physiological and patho-physiological processes of the brain. It is induced in the adult brain after injury or hypoxia and during neurodegeneration when it modulates and dampens inflammatory responses. After injury, although TGF-beta is neuroprotective, it may limit the self-repair of the brain by inhibiting neural stem cell proliferation. Similar to its effect on neural stem cells, TGF-beta reveals anti-proliferative control on most cell types; however, paradoxically, many brain tumors escape from TGF-beta control. Moreover, brain tumors develop mechanisms that change the anti-proliferative influence of TGF-beta into oncogenic cues, mainly by orchestrating a multitude of TGF-beta-mediated effects upon matrix, migration and invasion, angiogenesis, and, most importantly, immune escape mechanisms. Thus, TGF-beta is involved in tumor progression. This review focuses on TGF-beta and its role in the regulation and control of neural and of brain-cancer stem cells.

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“…3 and 4). Indeed, many soluble factors with immunoregulatory potential, not only neurotransmitters, peptides and hormones, but also cytokines (Johns et al, 1992;Breder et al, 1994;Tani and Ransahoff, 1994;Ericsson et al, 1995), neurotrophins, and smaller molecules such as nitric oxide (Valtschanoff et al, 1993), are present in the brain. Nonsecreted molecules, including adhesion molecules and extracellular matrix components, can also influence immune regulation (Romanic and Madri, 1994).…”

Section: Site-specific Responses and A Proposed Role For The Local Nementioning

confidence: 99%

“…Evidence from other experimental systems suggests that both of these factors are likely to play a role. When analyzed in vitro, astrocytes from different brain sites show heterogeneity in MHC regulation (Johns et al, 1992); the behavior of microglia from different sites must now be defined.…”

Section: Site-specific Responses and A Proposed Role For The Local Nementioning

confidence: 99%

Site-specific immune regulation in the brain: Differential modulation of major histocompatibility complex (MHC) proteins in brainstem vs. hippocampus

1999

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Transforming growth factor-β1 differentially regulates proliferation and MHC class-II antigen expression in forebrain and brainstem astrocyte primary cultures

Cited by 47 publications

References 26 publications

Astroglial-Conditioned Media and Growth Factors Modulate Proliferation and Differentiation of Astrocytes in Primary Culture

Astroglial-Conditioned Media and Growth Factors Modulate Proliferation and Differentiation of Astrocytes in Primary Culture

TGF-beta in neural stem cells and in tumors of the central nervous system

Site-specific immune regulation in the brain: Differential modulation of major histocompatibility complex (MHC) proteins in brainstem vs. hippocampus

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