Induction of TGF-β-inducible gene-h3 (βig-h3) by TGF-β1 in astrocytes: implications for astrocyte response to brain injury

Yun, Su Jin; Kim, Miok; Kim, Sung Ok; Park, Ji Ho; Kwon, Yunhee Kim; Kim, In San; Lee, Eunjoo H.

doi:10.1016/s0169-328x(02)00447-3

Cited by 40 publications

(28 citation statements)

References 47 publications

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“…Among them, tumor necrosis factor (TNF)-a, interleukin (IL)-1, and IL-6 have been classically considered to be major components in the response to injury (for review; Rothwell and Hopkins, 1995), acting on various cell types and producing secondary damaging effects that in turn lead to lymphocyte recruitment and activation and may cause neuronal cell death (Kopf et al, 1994;Lee and Benveniste, 1999;Yun et al, 2002;Hansson and Ronnback, 2003;Raivich et al, 2003). IL-6 is a cytokine that has important roles in normal brain function, including control of thermogenesis (Chai et al, 1996), body weight (Wallenius et al, 2002), and emotional behavior (Armario et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Effect of astrocyte‐targeted production of IL‐6 on traumatic brain injury and its impact on the cortical transcriptome

Quintana

Molinero

Borup

et al. 2007

Developmental Neurobiology

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Interleukin-6 (IL-6) is one of the key players in the response of the brain cortex to injury. We have described previously that astrocyte-driven production of IL-6 (GFAP-IL6) in transgenic mice, although causing spontaneous neuroinflammation and long term damage, is beneficial after an acute (freeze) injury in the cortex, increasing healing and decreasing oxidative stress and apoptosis. To determine the transcriptional basis for these responses here we analyzed the global gene expression profile of the cortex, at 0 (unlesioned), 1 or 4 days post lesion (dpl), in both GFAP-IL6 mice and their control littermates. GFAP-IL6 mice showed an increase in genes associated with the inflammatory response both at 1 dpl (Iftm1, Endod1) and 4 dpl (Gfap, C4b), decreased expression of proapoptotic genes (i.e. Gadd45b, Clic4, p21) as well as reduced expression of genes involved in the control of oxidative stress (Atf4). Furthermore, the presence of IL-6 altered the expression of genes involved in hemostasis (Vwf), cell migration and proliferation (Cap2), and synaptic activity (Vamp2). All these changes in gene expression could underlie the phenotype of the GFAP-IL6 mice after injury, but many other possible factors were also identified in this study, highlighting the utility of this approach for deciphering new pathways orchestrated by IL-6.

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Section: Introductionmentioning

confidence: 99%

Effect of astrocyte‐targeted production of IL‐6 on traumatic brain injury and its impact on the cortical transcriptome

Quintana

Molinero

Borup

et al. 2007

Developmental Neurobiology

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“…Thus, increased TGF-β1 mRNA expression or its protein production may not necessarily reflect parallel changes in TGF-β1 bioactivity. The TGF-β1 inducible gene-h3 (βig-h3) is a matrix protein that is regulated by TGF-β1 [18]. In case of chronic CsA nephrotoxicity, βig-h3 has been suggested as an index of TGF-β1 bioactivity, and represents the degree of tubulointerstitial injury in human [19]and rat kidneys [Sun et al: J Lab Clin Med, in press].…”

Section: Introductionmentioning

confidence: 99%

Blockade of Angiotensin II with Losartan Attenuates Transforming Growth Factor-β1 Inducible Gene-h3 (βig-h3) Expression in a Model of Chronic Cyclosporine Nephrotoxicity

Sun

Lim

et al. 2005

Nephron Exp Nephrol

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Background: We recently demonstrated that upregulation of the transforming growth factor (TGF)-β1 inducible gene-h3 (βig-h3) is associated with tubulointerstitial fibrosis (TIF) in a rat model of chronic cyclosporine A (CsA) nephrotoxicity. This study investigated the association between βig-h3 expression and TIF during losartan treatment in this model. Methods: Adult Sprague-Dawley rats kept on a salt-depleted diet (0.05% sodium) were treated daily for 4 weeks with vehicle (olive oil, 1 ml/kg), CsA (15 mg/kg) or both CsA and losartan (10 mg/kg in drinking water). The effect of losartan on βig-h3 expression was evaluated using in situ hybridization, immunohistochemistry and immunoblotting. Histopathology, expressions of TGF-β1 and intrarenal angiotensin II were compared across treatment groups. Results: Concurrent administration of losartan significantly attenuated βig-h3 mRNA and protein expression within the tubulointerstitium of CsA-treated kidneys. This was accompanied by the retardation of TIF (18 ± 5 vs. 39 ± 5%, p < 0.01 vs. CsA) and the expression of TGF-β1 mRNA (336 ± 49 vs. 685 ± 63%, p < 0.01 vs. CsA) and the number of angiotensin II-positive glomeruli (18 ± 5 vs. 38 ± 6, p < 0.05 vs. CsA). Conclusion: Losartan is capable of abrogating the upregulation of TGF-β1 and βig-h3 expression, and this is associated with attenuated tubulointerstitial fibrosis in chronic CsA nephrotoxicity.

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“…For example, culture and in vivo studies suggest that these molecules enhance neuron differentiation and survival directly through the mediation of chemokine and cytokine receptors (Plata-Salaman, 1991 ;Mehler and Kessler, 1995 ;Arakawa et al, 2003 ;Emsley and Hagg, 2003) . Chemokine and cytokine knockout mice are impaired in the migration Nakamura et al, 1998bNakamura et al, , 1999 GDN or PN-1 Simpson et al, 1994;Brenneman et al, 1997;Kim et al, 2004 Gard et al, 1995;Silberstein et al, 1996;Sjoborg et al, 1998;Pang et al, 2001;Nakagawa and Schwartz, 2004 TGFa mRNA ( in vitro ) Ma et al, 1994;Lisovoski et al, 1997;Li et al, 2002 TGFb Ma et al, 1994;De Groot et al, 1999;Li et al, 2002;Yun et al, 2002;Meeuwsen et al, 2003Meeuwsen et al, , 2005Nakagawa and Schwartz, 2004;…”

Section: The Role Of Immune Moleculesmentioning

confidence: 99%

Release of Trophic Factors and Immune Molecules from Astrocytes

Jean

Bagayogo²,

Dreyfus

2008

Astrocytes in (Patho)Physiology of the Nervous System

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It is now quite clear that as part of their support role, astrocytes produce and release multiple proteins that impact survival, migration, differentiation, and function of proximate neurons. This astrocyte role is particularly evident during development, remains in play in the normal adult brain, and is enhanced after injury. The molecules produced include those known traditionally as cytokines, chemokines, and trophic factors. Importantly, these proteins can serve as trophic or toxic agents and may be differentially regulated by the signals impacting on astrocytes at various stages of brain development and maturity ( Fig. 13.1 ). The story of proteins produced by astrocytes, then, is a complex one. Multiple trophic or toxic molecules V. Parpura and P.G. Haydon (eds.), Astrocytes in (Patho)Physiology of the Nervous System, 351

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Induction of TGF-β-inducible gene-h3 (βig-h3) by TGF-β1 in astrocytes: implications for astrocyte response to brain injury

Cited by 40 publications

References 47 publications

Effect of astrocyte‐targeted production of IL‐6 on traumatic brain injury and its impact on the cortical transcriptome

Effect of astrocyte‐targeted production of IL‐6 on traumatic brain injury and its impact on the cortical transcriptome

Blockade of Angiotensin II with Losartan Attenuates Transforming Growth Factor-β1 Inducible Gene-h3 (βig-h3) Expression in a Model of Chronic Cyclosporine Nephrotoxicity

Release of Trophic Factors and Immune Molecules from Astrocytes

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