Thymosin beta-4 upregulates anti-oxidative enzymes and protects human cornea epithelial cells against oxidative damage

Ho, Jcm; Tseng, K.-C.; Ma, W.-H.; Chen, K-H; Lee, O K-S; Su, Yeu

doi:10.1136/bjo.2007.136747

Cited by 55 publications

(54 citation statements)

References 24 publications

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“…The human HSC cell line LX-2 was used in this study because of its similarity to primary human stellate cells; LX-2 cells express α-SMA, vimentin, platelet derived growth factor receptor β (PDGF-Rβ), matrix metalloproteinase (MMP)-2, and tissue inhibitor of matrix metalloproteinase (TIMP)-2 [6]. PI3K (phosphoinositide 3-kinase) is composed of an 85-kDa regulatory subunit and a 110-kDa catalytic subunit, which is recruited to and activated by the activated PDGF receptor following HSC activation and growth factor stimulation [7,8,9]. It has been reported that the activation of the PI3K/Akt pathway can facilitate HSC proliferation and α1 collagen expression [7,10,11].…”

Section: Introductionmentioning

confidence: 99%

“…PI3K (phosphoinositide 3-kinase) is composed of an 85-kDa regulatory subunit and a 110-kDa catalytic subunit, which is recruited to and activated by the activated PDGF receptor following HSC activation and growth factor stimulation [7,8,9]. It has been reported that the activation of the PI3K/Akt pathway can facilitate HSC proliferation and α1 collagen expression [7,10,11]. In this regard, the activation of PI3K/Akt signaling significantly contributes to fibrotic progression.…”

Section: Introductionmentioning

confidence: 99%

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Depletion of Thymosin �4 Promotes the Proliferation, Migration, and Activation of Human Hepatic Stellate Cells

Xiao¹,

et al. 2014

Cell Physiol Biochem

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Background & Aims: It has recently been reported that thymosin beta-4 (Tβ4) has anti-fibrogenic effects in human hepatic stellate cells (HSCs) in vitro, but the mechanisms underlying these effects remain unclear. The aim of this study was to investigate the roles of Tβ4 in the proliferation, migration, and activation of HSCs. Methods: Enzyme-linked immunosorbent assays (ELISA), immunohistochemistry, and western blot assays were utilized to determine the expression levels of Tβ4 in serum, liver tissues, and LX-2 cells. Tβ4 was depleted in LX-2 cells using small interfering RNAs (siRNAs). Cell proliferation was analyzed using cell counting kit-8 (CCK-8) viability assays, and cell migration was investigated using wound-healing and transwell migration assays. Results: The expression of Tβ4 was significantly reduced during the progression of liver fibrosis. The depletion of Tβ4 significantly promoted the proliferation and migration of LX-2 cells via the activation of the PI3K/Akt signaling pathway. The pro-migratory and pro-proliferative effects of Tβ4 depletion in LX-2 cells can be counteracted by treatment with the Akt inhibitor MK-2206. In addition, Tβ4 depletion was also associated with the activation of HSCs via the enhanced expression of α-smooth muscle actin (α-SMA) and vimentin. Conclusions: Our results suggest that Tβ4 participates in liver fibrosis by inhibiting the migration, proliferation, and activation of HSCs and that Tβ4 may be an effective target in the treatment of liver fibrosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Depletion of Thymosin �4 Promotes the Proliferation, Migration, and Activation of Human Hepatic Stellate Cells

Xiao¹,

et al. 2014

Cell Physiol Biochem

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“…Mild effect of ROS may indirectly increased cell proliferation whereas the acute effect of high amount of ROS directly affects cell survival which are sensitive to apoptotic death (Moon et al 2004). Human corneal epithelial cells are protected by TB4P treatment through the expression of anti-oxidative enzymes such as manganese superoxide dismutase (SOD), copper/zinc SOD, and catalase (Ho et al 2008). We found that tumor cell density was increased by TB4P, which reduced by the treatment with NAC (Fig.…”

Section: Discussionmentioning

confidence: 90%

Actin-sequestering protein, thymosin beta-4, induces paclitaxel resistance through ROS/HIF-1α stabilization in HeLa human cervical tumor cells

Moon

2010

Life Sciences

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“…Therefore, it is not surprising that antioxidants and free radical scavengers have been used to attenuate ethanolinduced neurotoxicity in vitro and in vivo (Reyes et al 1993;Guerri et al 1994;Montoliu et al 1995;Heaton et al 2000;González et al 2007;Salazar et al 2008) and to prevent the damage of lipid peroxidation and consequent neurodegenerative diseases (Reyes et al 1993). One previous observation showed that Tb4 attenuated membrane lipid peroxidation and thus protected injured human cornea epithelial cells (Ho et al 2008). In the present study, we also detected that Tb4 can significantly eliminate ethanolinduced ROS accumulation and MDA production in astrocytes.…”

Section: Discussionmentioning

confidence: 95%

Thymosin-β4 Attenuates Ethanol-induced Neurotoxicity in Cultured Cerebral Cortical Astrocytes by Inhibiting Apoptosis

et al. 2009

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Thymosin-beta4 (Tbeta4) is a major actin monomer-binding peptide in mammalian tissues and plays a crucial role in the nervous system in synaptogenesis, neuronal survival and migration, axonal growth, and plastic changes of dendritic spines. However, it is unknown whether Tbeta4 is also involved in challenges with external stress such as ethanol-induced neurotoxicity. In the present study, we investigated the effects of Tbeta4 on ethanol-induced neurotoxicity in cultured cerebral cortical astrocytes and the underlying mechanisms. Primarily cultured astrocytes were treated with 1 microg/ml Tbeta4 2 h prior to administration of 100 mM ethanol for 0.5, 1, 3 and 6 days, respectively. The results showed that ethanol caused neurotoxicity in cultured astrocytes, as shown by declined cell viability, distinct astroglial apoptosis and increased intracellular peroxidation. Tbeta4 markedly promoted cell viability, ameliorated the injury of intracellular glial fibrillary acidic protein-immunopositive cytoskeletal structures, reduced the percentage of apoptotic astrocyte and cellular DNA fragmentation, suppressed caspase-3 activity and upregulated Bcl-2 expression, inhibited the accumulation of reactive oxygen species and production of malondialdehyde in ethanol-treated astrocytes in a time-dependent manner. These data indicated that Tbeta4 attenuates ethanol-induced neurotoxicity in cultured cortical astrocytes through inhibition of apoptosis signaling, and one of the mechanisms underlying the capacity of Tbeta4 to suppress apoptosis may in part be due to its effect of anti-peroxidation.

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Thymosin beta-4 upregulates anti-oxidative enzymes and protects human cornea epithelial cells against oxidative damage

Abstract: To the best of the authors' knowledge, this is the first report to show that T beta(4 )was capable of upregulating anti-oxidative enzymes in human corneal epithelial cells, and these findings further support its role in cornea protection.

Cited by 55 publications

References 24 publications

Depletion of Thymosin �4 Promotes the Proliferation, Migration, and Activation of Human Hepatic Stellate Cells

Depletion of Thymosin �4 Promotes the Proliferation, Migration, and Activation of Human Hepatic Stellate Cells

Actin-sequestering protein, thymosin beta-4, induces paclitaxel resistance through ROS/HIF-1α stabilization in HeLa human cervical tumor cells

Thymosin-β4 Attenuates Ethanol-induced Neurotoxicity in Cultured Cerebral Cortical Astrocytes by Inhibiting Apoptosis

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