Early alteration in TGF-β mRNA expression in irradiated rat liver

Seong, Joon Kyung; Kim, Sung Hee; Chung, Eun Ji; Lee, Won Jae; Suh, Chang‐Ok

doi:10.1016/s0360-3016(99)00401-0

Cited by 41 publications

(32 citation statements)

References 20 publications

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“…19 Since the observation that TGF-b1 was increased in a dose-dependent manner in irradiated rat liver, 20 multiple studies have demonstrated the involvement of TGF-b1 in direct radiation responses [21][22][23][24][25][26][27][28] and as an important mediator in RIBE. [10][11][12] It was suggested that TGF-b1 is induced by radiation at both transcriptional 23 and post-transcriptional levels.…”

Section: Introductionmentioning

confidence: 99%

MiR-663 inhibits radiation-induced bystander effects by targetingTGFB1in a feedback mode

Hu¹,

Xu²,

Yao

et al. 2014

RNA Biology

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The mechanisms of radiation-induced bystander effects (RIBE) have been investigated intensively over the past two decades. Although quite a few reports demonstrated that cytokines such as TGF-b1 are induced within the directly irradiated cells and play critical roles in mediating the bystander effects, little is known about the signaling pathways that occur in bystander cells. The crucial question as to why RIBE signals cannot be infinitely transmitted, therefore, remains unclear. In the present study, we showed that miR-663, a radiosensitive microRNA, participates in the regulation of biological effects in both directly irradiated and bystander cells via its targeting of TGF-b1. MiR-663 was downregulated, while TGFB1 was upregulated in directly irradiated cells. The regulation profile of miR-663 and TGFB1, on the other hand, was reversed in bystander cells, in which an elevated miR-663 expression was exhibited and led to downregulation of TGF-b1. Further studies revealed that miR-663 interacts with TGFB1 directly and that through its binding to the core regulation sequence, miR-663 suppresses the expression of TGFB1. Based on the results, we propose that miR-663 inhibits the propagation of RIBE in a feedback mode, in which the induction of TGF-b1 by reduced miR-663 in directly irradiated cells leads to increased level of miR-663 in bystander cells. The upregulation of miR-663 in turn suppresses the expression of TGF-b1 and limits further transmission of the bystander signals.

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Section: Introductionmentioning

confidence: 99%

MiR-663 inhibits radiation-induced bystander effects by targetingTGFB1in a feedback mode

Hu¹,

Xu²,

Yao

et al. 2014

RNA Biology

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“…This increased oxidative stress has been shown to be involved in the development and pathogenesis of late radiation-induced fibrosis in normal tissues (16). Both preclinical and clinical studies have pointed to a close relationship between the level of TGF-b and radiation-induced fibrosis (14,(17)(18)(19). Thus, TGF-b1 may play a role in radiation-induced effects by mediating multicellular interactions involving a cytokine activation cascade.…”

Section: Introductionmentioning

confidence: 99%

Radiation-Induced Liver Fibrosis Is Mitigated by Gene Therapy Inhibiting Transforming Growth Factor-β Signaling in the Rat

Du¹,

Mei²,

Zeng³

et al. 2010

International Journal of Radiation Oncology*Biology*Physics

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“…64 Within 24 hours of partial liver irradiation in rats, an increase in TGF-␤1 mRNA was reported. 65 The overexpression of TGF-␤1 was dose dependent and reached a peak at 28 days. Immunohistochemistry staining for TGF-␤1 showed an increased concentration around the central vein in nonhepatocytic cells.…”

Section: Radiation-induced Liver Fibrosismentioning

confidence: 99%

“…78 In another study with the same dose and frequency of IFN-␥, there also was a stabilization of visceral involvement. 79 A higher dose of IFN-␥ (150 mcg per day) induced a significant decrease in skin thickness compared with a lower dose (60 mcg per 17 Rat Intestines 0, 12 ISH Increased Wang et al 18 Rat Intestines 0, 12 CIA, IH Increased Hauer-Jensen et al 19 Rat Intestines 21 RTP, ISH Increased Zheng et al 20 Mouse Intestines 21 RTP, IH Inhibited by soluble TGF-␤ receptor Richter et al 23 Human Intestines NS IH Increased Bai et al 38 Rat Lungs 30 IH, ISH Increased Rube et al 39 Mouse Lungs 6, 12 IH, RTP Increased Rubin et al 43 Mouse Lungs 5 IH, ISH Increased Anscher et al 45 Human Lungs NS EIA Increased Randall and Coggle 50 Mouse Skin 50 PCR Increased Martin et al 51 Pig Skin 140 NBH, SBT, IF Increased Lefaix et al 55 Pig Skin 160 US, IH Inhibited by PTX and vit E Zhao et al 60 Rat Kidney 1-10 NBA Increased Robbins et al 61 Rat Kidney 10, 15, 20 IH Increased Zhao et al 62 Rat Kidney 1-10 WBA, LA Increased Datta et al 63 Rat Kidney 15 EIA Increased Seong et al 65 Rat Liver 25 IH Increased Geraci and Mariqno 66 Rat Liver 25 RH Increased Anscher et al 67 Rat Liver NS IH Increased TGF-␤: transforming growth factor beta; Gy: Gray; NS: not specified; IH: immunohistochemistry; RIS: radiation injury scoring; TBS: toluidine blue stain; ISH: in situ hybridization; CIA: computerized image analysis; RTP: reverse transcriptase polymerase; EIA: enzyme-linked immunosorbent assay; US: ultrasound; NBH: Northern blot hybridization; SBH: Southern blot hybridization; PCR: polymerase chain reaction; NBA: Northern blot analysis; WBA: Western blot analysis; LA: luciferase assay; RH: ribonucleic acid hybridization; PTX: pentoxifylline; vit E: vitamin E. day). 80 The beneficial effect of IFN-␥ on skin lesions also was reported in a randomized study: Mouth aperture and skin scores increased significantly in the treated group after 12 months of treatment with IFN-␥ (100 mcg per day).…”

Section: Sclerodermamentioning

confidence: 99%

Current concepts in radiation enteritis and implications for future clinical trials

Nguyen

Antoine

Dutta

et al. 2002

Cancer

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BACKGROUNDRadiation enteritis is one of the most feared complications of abdominal and pelvic radiation. Once its occurs, the process is relentless and may result in the patient's death. Available treatment is only supportive. Recent progress in molecular biology has shed some light on the pathogenesis of radiation enteritis and other diseases that are characterized by excessive fibrosis. New treatment modalities may be devised to improve the outcome of patients who are affected with this complication.METHODSA literature search was used to identify the common denominator between many radiation‐induced fibrotic conditions and other sclerotic diseases. Factors that affect the disease process and possible therapeutic interventions were evaluated.RESULTSThe hyperstimulation of transforming growth factor β1 (TGF‐β1) leads to increased fibrosis and, ultimately, organ failure. Interferon gamma (IFN‐γ) inhibits the effects of TGF‐β1 in the nucleus. The fibrotic process may be reverted by IFN‐γ in various pathologic conditions.CONCLUSIONSRadiation enteritis and other radiation‐induced, long‐term complications are characterized by excessive stimulation of TGF‐β1. Preliminary studies suggest that IFN‐γ may be effective in the treatment of patients with radiation‐induced cutaneous fibrosis. IFN‐γ should be considered in Phase I–II studies to assess its toxicity and efficacy in the treatment of patients with radiation enteritis. Cancer 2002;95:1151–63. © 2002 American Cancer Society.DOI 10.1002/cncr.10766

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Early alteration in TGF-β mRNA expression in irradiated rat liver

Cited by 41 publications

References 20 publications

MiR-663 inhibits radiation-induced bystander effects by targetingTGFB1in a feedback mode

MiR-663 inhibits radiation-induced bystander effects by targetingTGFB1in a feedback mode

Radiation-Induced Liver Fibrosis Is Mitigated by Gene Therapy Inhibiting Transforming Growth Factor-β Signaling in the Rat

Current concepts in radiation enteritis and implications for future clinical trials

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