Radioprotective Effect of Heat Shock Protein 25 on Submandibular Glands of Rats

Lee, Hae June; Lee, Yoon Jin; Kwon, Hee Chung; Bae, Sangwoo; Kim, Sung Hoon; Min, Jung Joon; Cho, Chul Koo; Lee, Yun Sil

doi:10.2353/ajpath.2006.060327

Cited by 39 publications

(24 citation statements)

References 44 publications

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“…An adequate balance between cell proliferation and programmed cell death or apoptosis is a key feature in the maintenance of the normal architecture and function of SMG (De la Cal et al 2006, Limesand et al 2006, Muhvic-Urek et al 2006, Lee et al 2006, Redman 2008, Avila et al 2009). …”

Section: Effect Of Histamine On Cell Proliferation and Apoptosis In Imentioning

confidence: 96%

Histamine prevents functional and morphological alterations of submandibular glands induced by ionising radiation

Medina

Prestifilippo²,

Croci³

et al. 2010

International Journal of Radiation Biology

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Section: Effect Of Histamine On Cell Proliferation and Apoptosis In Imentioning

confidence: 96%

Histamine prevents functional and morphological alterations of submandibular glands induced by ionising radiation

Medina

Prestifilippo²,

Croci³

et al. 2010

International Journal of Radiation Biology

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“…Sections were prepared at 3 Am in thickness, dewaxed, and then rehydrated. Sections were stained with ST6Gal I antibody and immunoperoxidase labeling was done as previously described (62).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Protein Sialylation by Sialyltransferase Involves Radiation Resistance

Lee

Bae

et al. 2008

Molecular Cancer Research

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Previously, we identified B-galactoside A(2,6)-sialyltransferase (ST6Gal I) as a candidate biomarker for ionizing radiation. The expression of ST6Gal I and the level of protein sialylation increased following radiation exposure in a dose-dependent manner. Radiation induced ST6Gal I cleavage and the cleaved form of ST6Gal I was soluble and secreted. Sialylation of integrin B1, a glycosylated cell surface protein, was stimulated by radiation exposure and this increased its stability. Overexpression of ST6Gal I in SW480 colon cancer cells that initially showed a low level of ST6Gal I expression increased the sialylation of integrin B1 and also increased the stability of the protein. Inhibition of sialylation by transfection with neuraminidase 2 or neuraminidase 3 or by treatment with short interfering RNA targeting ST6Gal I reversed the effects of ST6Gal I overexpression. In addition, ST6Gal I overexpression increased clonogenic survival following radiation exposure and reduced radiation-induced cell death and caspase 3 activation. However, removal of sialic acids by neuraminidase 2 or knockdown of expression by short interfering RNA targeting ST6Gal I restored radiation-induced cell death phenotypes. In conclusion, radiation exposure was found to increase the sialylation of glycoproteins such as integrin B1 by inducing the expression of ST6Gal I, and increased protein sialylation contributed to cellular radiation resistance. (Mol Cancer Res 2008;6(8):1316 -25)

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“…46 Their capability to protect cells against apoptosis has led to exploration of several HSPs, especially HSP25 as protective agents against the insults of chemotherapy and XRT. 47,48 The mechanism by which HSPs reduces apoptosis is unknown, but putative mechanisms include binding cytochrome c, 49 degradation of unfolded proteins via the ubiquitin pathway, 50 binding Daxx, 51 delaying cell growth, 52 inducing MnSOD expression, 53 downregulating ERK1/2 expressing, 54 and inhibiting PKCδ-mediated production of reactive oxygen species. 55 …”

Section: Heat Shock Protein 25mentioning

confidence: 99%

Gene therapy for radioprotection

Everett

Curiel

2015

Cancer Gene Ther

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Radiation therapy is a critical component of cancer treatment with over half of patients receiving radiation during their treatment. Despite advances in image guided therapy and dose fractionation, patients receiving radiation therapy are still at risk for side effects due to off-target radiation damage of normal tissues. To reduce normal tissue damage, researchers have sought radioprotectors, agents capable of protecting tissue against radiation by preventing radiation damage from occurring or by decreasing cell death in the presence of radiation damage. While much early research focused on small molecule radioprotectors, there has been a growing interest in gene therapy for radioprotection. The amenability of gene therapy vectors to targeting, as well as the flexibility of gene therapy to accomplish ablation or augmentation of biologically relevant genes, makes gene therapy an excellent strategy for radioprotection. Future improvements to vector targeting and delivery should greatly enhance radioprotection through gene therapy.

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Radioprotective Effect of Heat Shock Protein 25 on Submandibular Glands of Rats

Cited by 39 publications

References 44 publications

Histamine prevents functional and morphological alterations of submandibular glands induced by ionising radiation

Histamine prevents functional and morphological alterations of submandibular glands induced by ionising radiation

Protein Sialylation by Sialyltransferase Involves Radiation Resistance

Gene therapy for radioprotection

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