Effect of antisense oligonucleotide targeting bFGF on apoptosis of hepatoma cells

Qi, Jie-Lin; Wu, Ning; Li, Li; Bu, Bing; Zhou, Daohong; Zhang, Xiqin

doi:10.1007/s10330-008-0157-1

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“…In this study, we determined the effect that bFGF ASODN has on the proliferation and differentiation of NSCs in rat models with focal CI. Additionally, previous studies reported that treatment with bFGF ASODN can not only inhibit expression of bFGF protein, but it can also induce apoptosis in hepatoma HepG2 cells suggesting that there exists a different mechanism of bFGF in the treatment of CI [Qi et al, 2008]. Initially, MCAO þ ASODN group showed minor neurological deficits and less CI than the MCAO and MCAO þ NODN groups.…”

Section: Discussionmentioning

confidence: 91%

“…It was also revealed that bFGF was a promising treatment for preventing infarction [Ito et al, ]. Additionally, previous studies reported that treatment with bFGF ASODN can not only inhibit expression of bFGF protein, but it can also induce apoptosis in hepatoma HepG2 cells suggesting that there exists a different mechanism of bFGF in the treatment of CI [Qi et al, ].…”

Section: Discussionmentioning

confidence: 99%

“…DNA-like fragments are able to bind messenger RNA (mRNA) specific mRNA sequences and trigger intra-nuclear mRNA biodegradation [Winer et al, 2013]. Moreover, bFGF ASODN is able to suppress the expression of bFGF protein, promote apoptosis, and hinder the development of pulmonary fibrosis, possibly through the TGF-b1/Smad-based signaling mechanism [Qi et al, 2008;Chen et al, 2015]. Moreover, bFGF ASODN is able to suppress the expression of bFGF protein, promote apoptosis, and hinder the development of pulmonary fibrosis, possibly through the TGF-b1/Smad-based signaling mechanism [Qi et al, 2008;Chen et al, 2015].…”

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confidence: 99%

“…It has been proved that bFGF ASODN can inhibit tumor growth and angiogenesis [Cenni et al, 2005]. Moreover, bFGF ASODN is able to suppress the expression of bFGF protein, promote apoptosis, and hinder the development of pulmonary fibrosis, possibly through the TGF-b1/Smad-based signaling mechanism [Qi et al, 2008;Chen et al, 2015]. In order to explore the effects of bFGF ASODN on the proliferation and differentiation of NSCs, we conducted serval experiments and performed corresponding analysis in rat models with focal CI in the present study.…”

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confidence: 99%

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Retracted: Suppression of Basic Fibroblast Growth Factor Expression by Antisense Oligonucleotides Inhibits Neural Stem Cell Proliferation and Differentiation in Rat models With Focal Cerebral Infarction

Che

Shi

et al. 2017

J of Cellular Biochemistry

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This study is designed to investigate the role of basic fibroblast growth factor (bFGF) antisense oligonucleotide (ASODN) on the proliferation and differentiation of neural stem cells (NSCs) in rat models with focal cerebral infarction (CI). Seventy-five Sprague-Dawlay (SD) rats were randomly divided into the control, sham, middle cerebral artery occlusion (MCAO), MCAO + nonsense oligonucleotide (NODN), and MCAO + ASODN groups. Proliferation and differentiation of NSCs were detected by bromodeoxyuridine (BrdU) and immunofluorescence staining, respectively. ELISA was performed to detect the expressions of endogenous factors that include insulin-like growth factor 1 (IGF-1), glial cell line derived neurotrophic factor (GDNF), brain-derived neurotrophic factor (BDNF), transforming growth factor-α1 (TGF-α1), bFGF, and nerve growth factor (NGF). Results show significant neurological deficits and focal CI in the MCAO and MCAO + NODN groups. An obvious increase of NSC proliferation, reactive proliferation of astrocytes in CI areas, differentiation of newly proliferated NSCs into mature neuronal cells, and expressions of endogenous growth factors exhibited in the MCAO, MCAO + NODN and MCAO + ASODN groups. Compared to the MCAO and MACO + NODN groups, the MCAO + ASODN group showed a significant decrease NSC proliferation and differentiation in CI areas as well as decrease expressions of endogenous growth factors. These findings may offer insight to help us understand more as to how bFGF ASODN can effectively suppress the proliferation and differentiation of NSCs. These findings are expected to help contribute to research for new targets in the treatment of focal CI. J. Cell. Biochem. 118: 3875-3882, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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