Knockdown of HMGN5 Expression by RNA Interference Induces Cell Cycle Arrest in Human Lung Cancer Cells

Chen, Peng,Wang, Xiu-Li,Ma, Zhong-Sen,Xu, Zhong,Jia, Bo,Ren, Jin,Hu, Yu-Xin,Zhang, Qing-Hua,Ma, Tian-Gang,Yan, Bing-Di,Yan, Qing-Zhu,Li, Yan-Lei,Li, Zhen,Yu, Jin-Yan,Gao, Rong,Fan, Na,Li, Bo,Yang, Jun Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.7

HMGN5 is a typical member of the HMGN (high mobility group nucleosome-binding protein) family which may function as a nucleosomal binding and transcriptional activating protein. Overexpression of HMGN5 has been observed in several human tumors but its role in tumorigenesis has not been fully clarified. To investigate its significance for human lung cancer progression, we successfully constructed a shRNA expression lentiviral vector in which sense and antisense sequences targeting the human HMGN5 were linked with a 9-nucleotide loop. Inhibitory effects of siRNA on endogenous HMGN5 gene expression and protein synthesis were demonstrated via real-time RT-PCR and western blotting. We found HMGN5 silencing to significantly inhibit A549 and H1299 cell proliferation assessed by MTT, BrdU incorporation and colony formation assays. Furthermore, flow cytometry analysis showed that specific knockdown of HMGN5 slowed down the cell cycle at the G0/G1 phase and decreased the populations of A549 and H1299 cells at the S and G2/M phases. Taken together, these results suggest that HMGN5 is directly involved in regulation cell proliferation in A549 and H1299 cells by influencing signaling pathways involved in cell cycle progression. Thus, our finding suggests that targeting HMGN5 may be an effective strategy for human lung cancer treatment.

Picosecond Mid-Infrared 3.8 μm MgO:PPLN Optical Parametric Oscillator Laser with High Peak Power

Bing-Yan Chen,Yu-Heng Wang,Yong-Ji Yu,Guang-Yong Jin 한국광학회 2021 Current Optics and Photonics Vol.5 No.2

In this study, a compact, picosecond, mid-infrared 3.8 μm MgO:PPLN optical parametric oscillator(OPO) laser output with high peak power is realized using a master oscillator power amplifier (MOPA)1 μm solid-state laser seeded by a picosecond fiber laser as the pump source. The pump source was a 50MHz and 10 ps fiber seed source. After AOM pulse selection and two-stage solid-state amplification, a 1,064 nm laser output with a repetition frequency of 1–2 MHz, pulse width of 9.5 ps, and a maximum average power of 20 W was achieved. Furthermore, a compact short cavity with a unsynchronized pump is adopted through the design of an OPO cavity structure. When the injection pump power was 15 W and the repetition frequency was 1 MHz, the average output power of idler light was 1.19 W, and the corresponding peak power was 119 kW. The optical conversion efficiency was 7.93%. When the repetition frequency was increased to 2 MHz, the average output power of idler light was 1.63 W, the corresponding peak power was 81.5 kW, and the optical conversion efficiency was 10.87%. At the same time, the output wavelength was measured at 3,806 nm, and the beam quality was M X2 = 3.21 and M Y2 = 3.34.

Colorectal Cancer Screening in High-risk Populations: a Survey of Cognition among Medical Professionals in Jiangsu, China

Chen, Yao-Sheng,Xu, Song-Xin,Ding, Yan-Bing,Huang, Xin-En,Deng, Bin,Gao, Xue-Feng,Wu, Da-Cheng Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.11

To investigate the cognition of medical professionals when following screening guidelines for colorectal cancer (CRC) and barriers to CRC screening. Between February 2012 and December 2012, an anonymous survey with 19-questions based on several CRC screening guidelines was randomly administered to gastroenterologists, oncologists, general surgeons, and general practitioners in Jiangsu, a developed area in China where the incidence of CRC is relatively high. The average cognitive score was 26.4% among 924 respondents. Gastroenterologists and oncologists had higher scores compared with others (p<0.01 and p<0.01, respectively); doctor of medicine (M.D.) with or without doctor of philosophy (Ph.D.) or holders with bachelor of medical science (BMS) achieved higher scores than other lower degree holders (P<0.05). More importantly, doctors who finished CRC related education in the past year achieved higher scores than the others (p<0.001). The most commonly listed barriers to referring high-risk patients for CRC screening were "anxiety about colonoscopy without anesthesia", "lack of awareness of the current guidelines" and "lack of insurance reimbursement". Lack of cognition was detected among doctors when following CRC screening guidelines for high-risk populations. Educational programs should be recommended to improve their cognition and reduce barriers to CRC screening.

Ethanol extract of <i>Oenanthe javanica</i> increases cell proliferation and neuroblast differentiation in the adolescent rat dentate gyrus

Chen, Bai Hui,Park, Joon Ha,Cho, Jeong Hwi,Kim, In Hye,Shin, Bich Na,Ahn, Ji Hyeon,Hwang, Seok Joon,Yan, Bing Chun,Tae, Hyun Jin,Lee, Jae Chul,Bae, Eun Joo,Lee, Yun Lyul,Kim, Jong Dai,Won, Moo-Ho,Kang Medknow PublicationsMedia Pvt Ltd 2015 Neural regeneration research Vol.10 No.2

<P><I>Oenanthe javanica</I> is an aquatic perennial herb that belongs to the <I>Oenanthe genus</I> in Apiaceae family, and it displays well-known medicinal properties such as protective effects against glutamate-induced neurotoxicity. However, few studies regarding effects of <I>Oenanthe javanica</I> on neurogenesis in the brain have been reported. In this study, we examined the effects of a normal diet and a diet containing ethanol extract of <I>Oenanthe javanica</I> on cell proliferation and neuroblast differentiation in the subgranular zone of the hippocampal dentate gyrus of adolescent rats using Ki-67 (an endogenous marker for cell proliferation) and doublecortin (a marker for neuroblast). Our results showed that <I>Oenanthe javanica</I> extract significantly increased the number of Ki-67-immunoreactive cells and doublecortin-immunoreactive neuroblasts in the subgranular zone of the dentate gyrus in the adolescent rats. In addition, the immunoreactivity of brain-derived neurotrophic factor was significantly increased in the dentate gyrus of the <I>Oenanthe javanica</I> extract-treated group compared with the control group. However, we did not find that vascular endothelial growth factor expression was increased in the <I>Oenanthe javanica</I> extract-treated group compared with the control group. These results indicate that <I>Oenanthe javanica</I> extract improves cell proliferation and neuroblast differentiation by increasing brain-derived neurotrophic factor immunoreactivity in the rat dentate gyrus.</P>

Increased cyclooxygenase-2 and nuclear factor-κB/p65 expression in mouse hippocampi after systemic administration of tetanus toxin

YAN, BING CHUN,JEON, YONG HWAN,PARK, JOON HA,KIM, IN HYE,CHO, JEONG-HWI,AHN, JI HYEON,CHEN, BAI HUI,TAE, HYUN-JIN,LEE, JAE-CHUL,AHN, JI YUN,KIM, DONG WON,CHO, JUN HWI,WON, MOO-HO,HONG, SEONGKWEON SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.12 No.6

<P>Brain inflammation has a crucial role in various diseases of the central nervous system. The hippocampus in the mammalian brain exerts an important memory function, which is sensitive to various insults, including inflammation induced by exo/endotoxin stimuli. Tetanus toxin (TeT) is an exotoxin with the capacity for neuronal binding and internalization. The present study investigated changes in inflammatory mediators in the mouse hippocampus proper (CA1-3 regions) and dentate gyrus (DG) after TeT treatment. The experimental mice were intraperitoneally injected with TeT at a low dosage (100 ng/kg), while the control mice were injected with the same volume of saline. At 6, 12 and 24 h after TeT treatment, changes in the hippocampal levels of inflammatory mediators cyclooxygenase-2 (COX-2) and nuclear factor kappa-B (NF-κB/p65) were assessed using immunohistochemical and western blot analysis. In the control group, moderate COX-2 immunoreactivity was observed in the stratum pyramidal (SP) of the CA2-3 region, while almost no expression was identified in the CA1 region and the DG. COX-2 immunoreactivity was increased by TeT in the SP and granule cell layer (GCL) of the DG in a time-dependent manner. At 24 h post-treatment, COX-2 immunoreactivity in the SP of the CA1 region and in the GCL of the DG was high, and COX-2 immunoreactivity in the SP of the CA2/3 region was highest. Furthermore, the present study observed that NF-κB/p65 immunoreactivity was obviously increased in the SP and GCL at 6, 12 and 24 h after TeT treatment. In conclusion, the present study demonstrated that systemic treatment with TeT significantly increased the expression of COX-2 and NF-κB/p65 in the mouse hippo-campus, suggesting that increased COX-2 and NF-κB/65 expression may be associated with inflammation in the brain induced by exotoxins.</P>

Melatonin improves vascular cognitive impairment induced by ischemic stroke by remyelination via activation of ERK1/2 signaling and restoration of glutamatergic synapses in the gerbil hippocampus

Chen, Bai Hui,Park, Joon Ha,Lee, Yun Lyul,Kang, Il Jun,Kim, Dae Won,Hwang, In Koo,Lee, Choong-Hyun,Yan, Bing Chun,Kim, Young-Myeong,Lee, Tae-Kyeong,Lee, Jae Chul,Won, Moo-Ho,Ahn, Ji Hyeon Elsevier 2018 BIOMEDICINE AND PHARMACOTHERAPY Vol.108 No.-

<P><B>Abstract</B></P> <P>Vascular dementia affects cognition by damaging axons and myelin. Melatonin is pharmacologically associated with various neurological disorders. In this study, effects of melatonin on cognitive impairment and related mechanisms were investigated in an animal model of ischemic vascular dementia (IVD). Melatonin was intraperitoneally administered to adult gerbils after transient global cerebral ischemia (tGCI) for 25 days beginning 5 days after tGCI. Cognitive impairment was examined using a passive avoidance test and the Barnes maze test. To investigate mechanisms of restorative effects by melatonin, neuronal damage/death, myelin basic protein (MBP, a marker for myelin), Rip (a marker for oligodendrocyte), extracellular signal-regulated protein kinase1/2 (ERK1/2) and phospho-ERK1/2 (p-ERK1/2), and vesicular glutamate transporter (VGLUT)-1 (a glutamatergic synaptic marker) in the hippocampal Cornu Ammonis 1 area (CA1) were evaluated using immunohistochemistry. Melatonin treatment significantly improved tGCI-induced cognitive impairment. Death of CA1 pyramidal neurons after tGCI was not affected by melatonin treatment. However, melatonin treatment significantly increased MBP immunoreactivity and numbers of Rip-immunoreactive oligodendrocytes in the ischemic CA1. In addition, melatonin treatment significantly increased ERK1/2 and p-ERK1/2 immunoreactivities in oligodendrocytes in the ischemic CA1. Furthermore, melatonin treatment significantly increased VGLUT-1 immunoreactive structures in the ischemic CA1. These results indicate that long-term melatonin treatment after tGCI improves cognitive deficit <I>via</I> restoration of myelin, increase of oligodendrocytes which is closely related to the activation of ERK1/2 signaling, and increase of glutamatergic synapses in the ischemic brain area.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Melatonin (Mel) improved impaired memory function after ischemia. </LI> <LI> Mel did not protect ischemia-induced (i-i) neuronal loss in the hippocampus. </LI> <LI> Mel recovered i-i damaged myelinated nerve fibers and oligodendrocytes. </LI> <LI> Mel increased ERK1/2 and p-ERK1/2 in oligodendrocytes in i-i hippocampus. </LI> <LI> Mel increased i-i damaged VGLUT-1 in the hippocampus. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Gender-independent efficacy of mesenchymal stem cell therapy in sex hormone-deficient bone loss via immunosuppression and resident stem cell recovery

Bing-Dong Sui,Ji Chen,Xin-Yi Zhang,Tao He,Pan Zhao,Chen-Xi Zheng,Meng Li,Cheng-Hu Hu,Yan Jin 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-

Osteoporosis develops with high prevalence in both postmenopausal women and hypogonadal men. Osteoporosis results in significant morbidity, but no cure has been established. Mesenchymal stem cells (MSCs) critically contribute to bone homeostasis and possess potent immunomodulatory/anti-inflammatory capability. Here, we investigated the therapeutic efficacy of using an infusion of MSCs to treat sex hormone-deficient bone loss and its underlying mechanisms. In particular, we compared the impacts of MSC cytotherapy in the two genders with the aim of examining potential gender differences. Using the gonadectomy (GNX) model, we confirmed that the osteoporotic phenotypes were substantially consistent between female and male mice. Importantly, systemic MSC transplantation (MSCT) not only rescued trabecular bone loss in GNX mice but also restored cortical bone mass and bone quality. Unexpectedly, no differences were detected between the genders. Furthermore, MSCT demonstrated an equal efficiency in rectifying the bone remodeling balance in both genders of GNX animals, as proven by the comparable recovery of bone formation and parallel normalization of bone resorption. Mechanistically, using green fluorescent protein (GFP)-based cell-tracing, we demonstrated rapid engraftment but poor inhabitation of donor MSCs in the GNX recipient bone marrow of each gender. Alternatively, MSCT uniformly reduced the CD3+T-cell population and suppressed the serum levels of inflammatory cytokines in reversing female and male GNX osteoporosis, which was attributed to the ability of the MSC to induce T-cell apoptosis. Immunosuppression in the microenvironment eventually led to functional recovery of endogenous MSCs, which resulted in restored osteogenesis and normalized behavior to modulate osteoclastogenesis. Collectively, these data revealed recipient sexually monomorphic responses to MSC therapy in gonadal steroid deficiency-induced osteoporosis via immunosuppression/anti-inflammation and resident stem cell recovery.

Systemic administration of low dosage of tetanus toxin decreases cell proliferation and neuroblast differentiation in the mouse hippocampal dentate gyrus

Bing Chun Yan,In Hye Kim,Joon Ha Park,Ji Hyeon Ahn,Jeong-Hwi Cho,Bai Hui Chen,Jae-Chul Lee,Jung Hoon Choi,Ki-Yeon Yoo,Choong Hyun Lee,Jun Hwi Cho,Jong-Dai Kim,Moo-Ho Won 한국실험동물학회 2013 Laboratory Animal Research Vol.29 No.3

In the present study, we investigated the effect of Tetaus toxin (TeT) on cell proliferation and neuroblast differentiation using specific markers: 5-bromo-2-deoxyuridine (BrdU) as an exogenous marker for cell proliferation, Ki-67 as an endogenous marker for cell proliferation and doublecortin (DCX) as a marker for neuroblasts in the mouse hippocampal dentate gyrus (DG) after TeT treatment. Mice were intraperitoneally administered 2.5 and 10 ng/kg TeT and sacrificed 15 days after the treatment. In both the TeT-treated groups, no neuronal death occurred in any layers of the DG using neuronal nuclei (NeuN, a neuron nuclei maker) and Fluoro-Jade B (F-J B, a high-affinity fluorescent marker for the localization of neuronal degeneration). In addition, no significant change in glial activation in both the 2.5 and 10 ng/kg TeT-treated-groups was found by GFAP (a marker for astrocytes) and Iba-1 (a marker for microglia) immunohistochemistry. However, in the 2.5 ng/kg TeT-treated-group, the mean number of BrdU, Ki-67 and DCX immunoreactive cells, respectively, were apparently decreased compared to the control group, and the mean number of each in the 10 ng/kg TeT-treated-group was much more decreased. In addition, processes of DCX-immunoreactive cells, which projected into the molecular layer, were short compared to those in the control group. In brief, our present results show that low dosage (10 ng/kg) TeT treatment apparently decreased cell proliferation and neuroblast differentiation in the mouse hippocampal DG without distinct gliosis as well as any loss of adult neurons.

Melatonin attenuates scopolamine-induced cognitive impairment via protecting against demyelination through BDNF-TrkB signaling in the mouse dentate gyrus

Chen, Bai Hui,Park, Joon Ha,Lee, Tae-Kyeong,Song, Minah,Kim, Hyunjung,Lee, Jae Chul,Kim, Young-Myeong,Lee, Choong-Hyun,Hwang, In Koo,Kang, Il Jun,Yan, Bing Chun,Won, Moo-Ho,Ahn, Ji Hyeon Elsevier 2018 Chemico-biological interactions Vol.285 No.-

<P><B>Abstract</B></P> <P>Animal models of scopolamine-induced amnesia are widely used to study underlying mechanisms and treatment of cognitive impairment in neurodegenerative diseases such as Alzheimer's disease (AD). Previous studies have identified that melatonin improves cognitive dysfunction in animal models. In this study, using a mouse model of scopolamine-induced amnesia, we assessed spatial and short-term memory functions for 4 weeks, investigated the expression of myelin-basic protein (MBP) in the dentate gyrus, and examined whether melatonin and scopolamine cotreatment could keep cognitive function and MBP expression. In addition, to study functions of melatonin for keeping cognitive function and MBP expression, we examined expressions of brain-derived neurotrophic factor (BDNF) and tropomycin receptor kinase B (TrkB) in the mouse dentate gyrus. Scopolamine (1 mg/kg) and melatonin (10 mg/kg) were intraperitoneally treated for 2 and 4 weeks. Two and 4 weeks after scopolamine treatment, mice showed significant cognitive impairment; however, melatonin and scopolamine cotreatment recovered cognitive impairment. Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus. Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus. Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Long-term treatment of scopolamine (Sco) induces cognitive deficits. </LI> <LI> Long-term treatment of melatonin improves Sco-induced cognitive deficits. </LI> <LI> Sco significantly decreases MBP, BDNF, and TrkB in the dentate gyrus. </LI> <LI> Melatonin restores scopolamine-induced decreases in MBP, BDNF, and TrkB. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Helicobacter pylori Infection and the Risk of Colorectal Adenoma and Adenocarcinoma: an Updated Meta-analysis of Different Testing Methods

Chen, Yao-Sheng,Xu, Song-Xin,Ding, Yan-Bing,Huang, Xin-En,Deng, Bin Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.12

Background and Aims: Helicobacter pylori infection may be associated with an increased risk of colorectal carcinoma. However, as most studies on this subject were relatively small in size and differed at least partially in their designs, their results remain controversial. In this study, we aimed to carry out a meta-analysis to evaluate the potential association of H. pylori infection with colorectal adenoma and adenocarcinoma risk, covering all of the different testing methods. Methods: We conducted a search in PubMed, Medline, EBSCO, High Wire Press, OVID, and EMBASE covering all published papers up to March 2013. According to the established inclusion criteria, essential data were then extracted from the included studies and further analyzed by a systematic meta-analysis. Odds ratios were employed to evaluate the relationship between H. pylori infection and the risk of colorectal neoplasms. Results: Twenty-two studies were included, and the odds ratio for the association between H. pylori infection and colorectal cancer was 1.49 (95% confidence interval 1.30-1.72). No statistically significant heterogeneity was observed. Publication bias was ruled out. Conclusion: The pooled data suggest H. pylori infection indeed increases the risk of colorectal adenoma and adenocarcinoma.