Expression of exogenous LIN28 contributes to proliferation and survival of mouse primary cortical neurons in vitro

Bhuiyan, Mohammad Iqbal Hossain; Lee, J.-H.; Kim, Seong Yun; Cho, Kyung-Ok

doi:10.1016/j.neuroscience.2013.06.023

Cited by 23 publications

(20 citation statements)

References 52 publications

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“…As development proceeds, its Multi-expressed in several tissues such as cardiac and skeletal muscles [19, 20]. With research on Lin28 growing number of studies have found it also expressed in the central nervous system [21]. This is consistent with the results we saw in the expression of Lin28 in GeneCards.…”

Section: Introductionsupporting

confidence: 81%

LIN28 Expression in Rat Spinal Cord After Injury

et al. 2014

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LIN28, an RNA-binding protein, is known to be involved in the regulation of many cellular processes, such as embryonic stem cell proliferation, cell fate succession, developmental timing, and oncogenesis. However, its expression and function in central nervous system still unclear. In this study, we performed an acute spinal cord contusion injury (SCI) model in adult rats and investigated the dynamic changes of LIN28 expression in spinal cord. Western blot and immunohistochemistry analysis revealed that LIN28 was present in normal spinal cord. It gradually increased, reached a peak at 3 day, and then nearly declined to the basal level at 14 days after SCI. Double immunofluorescence staining showed that LIN28 immunoreactivity was found in neurons, astrocytes and a handful of microglia. Interestingly, LIN28 expression was increased predominantly in astrocytes but not in neurons. Moreover, the colocalization of LIN28 and proliferating cell nuclear antigen was detected after injury. Western blot showed that LIN28 participated in lipopolysaccharide (LPS) induced astrocytes inflammatory responses by NF-κB signaling pathway. These results suggested that LIN28 may be involved in the pathologic process of SCI, and further research is needed to have a good understanding of its function and mechanism.

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Section: Introductionsupporting

confidence: 81%

LIN28 Expression in Rat Spinal Cord After Injury

et al. 2014

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“…Tables and list the genes identified by miRDB related to miRNAs affected by PM 2.5 . Genes with the highest correlation score of 100 were selected (Walaas and Greengard, ; Elferink et al, ; Blanco et al, ; Wu and Belasco, ; Janssen and Marynen, ; Takahashi et al, ; Bhattacherjee et al, ; Bourguignon et al, ; Dauwerse et al, ; Claustre et al, ; Golan et al, ; Holian et al, ; Amsen, ; Hosakote et al, ; Kalivas, ; Katoh and Katoh, ; Lan et al, ; Shimojima et al, ; Kim et al, ; Mohan et al, ; Schlager et al, ; Tanaka et al, ; Sato et al, ; Schultz et al, ; Christopoulou et al, ; Hertel et al, ; Nishimura et al, ; Wilhelmsson et al, ; Xu et al, ; Bhuiyan et al, ; Cotter et al, ; Derlig et al, ; Dhanoa et al, ; Elton et al, ; Gaudin et al,. ; Gomez‐Hierro et al, ; Ivankova et al, ; Kobayashi et al, ; Kwon et al, ; Lovero et al, ; Luhrig et al, ; Mas et al, ; Watanabe et al, ; Ando et al, ; Born et al, ; Naj et al, ; Monsalve et al, ; Orre et al, ; Wright et al, ; Maeda, ; Rajkowska et al, ; Sirko et al, ; Srivastava et al, ; Wang et al, ; Werner et al, ).…”

Section: Resultsmentioning

confidence: 99%

Exposure to PM_2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus

Chao

Yang

Lin

et al. 2016

Environmental Toxicology

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PM travels along the respiratory tract and enters systemic blood circulation. Studies have shown that PM increases the incidence of various diseases not only in adults but also in newborn infants. It causes chronic inflammation in pregnant women and retards fetal development. In this study, pregnant rats were exposed to PM for extended periods of time and it was found that PM exposure increased immune cells in mother rats. In addition, cytokines and free radicals rapidly accumulated in the amniotic fluid and indirectly affected the fetuses. The authors collected cerebral cortex and hippocampus samples at E18 and analyzed changes of miRNA levels. Expression levels of cortical miR-6315, miR-3588, and miR-466b-5p were upregulated, and positively correlated with the genes Pkn2 (astrocyte migration), Gorab (neuritogenesis), and Mobp (allergic encephalomyelitis). In contrast, PM decreased expression of miR-338-5p and let-7e-5p, both related to mental development. Further, PM exposure increased miR-3560 and let-7b-5p in the hippocampus, two proteins that regulate genes Oxct1 and Lin28b that control ketogenesis and glycosylation, and neural cell differentiation, respectively. miR-99b-5p, miR-92b-5p, and miR-99a-5p were decreased, leading to reduced expression of Kbtbd8 and Adam11 which reduced cell mitosis, migration, and differentiation, and inhibited learning abilities and motor coordination of the fetus. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1412-1425, 2017.

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“…Abnormal expression of Lin28a/b has also been linked to different kinds of tumors ( Nguyen et al, 2014 ; Tu et al, 2015 ; Urbach et al, 2014 ; Viswanathan et al, 2009 ; Wang et al, 2015 ; West et al, 2009 ). To our knowledge, the roles of Lin28 signaling in postmitotic neurons were only explored in three studies ( Amen et al, 2017 ; Bhuiyan et al, 2013 ; Huang et al, 2012 ). Lin28a/b mainly functions through let-7 microRNA (miRNA) family-dependent manners by posttranscriptionally blocking the biogenesis of mature let-7 miRNAs ( Heo et al, 2008 ; Nam et al, 2011 ; Newman et al, 2008 ; Rybak et al, 2008 ; Thornton et al, 2012 ; Viswanathan et al, 2008 ).…”

Section: Introductionmentioning

confidence: 99%

Lin28 Signaling Supports Mammalian PNS and CNS Axon Regeneration

et al. 2018

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SUMMARYRNA-binding proteins Lin28a/b regulate cellular growth and tissue regeneration. Here, we investigated the role of Lin28 in the control of axon regeneration in postmitotic neurons. We find that Lin28a/b are both necessary and sufficient for supporting axon regeneration in mature sensory neurons through their regulatory partners, let-7 microRNAs (miRNAs). More importantly, overexpression of Lin28a in mature retinal ganglion cells (RGCs) produces robust and sustained optic nerve regeneration. Additionally, combined overexpression of Lin28a and downregulation of Pten in RGCs act additively to promote optic nerve regeneration, potentially by reducing the backward turning of regenerating RGC axons. Our findings not only reveal a vital role of Lin28 signaling in regulating mammalian axon regeneration but also identify a signaling pathway that can promote axon regeneration in the central nervous system (CNS).

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Expression of exogenous LIN28 contributes to proliferation and survival of mouse primary cortical neurons in vitro

Cited by 23 publications

References 52 publications

LIN28 Expression in Rat Spinal Cord After Injury

LIN28 Expression in Rat Spinal Cord After Injury

Exposure to PM_2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus

Lin28 Signaling Supports Mammalian PNS and CNS Axon Regeneration

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Expression of exogenous LIN28 contributes to proliferation and survival of mouse primary cortical neurons in vitro

Cited by 23 publications

References 52 publications

LIN28 Expression in Rat Spinal Cord After Injury

LIN28 Expression in Rat Spinal Cord After Injury

Exposure to PM2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus

Lin28 Signaling Supports Mammalian PNS and CNS Axon Regeneration

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Exposure to PM_2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus