TIA1 interacts with annexin A7 in regulating vascular endothelial cell autophagy

Huang, Shuya; Liu, Ning; Li, Haiying; Zhao, Jing; Su, Le; Zhang, Yun; Zhang, Shangli; Zhao, Bao‐Xiang; Jiang, Miao

doi:10.1016/j.biocel.2014.10.015

Cited by 23 publications

(14 citation statements)

References 28 publications

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“…Our previous data suggested that ABO is an appropriate molecule for finding new factors which could inhibit VEC apoptosis 20 21 22 23 24 . By morphological observation, AO staining and TUNEL assay, we confirmed that ABO efficiently inhibited the serum and FGF-2 starvation-induced apoptosis in HUVECs ( Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

Huang

et al. 2016

Sci Rep

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Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) are key regulators of multiple biological processes by altering gene expression at various levels. Apoptosis in vascular endothelial cells (VECs) is closely linked to numerous cardiovascular diseases, such as arteriosclerosis, thrombus formation and plaque erosion. However, studies on lncRNAs in the cardiovascular system are just beginning. And thus far, no anti-apoptosis lncRNAs have been identified in VECs. Here, we focused on the anti-apoptosis roles of lncRNAs in the serum and FGF-2 starvation-induced apoptosis of VECs. Using microarray analysis, we found a novel lncRNA LOC100129973 which acted as an apoptosis inhibitor in VECs. Through sponging miR-4707-5p and miR-4767, lncRNA LOC100129973 upregulated the expression of two apoptosis repressors gene, Apoptosis Inhibitor 5 (API5) and BCL2 like 12 (BCL2L12), and thus alleviated the serum and FGF-2 starvation-induced apoptosis in VECs. This evidence suggests that lncRNA LOC100129973 is an attractive target to improve endothelial function and for therapy of apoptosis related cardiovascular diseases.

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Section: Resultsmentioning

confidence: 99%

Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

Huang

et al. 2016

Sci Rep

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“…Activated LIMK2 then phosphorylates cofilin to promote actin reorganization [ 57 ]. We previously reported that ABO-induced inhibition of ANXA7 GTPase activity decreased the phosphorylation of GCA and TIA-1 [ 27 , 58 ]. In the current study, SEC-activated ANXA7 GTPase increased the phosphorylation of ITGB4.…”

Section: Discussionmentioning

confidence: 99%

A small molecule induces integrin β4 nuclear translocation and apoptosis selectively in cancer cells with high expression of integrin β4

et al. 2016

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Increased integrin β4 (ITGB4) level is accompanied by malignant progression of multiple carcinomas. However, selective therapeutic strategies against cancer cells expressing a high level of ITGB4 have not been reported. Here, for the first time, we report that a chiral small molecule, SEC, selectively promotes apoptosis in cancer cells expressing a high level of ITGB4 by inducing ITGB4 nuclear translocation. Nuclear ITGB4 can bind to the ATF3 promoter region and activate the expression of ATF3, then upregulate the downstream pro-apoptosis genes. Furthermore, SEC promoted the binding of annexin A7 (ANXA7) to ITGB4 and increased ANXA7 GTPase activity. Activated ANXA7 promoted ITGB4 nuclear translocation by triggering ITGB4 phosphorylation at Y1494. SEC also inhibited the growth of xenograft tumors in the avian embryo model. We identified a small molecule, SEC, with selective pro-apoptosis effects on cancer cells with high expression of ITGB4, both in vitro and in vivo, by triggering the binding of ITGB4 and ANXA7, ITGB4 nuclear trafficking, and pro-apoptosis gene expression.

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“…Finally, loss- and gain-of-function of TIA1 can trigger autophagic phenotypes [17, 18, 33]. Increasing evidence suggests that some proteins, including annexin A7 [74], as well as long non-coding RNAs, such as FLJ11812/TGFB2-OT1 [75, 76] and MALAT1 [77], regulate autophagy through modulating TIA1 phosphorylation, to suppress the microRNA-mediated deregulation of some autophagic components in vascular endothelial cells [74–76]. Our results are in agreement with this scenario.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome-wide analysis links the short-term expression of the b isoforms of TIA proteins to protective proteostasis-mediated cell quiescence response

et al. 2018

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Control of gene expression depends on genetics and environmental factors. The T-cell intracellular antigens T-cell intracellular antigen 1 (TIA1), TIA1-like/related protein (TIAL1/TIAR) and human antigen R (HuR/ELAVL1) are RNA-binding proteins that play crucial roles in regulating gene expression in both situations. This study used massive sequencing analysis to uncover molecular and functional mechanisms resulting from the short-time expression of the b isoforms of TIA1 and TIAR, and of HuR in HEK293 cells. Our gene profiling analysis identified several hundred differentially expressed genes (DEGs) and tens of alternative splicing events associated with TIA1b, TIARb and HuR overexpression. Gene ontology analysis revealed that the controlled expression of these proteins strongly influences the patterns of DEGs and RNA variants preferentially associated with development, reproduction, cell cycle, metabolism, autophagy and apoptosis. Mechanistically, TIA1b and TIARb isoforms display both common and differential effects on the regulation of gene expression, involving systematic perturbations of cell biosynthetic machineries (splicing and translation). The transcriptome outputs were validated using functional assays of the targeted cellular processes as well as expression analysis for selected genes. Collectively, our observations suggest that early TIA1b and TIARb expression operates to connect the regulatory crossroads to protective proteostasis responses associated with a survival quiescence phenotype.

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TIA1 interacts with annexin A7 in regulating vascular endothelial cell autophagy

Cited by 23 publications

References 28 publications

Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

Long Noncoding RNA LOC100129973 Suppresses Apoptosis by Targeting miR-4707-5p and miR-4767 in Vascular Endothelial Cells

A small molecule induces integrin β4 nuclear translocation and apoptosis selectively in cancer cells with high expression of integrin β4

Transcriptome-wide analysis links the short-term expression of the b isoforms of TIA proteins to protective proteostasis-mediated cell quiescence response

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