Gene expression profiling of the ageing rat vibrissa follicle

Yang, Connie L.; T, Kurczab; Down, Gareth A.; Kealey, Terence; Langlands, Kenneth

doi:10.1111/j.1365-2133.2005.06550.x

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…Effectively, in cultured cells, apoD expression is associated with cellular growth arrest, senescence and inflammation. In agreement with these facts, apoD is also upregulated in aging rats [19] and humans [20,21] and this senescence characteristic, which is an irreversible growtharrested state in contrary to quiescence, is also considered as a physiological mechanism capable of counteracting tumour proliferation [22][23][24][25][26].…”

Section: Introductionsupporting

confidence: 60%

Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities

Levros

Carmo

Edouard

et al. 2010

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Human Apolipoprotein D (apoD) is upregulated under several stress conditions and pathological situations such as neurodegenerative diseases and cancers. We previously showed that apoD mRNA expression is induced in growth-arrested cells and demonstrated the specific binding of nuclear proteins to the region -514 to -475 of the promoter. Such region contains a pair of Serum Responsive Elements (SRE), an Ets-Binding Site (EBS) and a Glucocorticoid Responsive Element (GRE). In this study, we show that Parp-1, HnRNP-U, CBF-A, BUB-3, Kif4, APEX-1 and Ifi204 bind these regulatory elements of the apoD promoter. Specific binding of HnRNP-U and Parp-1 was confirmed by Electrophoretic Mobility Shift Assay (EMSA). In a biotin pull-down assay, Kif4 and BUB-3 bind preferentially the SRE1 and the EBS-GRE sites, respectively, while APEX-1 seems recruited indirectly to these elements. We found that the mRNA expression of some of these binding factors is upregulated in growth-arrested cells and that these proteins also transactivate the apoD promoter. In agreement with these results, mutants of APEX-1 and of Parp-1 defective for their DNA-binding and catalytic activities could not transactivate the promoter. The knockdown of Parp-1 and HnRNP-U and the use of specific inhibitors of MEK1/2 and of Parp-1 also inhibited the induction of apoD gene expression. Moreover, ERK1/2 was found activated in a biphasic manner post serum-starvation and the inhibition of Parp-1 causes a sustained activation of ERK2 but not ERK1 for up to 2h. Altogether, these findings demonstrate the importance of Parp-1, APEX-1 and ERK1/2 catalytic activities in the growth arrest-induced apoD gene expression.

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Section: Introductionsupporting

confidence: 60%

Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities

Levros

Carmo

Edouard

et al. 2010

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…However, the same staining pattern was seen in Id1 null lungs, indicating that ID1 staining of pulmonary VSMCs using this antibody is unreliable. This negative finding is of importance, since a number of studies have used this antibody to identify the cellular localization of ID1 in a variety of different tissues, including the lung (1,3,4,6,8,10,17,18,30,41,44,47,52). Id2 null mice were not available for these studies, so our analyses of ID2 regulation and localization have to be interpreted with caution.…”

Section: Discussionmentioning

confidence: 91%

“…We first evaluated the specificity of three different commercially available ID1 antibodies by comparing staining of lung sections from wild-type and Id1 null mice exposed to 1-wk hypoxia. The first antibody we tested, a rabbit polyclonal anti-ID1 antibody from Santa Cruz (C-20, SC-488), has been used extensively to evaluate ID1 expression domains in a variety of different tissues (1,3,4,6,8,10,17,18,30,41,44,47,52). This antibody gave weak but selective staining of pulmonary ECs in wild-type but not Id1 null mice (Supplemental Fig.…”

Section: Regulation Of Pulmonary Id1-3 Expression Levels By Hypoxiamentioning

confidence: 99%

ID family protein expression and regulation in hypoxic pulmonary hypertension

Lowery¹,

Frump²,

Anderson

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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To address this, we evaluated pulmonary expression of ID proteins in a mouse model of hypoxia-induced PH. There is selective induction of ID1 and ID3 expression in hypoxic pulmonary vascular smooth muscle cells (VSMCs) in vivo, and ID1 and ID3 expression are increased by hypoxia in cultured pulmonary VSMCs in a BMPdependent fashion. ID4 protein is barely detectable in the mouse lung, and while ID2 is induced in hypoxic peripheral VSMCs in vivo, it is not increased by hypoxia or BMP signaling in cultured pulmonary VSMCs. In addition, the PH response to chronic hypoxia is indistinguishable between wild type and Id1 null mice. This is associated with a compensatory increase in ID3 but not ID2 expression in pulmonary VSMCs of Id1 null mice. These findings indicate that ID1 is dispensable for mounting a normal pulmonary vascular response to hypoxia, but suggest that ID3 may compensate for loss of ID1 expression in pulmonary VSMCs. Taken together, these findings indicate that ID1 and ID3 expression are regulated in a BMP-dependent fashion in hypoxic pulmonary VSMCs, and that ID1 and ID3 may play a cooperative role in regulating BMP-dependent VSMC responses to chronic hypoxia. hypoxia; bone morphogenetic protein signaling; ID1; ID2; ID3; vascular smooth muscle cells; endothelial cells GENETIC STUDIES IN PATIENTS with hereditary pulmonary arterial hypertension (HPAH) indicate that defective bone morphogenetic protein (BMP) type 2 receptor (BMPR2) signaling plays a critical role in promoting pulmonary hypertension (PH) and obliterative pulmonary vascular remodeling in this disease (16,25). Studies in mice carrying heterozygous null and hypomorphic germ line Bmpr2 mutations show that these mice do not develop spontaneous PH, but they have increased susceptibility to PH in response to inflammatory mediators and serotonin (22,38,39) or to chronic hypoxia (9). Conditional deletion of Bmpr2 in endothelial cells (ECs) promotes spontaneous PH in a subset of affected mice (11), indicating that defective BMPR2 signaling plays a role in regulating EC function. However, interference with BMPR2 signaling in vascular smooth muscle cells (VSMCs) by overexpression of a dominant negative BMPR2 mutation also promotes spontaneous PH in mice (45). Furthermore, conditional deletion of the BMP type 1 receptor ALK3 in VSMCs reduces hypoxic pulmonary vascular remodeling and VSMC proliferation (7). These findings indicate that defective BMPR2 signaling influences both the EC and VSMC compartments in the pulmonary vasculature. However, the relationship between defective BMP signaling and vascular cell phenotypes in HPAH is complex and poorly understood (23).One approach to explore this has been to investigate the downstream signaling pathways that mediate the effects of BMP receptor mutations in different pulmonary vascular cell types. These studies also enable us to interrogate PH-associated alterations in BMP signaling that occur in the pulmonary vasculature in the absence of BMPR2 mutations. Activation of the BMP receptors leads to COOH-termi...

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The biological role of arachidonic acid 12-lipoxygenase (ALOX12) in various human diseases

Zheng

Jin

et al. 2020

Biomedicine & Pharmacotherapy

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Gene expression profiling of the ageing rat vibrissa follicle

Abstract: Follicular ageing is characterized by transcriptional changes associated with diverse aspects of keratinocyte metabolism, proliferation and development.

Cited by 4 publications

References 31 publications

Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities

Characterization of nuclear factors modulating the apolipoprotein D promoter during growth arrest: Implication of PARP-1, APEX-1 and ERK1/2 catalytic activities

ID family protein expression and regulation in hypoxic pulmonary hypertension

The biological role of arachidonic acid 12-lipoxygenase (ALOX12) in various human diseases

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