Glucocorticoids increase skeletal muscle <scp>NF</scp>‐<i>κ</i>B inducing kinase (<scp>NIK</scp>): links to muscle atrophy

Fry, Christopher S.; Nayeem, Syed Z.; Dillon, E. Lichar; Sarkar, Partha S.; Tumurbaatar, Batbayar; Urban, Randall J.; Wright, Traver J.; Sheffield‐Moore, Melinda; Tilton, Ronald G.; Choudhary, Sanjeev

doi:10.14814/phy2.13014

Cited by 36 publications

(24 citation statements)

References 49 publications

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“… 54 It was also reported that methylprednisolone is able to increase the NFκB-inducing kinase expression in human skeletal muscle. 55 Further studies are required for the new IT-inducing pharmacological therapy for patients with PDA.…”

Section: Discussionmentioning

confidence: 99%

Fibulin-1 Integrates Subendothelial Extracellular Matrices and Contributes to Anatomical Closure of the Ductus Arteriosus

Ito

Yokoyama

Nakakoji

et al. 2020

ATVB

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Objective: The ductus arteriosus (DA) is a fetal artery connecting the aorta and pulmonary arteries. Progressive matrix remodeling, that is, intimal thickening (IT), occurs in the subendothelial region of DA to bring anatomic DA closure. IT is comprised of multiple ECMs (extracellular matrices) and migrated smooth muscle cells (SMCs). Because glycoprotein fibulin-1 binds to multiple ECMs and regulates morphogenesis during development, we investigated the role of fibulin-1 in DA closure. Approach and Results: Fibulin-1–deficient ( Fbln1 −/− ) mice exhibited patent DA with hypoplastic IT. An unbiased transcriptome analysis revealed that EP4 (prostaglandin E receptor 4) stimulation markedly increased fibulin-1 in DA-SMCs via phospholipase C-NFκB (nuclear factor κB) signaling pathways. Fluorescence-activated cell sorting (FACS) analysis demonstrated that fibulin-1 binding protein versican was derived from DA-endothelial cells (ECs). We examined the effect of fibulin-1 on directional migration toward ECs in association with versican by using cocultured DA-SMCs and ECs. EP4 stimulation promoted directional DA-SMC migration toward ECs, which was attenuated by either silencing fibulin-1 or versican. Immunofluorescence demonstrated that fibulin-1 and versican V0/V1 were coexpressed at the IT of wild-type DA, whereas 30% of versican-deleted mice lacking a hyaluronan binding site displayed patent DA. Fibulin-1 expression was attenuated in the EP4-deficient mouse ( Ptger4 −/− ) DA, which exhibits patent DA with hypoplastic IT, and fibulin-1 protein administration restored IT formation. In human DA, fibulin-1 and versican were abundantly expressed in SMCs and ECs, respectively. Conclusions: Fibulin-1 contributes to DA closure by forming an environment favoring directional SMC migration toward the subendothelial region, at least, in part, in combination with EC-derived versican and its binding partner hyaluronan.

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Section: Discussionmentioning

confidence: 99%

Fibulin-1 Integrates Subendothelial Extracellular Matrices and Contributes to Anatomical Closure of the Ductus Arteriosus

Ito

Yokoyama

Nakakoji

et al. 2020

ATVB

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“…), and NFкB (Fry et al . ). Hence, due to continual basal stress, aged muscle is unable to further upregulate crucial stress responsive proteins, demonstrating a marked loss in age‐dependent adaptability when challenged with an acute exercise bout (Vasilaki et al .…”

Section: Introductionmentioning

confidence: 97%

The role of declining adaptive homeostasis in ageing

Pomatto

Davies

2017

The Journal of Physiology

162

108

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Adaptive homeostasis is "the transient expansion or contraction of the homeostatic range for any given physiological parameter in response to exposure to sub-toxic, non-damaging, signalling molecules or events, or the removal or cessation of such molecules or events" (Davies, 2016). Adaptive homeostasis enables biological systems to make continuous short-term adjustments for optimal functioning despite ever-changing internal and external environments. Initiation of adaptation in response to an appropriate signal allows organisms to successfully cope with much greater, normally toxic, stresses. These short-term responses are initiated following effective signals, including hypoxia, cold shock, heat shock, oxidative stress, exercise-induced adaptation, caloric restriction, osmotic stress, mechanical stress, immune response, and even emotional stress. There is now substantial literature detailing a decline in adaptive homeostasis that, unfortunately, appears to manifest with ageing, especially in the last third of the lifespan. In this review, we present the hypothesis that one hallmark of the ageing process is a significant decline in adaptive homeostasis capacity. We discuss the mechanistic importance of diminished capacity for short-term (reversible) adaptive responses (both biochemical and signal transduction/gene expression-based) to changing internal and external conditions, for short-term survival and for lifespan and healthspan. Studies of cultured mammalian cells, worms, flies, rodents, simians, apes, and even humans, all indicate declining adaptive homeostasis as a potential contributor to age-dependent senescence, increased risk of disease, and even mortality. Emerging work points to Nrf2-Keap1 signal transduction pathway inhibitors, including Bach1 and c-Myc, both of whose tissue concentrations increase with age, as possible major causes for age-dependent loss of adaptive homeostasis.

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“…Upstream regulation of NF-κB activation was reported to occur in skeletal muscle atrophy via increasing in vivo expression of NF-κB inducing kinase following glucocorticoid administration [25]. Early and intermediate stage supraspinatus tendon disease increased expression of genes and proteins regulated by NF-κB activation pathways [26].…”

Section: Discussionmentioning

confidence: 99%

Dexamethasone Facilitates NF-��B Signal Pathway in TNF-�� Stimulated Rotator Cuff Tenocytes

Kim

Patel

et al. 2019

Journal of Microbiology and Biotechnology

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Corticosteroids are commonly used for pain control in rotator cuff tear. Deregulated NF-κB activation is a hallmark of chronic inflammatory diseases and has been responsible for the pathogenesis of rotator cuff tear. The Dexamethasone(DEXA) is a synthetic corticosteroid. The purpose of this study was to examine the exact effect of dexamethasone on NF-κB signaling in rotator cuff tear. We measured NF-κB expression in four groups: control, TNF-α-treated, DEXA-treated, and combined treatment with TNF-α and DEXA. Tenocytes were isolated from patients with rotator cuff tears and pre-incubated with TNF-α (10 ng/ml), DEXA (1 μM), or both of them for 10 min, 1 h, and 2 h. Expression of p65, p50, and p52 in the nuclei and cytosol was analyzed by western blotting and immunofluorescence imaging using confocal microscopy. We also evaluated nucleus/cytosol (N/C) ratios of p65, p50, and p52. In our study, the combined treatment with DEXA and TNF-α showed increased N/C ratios of p65, p50, and p52 compared with those in the TNF-α group at all time points. Additionally, in the DEXA group, N/C ratios of p65, p50, and p52 gradually increased from 10 min to 2 h. In conclusion, DEXA promoted the nuclear localization of p65, p50, and p52, but was not effective in inhibiting the inflammatory response of TNF-α-stimulated rotator cuff tear.

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Glucocorticoids increase skeletal muscle NF‐κB inducing kinase (NIK): links to muscle atrophy

Cited by 36 publications

References 49 publications

Fibulin-1 Integrates Subendothelial Extracellular Matrices and Contributes to Anatomical Closure of the Ductus Arteriosus

Fibulin-1 Integrates Subendothelial Extracellular Matrices and Contributes to Anatomical Closure of the Ductus Arteriosus

The role of declining adaptive homeostasis in ageing

Dexamethasone Facilitates NF-��B Signal Pathway in TNF-�� Stimulated Rotator Cuff Tenocytes

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