High level of reactive oxygen species impaired mesenchymal stem cell migration via overpolymerization of F-actin cytoskeleton in systemic lupus erythematosus

Shi, Dongyan; Li, X.; Chen, H.; Che, Nan; Zhou, Shiliang; Lù, Zhongwen; Shi, Songtao; Sun, Lingyun

doi:10.1016/j.patbio.2014.07.009

Cited by 31 publications

(23 citation statements)

References 24 publications

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“…A previous study documented that CXCL-8 reduced damage to microfilaments and microtubules caused by reactive oxygen species, and promoted the chemotactic movement of HUVECs (52). In the current study, the effects of CXCL-8 on HUVEC cells were blocked by Akt inhibitors, resulting in reduced proliferation and migration, thus suggesting that Akt may serve a key role in the process of HUVEC migration (53).…”

Section: Discussionsupporting

confidence: 63%

C-X-C motif chemokine ligand 8 promotes endothelial cell homing via the Akt-signal transducer and activator of transcription pathway to accelerate healing of ischemic and hypoxic skin ulcers

Shen

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. C-X-C motif chemokine ligand 8 (CXCL-8) promotes cell homing and angiogenesis. However, under hypoxic conditions, the role of CXCL-8 in the homing of human umbilical vein endothelial cells (HUVECs), and its effect on the healing of skin ulcers caused by ischemia and hypoxia remain unknown. In the current study, assays measuring cell proliferation, in vitro angiogenesis and cell migration were performed to evaluate alterations in the proliferation, angiogenic capacity and chemotaxis of HUVECs treated with CXCL-8 protein and/or an Akt inhibitor (AZD5363 group) under hypoxic conditions. Changes in the levels of Akt, signal transducer and activator of transcription 3 (STAT3), vascular endothelial growth factor (VEGF), malondialdehyde (MDA) and total-superoxide dismutase (total-SOD) were also detected by western blotting and ELISA. In addition, in vivo experiments were performed using a skin ulcer model in mice. Ischemic and hypoxic skin ulcers were created on the thighs of C57BL/6J mice, and the effects of CXCL-8 and HUVEC transplantation on the healing capacity of skin ulcers was determined by injecting mice with HUVECs and/or CXCL-8 recombinant protein (CXCL-8, HUVEC and HUVEC + CXCL-8 groups). Vascular endothelial cell homing, changes in vascular density and the expression of VEGF, SOD, EGF and MDA within the ulcer tissue were subsequently measured. In vitro experiments demonstrated that HUVEC proliferation, migration and tube forming capacity were significantly increased by CXCL-8 under hypoxic conditions. Additionally, levels of VEGF, MDA and SOD were significantly higher in the CXCL-8 group, though were significantly decreased by the Akt and STAT3 inhibitors. In vivo experiments demonstrated that the expression of VEGF, total-SOD and EGF proteins were higher in the skin ulcer tissue of mice treated with CXCL-8 + HUVEC, relative to mice treated with HUVECs alone. Furthermore, vascular endothelial cell homing and vascular density were significantly increased in the CXCL-8 + HUVEC group, indicating that combined use of HUVECs and CXCL-8 may promote the healing of ischemic skin ulcers. The present results demonstrate that CXCL-8 may stimulate vascular endothelial cells to secrete VEGF, SOD and other cytokines via the Akt-STAT3 pathway, which in turn serves a key regulatory role in the recruitment of vascular endothelial cells, reduction of hypoxia-related injury and promotion of tissue repair following hypoxic/ischemic injury.

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Section: Discussionsupporting

confidence: 63%

C-X-C motif chemokine ligand 8 promotes endothelial cell homing via the Akt-signal transducer and activator of transcription pathway to accelerate healing of ischemic and hypoxic skin ulcers

Shen

Zhang

et al. 2017

Experimental and Therapeutic Medicine

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“…An in vivo study has also shown that actin cytoskeleton remodeling attenuates myocardial fibrosis following myocardial infarction in rats [22] . A series of studies have demonstrated that high level of ROS can impair the integrity and function of cytoskeleton in a variety of cells including fibroblasts, and reduction of ROS production via antioxidant therapy can stabilize cytoskeleton by targeting the ROCK1 pathway [23,24] . While it is known that glucose and Ang II are strong stimuli for ROS production, the effects of glucose and Ang II on cytoskeleton organization in cardiac fibroblasts have not been previously studied.…”

Section: Discussionmentioning

confidence: 99%

Effects of linagliptin and liraglutide on glucose- and angiotensin II-induced collagen formation and cytoskeleton degradation in cardiac fibroblasts in vitro

et al. 2016

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Aim: Glucagon-like peptide-1 (GLP-1) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors can not only lower blood glucose levels, but also alleviate cardiac remodeling after myocardial ischemia and hypertension. In the present study, we investigated the effects of a DPP-4 inhibitor (linagliptin) and a GLP-1 activator (liraglutide) on glucose-and angiotensin II (Ang II)-induced collagen formation and cytoskeleton reorganization in cardiac fibroblasts in vitro, and elucidated the related mechanisms. Methods: Cardiac fibroblasts were isolated from the hearts of 6-week-old C57BL/6 mice, and then exposed to different concentrations of glucose or Ang II for 24 h. The expression of fibrotic signals (fibronectin, collagen-1, -3 and -4), as well as ERK1/2 and NF-κB-p65 in the fibroblasts was examined using Western blotting assays. F-actin degradation was detected under inverted laser confocal microscope in fibroblasts stained with Rhodamine phalloidin. Results: Glucose (1-40 mmol/L) and Ang II (10-5 mol/L) dose-dependently increased the expression of fibronectin, collagens, phospho-ERK1/2 and phospho-NF-κB-p65 in cardiac fibroblasts. High concentrations of glucose (≥40 mmol/L) and Ang II (≥10 -6 mol/L) caused a significant degradation of F-actin (less assembly F-actin fibers and more disassembly fibers). ERK1/2 inhibitor U0126 (10 μmol/L) and NF-κB inhibitor JSH-23 (10 μmol/L) both markedly suppressed glucose-and angiotensin II-induced fibronectin and collagen expressions in cardiac fibroblasts. Furthermore, pretreatment with liraglutide (10-100 nmol/L) or linagliptin (3 and 30 nmol/L) significantly decreased glucose-and Ang II-induced expression of fibrotic signals, phospho-ERK1/2 and phospho-NF-κB-p65 in cardiac fibroblasts. Moreover, pretreatment with liraglutide (30 nmol/L) or liraglutide (100 nmol/L) markedly inhibited glucose-induced F-actin degradation, however, only liraglutide inhibited Ang II-induced F-actin degradation. Conclusion: Linagliptin and liraglutide inhibit glucose-and Ang II-induced collagen formation in cardiac fibroblasts via activation of the ERK/NF-κB/pathway. Linagliptin and liraglutide also markedly inhibit glucose-induced F-actin degradation in cardiac fibroblasts, but only liraglutide inhibits Ang II-induced F-actin degradation.

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“…The actin cytoskeleton is balanced by actin polymerization and depolymerization. The distribution of F‐actin is higher in aged then in young human skin (Schulze et al, ), and this overabundance is associated with impairments in cell proliferation and migration (Shi et al, ). Consistent with these reports, we found that aged bovine OECs possess a cytoskeleton enriched in F‐actin, and that their functional capacities, including villous movement and cell proliferation, were decreased compared with young OECs.…”

Section: Discussionmentioning

confidence: 99%

Age-dependent changes in inflammation and extracellular matrix in bovine oviduct epithelial cells during the post-ovulatory phase

et al. 2016

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The mammalian oviduct is an essential site for sperm storage, the transport of gametes, fertilization, and embryo development-functions that are aided by cytokines secreted from oviduct epithelial cells (OECs). Aging leads to cellular and organ dysfunction, with infertility associated with advanced maternal age. Few studies have investigated age-dependent changes in the oviduct as a possible cause of infertility, so we compared OECs from young (30-50 months) versus aged (more than 120 months) cattle. Next-generation sequencing was first used to identify age-related differences in gene expression. Several proinflammatory-related genes (including IL1B, IL1A, IL17C, IL8, S100A8, S100A9, and TNFA) were activated in OECs from aged (more than 120 months) compare to young (30-50 months) individuals, whereas genes associated with extracellular matrix-related factors (COLs, POSTN, BGN, and LUM) were down-regulation in aged OECs. Indeed, IL1 B and IL8 abundance was higher in aged OECs than in young OECs. Young OECs also tended to proliferate faster, and the revolution frequency of young, ciliated OECs was higher than that of their aged counterparts. In contrast, aged OECs possessed more F-actin, an actin cytoskeleton marker associated with reduced elasticity, and contained high levels of reactive oxygen species, which are mediators of inflammation and senescence. These different functional characteristics of bovine OECs during the post-ovulatory phase support the emerging concept of "inflammaging," that is, age-dependent inflammation. Mol. Reprod. Dev. 83: 815-826, 2016 © 2016 Wiley Periodicals, Inc.

show abstract

High level of reactive oxygen species impaired mesenchymal stem cell migration via overpolymerization of F-actin cytoskeleton in systemic lupus erythematosus

Cited by 31 publications

References 24 publications

C-X-C motif chemokine ligand 8 promotes endothelial cell homing via the Akt-signal transducer and activator of transcription pathway to accelerate healing of ischemic and hypoxic skin ulcers

C-X-C motif chemokine ligand 8 promotes endothelial cell homing via the Akt-signal transducer and activator of transcription pathway to accelerate healing of ischemic and hypoxic skin ulcers

Effects of linagliptin and liraglutide on glucose- and angiotensin II-induced collagen formation and cytoskeleton degradation in cardiac fibroblasts in vitro

Age-dependent changes in inflammation and extracellular matrix in bovine oviduct epithelial cells during the post-ovulatory phase

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