Interleukin-10 overexpression improves the function of endothelial progenitor cells stimulated with TNF-α through the activation of the STAT3 signaling pathway

Wáng, Ying; Chen, Qingzhong; Zhang, Zhuhong; Jiang, Feng; Meng, Xiangda; Yan, Hua

doi:10.3892/ijmm.2014.2034

Cited by 23 publications

(18 citation statements)

References 32 publications

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“…Previous studies have shown that IL-10 improves endothelial progenitor cell survival and function under hypoxic conditions via the STAT3/VEGF signaling pathway [ 37 ]. In addition, IL-10 overexpression improves endothelial progenitor cell function following TNF-α stimulation via the STAT3 pathway [ 38 ]. To date, the IL-10/STAT3 signaling pathway has been reported to play an important part in tumor progression, chemotherapy resistance [ 39 ] and the anti-inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 attenuates impairment of the blood-brain barrier in a severe acute pancreatitis rat model

Lin

Chen

et al. 2018

J Inflamm

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BackgroundImpairment of the blood-brain barrier (BBB) in severe acute pancreatitis (SAP) could result in life-threatening pancreatic encephalopathy. Interleukin-10 (IL-10) is a classical cytokine that is well-known for its strong immunoregulatory and anti-inflammatory abilities. However, whether and how IL-10 protects the BBB in SAP are still unclear.MethodsThis study includes in vivo experiments using a SAP rat model and in vitro experiments using an in vitro BBB model consisting of a monolayer of brain microvascular endothelial cells (BMECs). The study groups are divided into the control, SAP (in vivo)/TNF-α (in vitro), IL-10 treatment, IL-10 + signal transducer and activator of transcription 3 (STAT3) inhibitor S3I-201 treatment groups. Pancreatic pathological scores, serum amylase, serum TNF-α levels and BBB permeability by Evan’s blue assay in SAP rat models were evaluated. BMEC apoptosis in SAP rats or induced by TNF-αin vitro was detected by terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) and flow cytometry, separately. Expression levels of claudin-5 and proteins involved in the STAT3 signaling pathway were measured by Western blotting. Location and changes of junctional structure of claudin-5 on BMECs were assessed by immunohistochemistry and immunofluorescence.ResultsIn vivo, IL-10 alleviated the severity of inflammation, attenuated the increased BBB permeability in SAP rat models by reducing BMEC apoptosis via the STAT3 pathway and ameliorated the down-regulation of claudin-5 expression in BMECs; in vitro, IL-10 improved BBB integrity against TNF-α by attenuating BMEC apoptosis via the STAT3 pathway, the impairment of tight junction structure and the down-regulation of claudin-5 expression in BMECs.ConclusionsIL-10 improves BBB properties in SAP by attenuating the down-regulation of claudin-5 expression and the impairment of tight junctions and by STAT3 pathway-mediated anti-apoptotic effects on BMECs.

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Section: Discussionmentioning

confidence: 99%

Interleukin-10 attenuates impairment of the blood-brain barrier in a severe acute pancreatitis rat model

Lin

Chen

et al. 2018

J Inflamm

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“…Modeling vessel formation involves plating vascular cells, such as endothelial cells, in basement membrane matrix that promotes cell organization and formation of vessel networks 8 9 10 . Typically, following overnight incubation, images of cell networks are captured at a single time point, resulting in a small number of images for analysis 11 12 13 . Therefore, analytic approaches have largely been developed and optimized for single time point assessments 10 14 .…”

Section: Introductionmentioning

confidence: 99%

Kinetic Analysis of Vasculogenesis Quantifies Dynamics of Vasculogenesis and Angiogenesis <em>In Vitro</em>

Varberg

Winfree

Dunn

et al. 2018

JoVE

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Vasculogenesis is a complex process by which endothelial stem and progenitor cells undergo de novo vessel formation. Quantitative assessment of vasculogenesis has become a central readout of endothelial progenitor cell functionality, and therefore, several attempts have been made to improve both in vitro and in vivo vasculogenesis models. However, standard methods are limited in scope, with static measurements failing to capture many aspects of this highly dynamic process. Therefore, the goal of developing this novel protocol was to assess the kinetics of in vitro vasculogenesis in order to quantitate rates of network formation and stabilization, as well as provide insight into potential mechanisms underlying vascular dysfunction. Application of this protocol is demonstrated using fetal endothelial colony forming cells (ECFCs) exposed to maternal diabetes mellitus. Fetal ECFCs were derived from umbilical cord blood following birth, cultured, and plated in slides containing basement membrane matrix, where they underwent vasculogenesis. Images of the entire slide wells were acquired using time-lapse phase contrast microscopy over 15 hours. Images were analyzed for derivation of quantitative data using an analysis software called Kinetic Analysis of Vasculogenesis (KAV). KAV uses image segmentation followed by skeletonization to analyze network components from stacks of multi-time point phase contrast images to derive ten parameters (9 measured, 1 calculated) of network structure including: closed networks, network areas, nodes, branches, total branch length, average branch length, triple-branched nodes, quad-branched nodes, network structures, and the branch to node ratio. Application of this protocol identified altered rates of vasculogenesis in ECFCs obtained from pregnancies complicated by diabetes mellitus. However, this technique has broad implications beyond the scope reported here. Implementation of this approach will enhance mechanistic assessment and improve functional readouts of vasculogenesis and other biologically important branching processes in numerous cell types or disease states.

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“…TNF-a mediates downexpression of VEGF-receptor 1 and SDF-1 as well as the inducible and endothelial forms of NOS [115]. Interestingly, some studies have shown that TNF-a enhances EPCs migration, adhesion, and tubule formation [95], but these results were not replicated by other researchers.…”

Section: Endocrinementioning

confidence: 96%

“…Furthermore, IL-10 alone has no effect on EPCs migration and differentiation. However, it significantly increases the expression of VEGF and matrix metallopeptidase-9 (MMP-9) and potentiates the detrimental effects of TNF-a on EPCs [95].…”

Section: C-reactive Protein (Crp)mentioning

confidence: 99%

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

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Interleukin-10 overexpression improves the function of endothelial progenitor cells stimulated with TNF-α through the activation of the STAT3 signaling pathway

Cited by 23 publications

References 32 publications

Interleukin-10 attenuates impairment of the blood-brain barrier in a severe acute pancreatitis rat model

Interleukin-10 attenuates impairment of the blood-brain barrier in a severe acute pancreatitis rat model

Kinetic Analysis of Vasculogenesis Quantifies Dynamics of Vasculogenesis and Angiogenesis <em>In Vitro</em>

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

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