Endothelial progenitor cells (EPCs) in ageing and age-related diseases: How currently available treatment modalities affect EPC biology, atherosclerosis, and cardiovascular outcomes

Altabas, Velimir; Altabas, Karmela; Kirigin, Lora Stanka

doi:10.1016/j.mad.2016.02.009

Cited by 42 publications

(34 citation statements)

References 160 publications

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“…Endothelial dysfunction eventually represents an imbalance between the magnitude of injury and the ability for repair [30]. Endothelial cells, the most abundant cells in the endothelium, do not have significant replicative capacity; however, EPCs also participate in vascular repair [31]. EPCs proliferate in the bone marrow and other tissues, and are released in response to vascular damage, migrate to the site of injury and further replicate and maturate to endothelial cells [31].…”

Section: Discussionmentioning

confidence: 99%

“…Endothelial cells, the most abundant cells in the endothelium, do not have significant replicative capacity; however, EPCs also participate in vascular repair [31]. EPCs proliferate in the bone marrow and other tissues, and are released in response to vascular damage, migrate to the site of injury and further replicate and maturate to endothelial cells [31]. This whole process is called endothelial (vascular) repair.…”

Section: Discussionmentioning

confidence: 99%

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Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB

Yang

Pan

et al. 2016

Cell Physiol Biochem

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Background/Aims: Tanshinone IIA (Tan IIA) is effective in the treatment of inflammation and atherosclerosis. The adhesion of inflammatory cells to vascular endothelium plays important role in atherogenic processes. This study examined the effects of Tan IIA on expression of adhesion molecules in tumor necrosis factor-α (TNF-α)-induced endothelial progenitor cells (EPCs). Methods: EPCs were pretreated with Tan IIA and stimulated with TNF-α. Mononuclear cell (MNC) adhesion assay was performed to assess the effects of Tan IIA on TNF-α-induced MNC adhesion. Expression of vascular cell adhesion molecule-1 (VCAM-1)/intracellular adhesion molecule-1 (ICAM-1) and activation of Nuclear factor κB (NF-κB) signaling pathway were measured. Results: The results showed that the adhesion of MNCs to TNF-α-induced EPCs and expression of VCAM-1/ICAM-1 in EPCs were promoted by TNF-α, which were reduced by Tan IIA. TNF-α increased the amount of phosphorylation of NF-κB, IκB-α and IKKα/β in cytosolic fractions and NF-κB p65 in nucleus, while Tan IIA reduced its amount. Conclusion: This study demonstrated a novel mechanism for the anti-inflammatory/anti-atherosclerotic activity of Tan IIA, which may involve down-regulation of VCAM-1 and ICAM-1 through partial blockage of TNF-α-induced NF-κB activation and IκB-α phosphorylation by the inhibition of IKKα/β pathway in EPCs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB

Yang

Pan

et al. 2016

Cell Physiol Biochem

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“…Endothelial progenitor cells (EPCs) are the precursor cells of endothelial cells, which mainly exist in bone marrow, cord blood, and peripheral blood (Murohara et al, 2000). EPCs are quite capable of repairing damaged vascular endothelium and regenerating blood vessel (Altabas et al, 2016;Kiewisz et al, 2016). Therefore, EPCs have a broad prospect in the research and treatment of cardiovascular and cerebrovascular diseases, diabetes, peripheral vascular diseases, and other vascular injury diseases.…”

Section: Introductionmentioning

confidence: 99%

Rhynchophylline Attenuates Senescence of Endothelial Progenitor Cells by Enhancing Autophagy

Lin

Zhang

et al. 2020

Front. Pharmacol.

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The increase of blood pressure accelerates endothelial progenitor cells (EPCs) senescence, hence a significant reduction in the number of EPCs is common in patients with hypertension. Autophagy is a defense and stress regulation mechanism to assist cell homeostasis and organelle renewal. A growing number of studies have found that autophagy has a positive role in repairing vascular injury, but the potential mechanism between autophagy and senescence of EPCs induced by hypertension has rarely been studied. Therefore, in this study, we aim to explore the relationship between senescence and autophagy, and investigate the protective effect of rhynchophylline (Rhy) on EPCs. In angiotensin II (Ang II)treated EPCs, enhancing autophagy through rapamycin mitigated Ang II-induced cell senescence, on the contrary, 3-methyladenine aggravated the senescence by weakening autophagy. Similarly, Rhy attenuated senescence and improved cellular function by rescuing the impaired autophagy in Ang II-treated EPCs. Furthermore, we found that Rhy promoted autophagy by activating AMP-activated protein kinase (AMPK) signaling pathway. Our results show that enhanced autophagy attenuates EPCs senescence and Rhy rescues autophagy impairment to protect EPCs against Ang II injury.

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“…as potential measures for both improving number and functionality of EPCs, delaying the rate of ageing and consequently the onset of the most common age-related diseases, i.e. atherosclerosis (Altabas et al, 2016).…”

mentioning

confidence: 99%

Endothelial progenitor cells in ageing

Olivieri

Pompilio

Balistreri

2016

Mechanisms of Ageing and Development

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Endothelial progenitor cells (EPCs) in ageing and age-related diseases: How currently available treatment modalities affect EPC biology, atherosclerosis, and cardiovascular outcomes

Cited by 42 publications

References 160 publications

Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB

Tanshinone II A Attenuates TNF-α-Induced Expression of VCAM-1 and ICAM-1 in Endothelial Progenitor Cells by Blocking Activation of NF-κB

Rhynchophylline Attenuates Senescence of Endothelial Progenitor Cells by Enhancing Autophagy

Endothelial progenitor cells in ageing

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