CD147 induces up-regulation of vascular endothelial growth factor in U937-derived foam cells through PI3K/AKT pathway

Zong, JiaXin; Li, Yuntian; Du, Da-Yong; Liu, Yang; Yin, Yongjun

doi:10.1016/j.abb.2016.09.001

Cited by 11 publications

(14 citation statements)

References 35 publications

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“…PI3K is activated mainly by G-protein-coupled receptor stimulation and plays a crucial role in repairing angiogenesis. Zong et al demonstrated that CD147 induced the upregulation of VEGF in U937-derived foam cells, further promoting intraplaque angiogenesis (Zong et al, 2016).…”

Section: Effects Of Pi3k On Atherosclerotic Plaque Formationmentioning

confidence: 99%

Role of PI3K in the Progression and Regression of Atherosclerosis

et al. 2021

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Phosphatidylinositol 3 kinase (PI3K) is a key molecule in the initiation of signal transduction pathways after the binding of extracellular signals to cell surface receptors. An intracellular kinase, PI3K activates multiple intracellular signaling pathways that affect cell growth, proliferation, migration, secretion, differentiation, transcription and translation. Dysregulation of PI3K activity, and as aberrant PI3K signaling, lead to a broad range of human diseases, such as cancer, immune disorders, diabetes, and cardiovascular diseases. A growing number of studies have shown that PI3K and its signaling pathways play key roles in the pathophysiological process of atherosclerosis. Furthermore, drugs targeting PI3K and its related signaling pathways are promising treatments for atherosclerosis. Therefore, we have reviewed how PI3K, an important regulatory factor, mediates the development of atherosclerosis and how targeting PI3K can be used to prevent and treat atherosclerosis.

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Section: Effects Of Pi3k On Atherosclerotic Plaque Formationmentioning

confidence: 99%

Role of PI3K in the Progression and Regression of Atherosclerosis

et al. 2021

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“…Another research group has suggested that the PI3K/Akt pathway may underlie CD147-induced upregulation of VEGF in U937-derived foam cells [ 37 ]. When the cell culture was transfected with CD147 stealth siRNA, the extent to which VEGF production was reduced depended on the inhibition efficiency of CD147 siRNAs.…”

Section: Targeting the Mmp Familymentioning

confidence: 99%

Implications of Angiogenesis Involvement in Arthritis

MacDonald

Liu

et al. 2018

IJMS

159

117

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Angiogenesis, the growth of new blood vessels, is essential in the pathogenesis of joint inflammatory disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA), facilitating the invasion of inflammatory cells and increase in local pain receptors that contribute to structural damage and pain. The angiogenic process is perpetuated by various mediators such as growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as proinflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases, and others. Despite the development of potent, well-tolerated nonbiologic (conventional) and biologic disease-modifying agents that have greatly improved outcomes for patients with RA, many remain resistant to these therapies, are only partial responders, or cannot tolerate biologics. The only approved therapies for OA include symptom-modifying agents, such as analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), steroids, and hyaluronic acid. None of the available treatments slow the disease progression, restore the original structure or enable a return to function of the damaged joint. Moreover, a number of safety concerns surround current therapies for RA and OA. New treatments are needed that not only target inflamed joints and control articular inflammation in RA and OA, but also selectively inhibit synovial angiogenesis, while preventing healthy tissue damage. This narrative review of the literature in PubMed focuses on the evidence illustrating the therapeutic benefits of modulating angiogenic activity in experimental RA and OA. This evidence points to new treatment targets in these diseases.

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“…One of the outcomes of this signaling pathway is the regulation of VEGF production (Paplomata & OʹRegan 2014). A previous study by Zong et al (2016) showed that in U937-derived foam cells, VEGF may be upregulated by CD147 through the PI3K/AKT pathway. The PI3K/AKT pathway can activate many transcription factors, including SP transcription factors (Archer 2011).…”

Section: Discussionmentioning

confidence: 99%

Decreased levels of sRAGE in follicular fluid from patients with PCOS

Asan¹,

Li²,

Yang³

et al. 2017

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This study aimed to explore the association between soluble receptor for advanced glycation end products (sRAGE) levels in follicular fluid and the number of oocytes retrieved and to evaluate the effect of sRAGE on vascular endothelial growth factor (VEGF) in granulosa cells in patients with polycystic ovarian syndrome (PCOS). Two sets of experiments were performed in this study. In part one, sRAGE and VEGF protein levels in follicular fluid samples from 39 patients with PCOS and 35 non-PCOS patients were measured by ELISA. In part two, ovarian granulosa cells were isolated from an additional 10 patients with PCOS and cultured. VEGF and SP1 mRNA and protein levels, as well as pAKT levels, were detected by real-time PCR and Western blotting after cultured cells were treated with different concentrations of sRAGE. Compared with the non-PCOS patients, patients with PCOS had lower sRAGE levels in follicular fluid. Multi-adjusted regression analysis showed that high sRAGE levels in follicular fluid predicted a lower Gn dose, more oocytes retrieved, and a better IVF outcome in the non-PCOS group. Logistic regression analysis showed that higher sRAGE levels predicted favorably IVF outcomes in the non-PCOS group. Multi-adjusted regression analysis also showed that high sRAGE levels in follicular fluid predicted a lower Gn dose in the PCOS group. Treating granulosa cells isolated from patients with PCOS with recombinant sRAGE decreased VEGF and SP1 mRNA and protein expression and pAKT levels in a dose-dependent manner.

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CD147 induces up-regulation of vascular endothelial growth factor in U937-derived foam cells through PI3K/AKT pathway

Cited by 11 publications

References 35 publications

Role of PI3K in the Progression and Regression of Atherosclerosis

Role of PI3K in the Progression and Regression of Atherosclerosis

Implications of Angiogenesis Involvement in Arthritis

Decreased levels of sRAGE in follicular fluid from patients with PCOS

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