CD147 Aggravated Inflammatory Bowel Disease by Triggering NF‐<i>κ</i>B‐Mediated Pyroptosis

Xu, Zhiqiang; Liu, Ruitao; Huang, Ling; Xu, Yuxin; Su, Mingmin; Chen, Jiayu; Geng, Lanlan; Xu, Wei; Gong, Sitang

doi:10.1155/2020/5341247

Cited by 16 publications

(14 citation statements)

References 49 publications

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“…CD147 also serves as a novel receptor on platelets that activates platelets and aggravates inflammation in monocytes ( Schmidt et al, 2008 ). Several studies have shown that CD147 is strongly involved in the development of various inflammatory diseases, such as COVID-19 ( Wang et al, 2020 ), rheumatoid arthritis ( Guo et al, 2019 ), and inflammatory bowel disease ( Xu et al, 2020 ). Our previous studies have shown that CD147 participates in reprogramming of glucose metabolism ( Huang et al, 2014 ) as well as in lipid metabolism ( Li J. et al, 2015 ) in hepatocellular carcinoma, including de novo lipogenesis and fatty acid-oxidation.…”

Section: Introductionmentioning

confidence: 99%

Blockade of Macrophage CD147 Protects Against Foam Cell Formation in Atherosclerosis

Wang

Cui

et al. 2021

Front. Cell Dev. Biol.

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The persistence of macrophage-derived foam cells in the artery wall fuels atherosclerosis development. However, the mechanism of foam cell formation regulation remains elusive. We are committed to determining the role that CD147 might play in macrophage foam cell formation during atherosclerosis. In this study, we found that CD147 expression was primarily increased in mouse and human atherosclerotic lesions that were rich in macrophages and could be upregulated by ox-LDL. High-throughput compound screening indicated that ox-LDL-induced CD147 upregulation in macrophages was achieved through PI3K/Akt/mTOR signaling. Genetic deletion of macrophage CD147 protected against foam cell formation by impeding cholesterol uptake, probably through the scavenger receptor CD36. The opposite effect was observed in primary macrophages isolated from macrophage-specific CD147-overexpressing mice. Moreover, bioinformatics results indicated that CD147 suppression might exert an atheroprotective effect via various processes, such as cholesterol biosynthetic and metabolic processes, LDL and plasma lipoprotein clearance, and decreased platelet aggregation and collagen degradation. Our findings identify CD147 as a potential target for prevention and treatment of atherosclerosis in the future.

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Section: Introductionmentioning

confidence: 99%

Blockade of Macrophage CD147 Protects Against Foam Cell Formation in Atherosclerosis

Wang

Cui

et al. 2021

Front. Cell Dev. Biol.

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“…In cancer, CD147 interacted with a variety of proteins, induces the secretion of MMPs, and promoted tumor invasion and metastasis [129,[133][134][135][136]. Recent studies have shown that CD147 was significantly increased in intestinal mucosa of IBD patients and aggravated IBD inflammatory response by activating NF-κB [137]. This indicates the important significance of CD147 in inflammatory diseases, and further confirms the results of previous studies [116][117][118][119][120][121][122][123][124] that eCypA firstly bound to CD147 on cell surface, and activated multiple signal pathways to regulate inflammatory cells, then promoted the expression of MMPs and other factors that can promote the occurrence and development of inflammation such as IBD, expecially UC.…”

Section: Cypamentioning

confidence: 99%

The Role of Cyclophilins in Inflammatory Bowel Disease and Colorectal Cancer

Liang¹,

Lin²,

Xie³

et al. 2021

Int. J. Biol. Sci.

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Cyclophilins (Cyps) is a kind of ubiquitous protein family in organisms, which has biological functions such as promoting intracellular protein folding and participating in the pathological processes of inflammation and tumor. Inflammatory bowel disease (IBD) and colorectal cancer (CRC) are two common intestinal diseases, but the etiology and pathogenesis of these two diseases are still unclear. IBD and CRC are closely associated, IBD has always been considered as one of the main risks of CRC. However, the role of Cyps in these two related intestinal diseases is rarely studied and reported. In this review, the expression of CypA, CypB and CypD in IBD, especially ulcerative colitis (UC), and CRC, their relationship with the development of these two intestinal diseases, as well as the possible pathogenesis, were briefly summarized, so as to provide modest reference for clinical researches and treatments in future.

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“…At present, a compelling body of evidence supports the fact that increased sRAGE levels correlate with a decrease in the RAGE activation-mediated inflammatory responses in many clinical entities[ 60 - 63 ]. In this context, it is important to highlight that CD147 significantly contributes to epithelial inflammation in many clinical entities including IBD[ 64 , 65 ], and it has been recently shown to act as a receptor for SARS-CoV-2[ 66 ]. Noteworthy, the inhibition of RAGE activation-mediated inflammatory response leads to a reduced expression of CD147[ 67 ].…”

Section: Rage Axis Activation In Ibdmentioning

confidence: 99%

Receptor for advanced glycation end-products axis and coronavirus disease 2019 in inflammatory bowel diseases: A dangerous liaison?

Rojas

Schneider

Lindner

et al. 2021

WJG

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Compelling evidence supports the crucial role of the receptor for advanced glycation end-products (RAGE) axis activation in many clinical entities. Since the beginning of the coronavirus disease 2019 pandemic, there is an increasing concern about the risk and handling of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in inflammatory gastrointestinal disorders, such as inflammatory bowel diseases (IBD). However, clinical data raised during pandemic suggests that IBD patients do not have an increased risk of contracting SARS-CoV-2 infection or develop a more severe course of infection. In the present review, we intend to highlight how two potentially important contributors to the inflammatory response to SARS-CoV-2 infection in IBD patients, the RAGE axis activation as well as the cross-talk with the renin-angiotensin system, are dampened by the high expression of soluble forms of both RAGE and the angiotensin-converting enzyme (ACE) 2. The soluble form of RAGE functions as a decoy for its ligands, and soluble ACE2 seems to be an additionally attenuating contributor to RAGE axis activation, particularly by avoiding the transactivation of the RAGE axis that can be produced by the virus-mediated imbalance of the ACE/angiotensin II/angiotensin II receptor type 1 pathway.

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CD147 Aggravated Inflammatory Bowel Disease by Triggering NF‐κB‐Mediated Pyroptosis

Cited by 16 publications

References 49 publications

Blockade of Macrophage CD147 Protects Against Foam Cell Formation in Atherosclerosis

Blockade of Macrophage CD147 Protects Against Foam Cell Formation in Atherosclerosis

The Role of Cyclophilins in Inflammatory Bowel Disease and Colorectal Cancer

Receptor for advanced glycation end-products axis and coronavirus disease 2019 in inflammatory bowel diseases: A dangerous liaison?

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