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• W2890862843 abstract "Background Although macrophage migration inhibitory factor ( MIF ) has been demonstrated to mediate cardioprotection in ischemia/reperfusion injury and antagonize fibrotic effects through its receptor, CD 74, the function of the soluble CD 74 receptor ectodomain ( sCD 74) and its interaction with circulating MIF have not been explored in cardiac disease. Methods and Results Cardiac fibroblasts were isolated from hearts of neonatal mice and differentiated into myofibroblasts. Co‐treatment with recombinant MIF and sCD 74 induced cell death ( P <0.001), which was mediated by receptor‐interacting serine/threonine‐protein kinase ( RIP) 1/ RIP 3‐dependent necroptosis ( P =0.0376). This effect was specific for cardiac fibroblasts and did not affect cardiomyocytes. Gene expression analyses using microarray and RT ‐ qPCR technology revealed a 4‐fold upregulation of several interferon‐induced genes upon co‐treatment of myofibroblasts with sCD 74 and MIF (Ifi44: P =0.011; Irg1: P =0.022; Clec4e: P =0.011). Furthermore, Western blot analysis confirmed the role of sCD 74 as a modulator of MIF signaling by diminishing MIF ‐mediated protein kinase B ( AKT) activation ( P =0.0197) and triggering p38 activation ( P =0.0641). We obtained evidence that sCD 74 inhibits MIF ‐mediated survival pathway through the C‐X‐C chemokine receptor 4/ AKT axis, enabling the induction of CD 74‐dependent necroptotic processes in cardiac myofibroblasts. Preliminary clinical data revealed a lowered sCD 74/ MIF ratio in heart failure patients (17.47±10.09 versus 1.413±0.6244). Conclusions These findings suggest that treatment of cardiac myofibroblasts with sCD 74 and MIF induces necroptosis, offering new insights into the mechanism of myofibroblast depletion during scar maturation. Preliminary clinical data provided first evidence about a clinical relevance of the sCD 74/ MIF axis in heart failure, suggesting that these proteins may be a promising target to modulate cardiac remodeling and disease progression in heart failure." @default.
• W2890862843 created "2018-09-27" @default.
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• W2890862843 date "2018-09-04" @default.
• W2890862843 modified "2023-10-14" @default.
• W2890862843 title "Soluble CD74 Reroutes MIF/CXCR4/AKT‐Mediated Survival of Cardiac Myofibroblasts to Necroptosis" @default.
• W2890862843 cites W169488438 @default.
• W2890862843 cites W1846616615 @default.
• W2890862843 cites W1892014140 @default.
• W2890862843 cites W1963971594 @default.
• W2890862843 cites W1968476414 @default.
• W2890862843 cites W1975349664 @default.
• W2890862843 cites W1979032223 @default.
• W2890862843 cites W1987213099 @default.
• W2890862843 cites W1989832114 @default.
• W2890862843 cites W1994537999 @default.
• W2890862843 cites W1997064567 @default.
• W2890862843 cites W1997868017 @default.
• W2890862843 cites W2000541661 @default.
• W2890862843 cites W2004656949 @default.
• W2890862843 cites W2008757142 @default.
• W2890862843 cites W2012759923 @default.
• W2890862843 cites W2018237850 @default.
• W2890862843 cites W2020087937 @default.
• W2890862843 cites W2027952618 @default.
• W2890862843 cites W2029174607 @default.
• W2890862843 cites W2034624097 @default.
• W2890862843 cites W2039411604 @default.
• W2890862843 cites W2045853353 @default.
• W2890862843 cites W2046666360 @default.
• W2890862843 cites W2047308155 @default.
• W2890862843 cites W2049780044 @default.
• W2890862843 cites W2051521455 @default.
• W2890862843 cites W2052605153 @default.
• W2890862843 cites W2053570926 @default.
• W2890862843 cites W2056442594 @default.
• W2890862843 cites W2064535683 @default.
• W2890862843 cites W2075089814 @default.
• W2890862843 cites W2086514569 @default.
• W2890862843 cites W2087107619 @default.
• W2890862843 cites W2089892676 @default.
• W2890862843 cites W2092585655 @default.
• W2890862843 cites W2093032251 @default.
• W2890862843 cites W2093552166 @default.
• W2890862843 cites W2094055083 @default.
• W2890862843 cites W2096233114 @default.
• W2890862843 cites W2098030130 @default.
• W2890862843 cites W2104806243 @default.
• W2890862843 cites W2106448072 @default.
• W2890862843 cites W2109732289 @default.
• W2890862843 cites W2113808060 @default.
• W2890862843 cites W2117037612 @default.
• W2890862843 cites W2117810566 @default.
• W2890862843 cites W2129328611 @default.
• W2890862843 cites W2131357993 @default.
• W2890862843 cites W2134518567 @default.
• W2890862843 cites W2135647797 @default.
• W2890862843 cites W2144621689 @default.
• W2890862843 cites W2149385441 @default.
• W2890862843 cites W2150913500 @default.
• W2890862843 cites W2151702576 @default.
• W2890862843 cites W2152832086 @default.
• W2890862843 cites W2156811335 @default.
• W2890862843 cites W2158858936 @default.
• W2890862843 cites W2161048718 @default.
• W2890862843 cites W2167733945 @default.
• W2890862843 cites W2169512063 @default.
• W2890862843 cites W2169813623 @default.
• W2890862843 cites W2184817776 @default.
• W2890862843 cites W2272325731 @default.
• W2890862843 cites W2328339150 @default.
• W2890862843 cites W2399314948 @default.
• W2890862843 cites W2423947669 @default.
• W2890862843 cites W2480151737 @default.
• W2890862843 cites W2485948342 @default.
• W2890862843 cites W2566236348 @default.
• W2890862843 cites W2614781785 @default.
• W2890862843 cites W2616672581 @default.
• W2890862843 cites W2772144112 @default.
• W2890862843 cites W2772714692 @default.
• W2890862843 cites W2890862843 @default.
• W2890862843 cites W2915142973 @default.
• W2890862843 doi "https://doi.org/10.1161/jaha.118.009384" @default.
• W2890862843 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6201423" @default.
• W2890862843 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30371153" @default.
• W2890862843 hasPublicationYear "2018" @default.
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