RBM3 and CIRP expressions in targeted temperature management treated cardiac arrest patients—A prospective single center study

Abstract

BackgroundManagement of cardiac arrest patients includes active body temperature control and strict prevention of fever to avoid further neurological damage. Cold-shock proteins RNA-binding motif 3 (RBM3) and cold inducible RNA-binding protein (CIRP) expressions are induced in vitro in response to hypothermia and play a key role in hypothermia-induced neuroprotection.ObjectiveTo measure gene expressions of RBM3, CIRP, and inflammatory biomarkers in whole blood samples from targeted temperature management (TTM)-treated post-cardiac arrest patients for the potential application as clinical biomarkers for the efficacy of TTM treatment.MethodsA prospective single center trial with the inclusion of 22 cardiac arrest patients who were treated with TTM (33°C for 24 hours) after ROSC was performed. RBM3, CIRP, interleukin 6 (IL-6), monocyte chemotactic protein 1 (MCP-1), and inducible nitric oxide synthase (iNOS) mRNA expressions were quantified by RT-qPCR. Serum RBM3 protein concentration was quantified using an enzyme-linked immunosorbent assay (ELISA).ResultsRBM3 mRNA expression was significantly induced in post-cardiac arrest patients in response to TTM. RBM3 mRNA was increased 2.2-fold compared to before TTM. A similar expression kinetic of 1.4-fold increase was observed for CIRP mRNA, but did not reached significancy. Serum RBM3 protein was not increased in response to TTM. IL-6 and MCP-1 expression peaked after ROSC and then significantly decreased. iNOS expression was significantly increased 24h after return of spontaneous circulation (ROSC) and TTM.ConclusionsRBM3 is temperature regulated in patients treated with TTM after CA and ROSC. RBM3 is a possible biomarker candidate to ensure the efficacy of TTM treatment in post-cardiac arrest patients and its pharmacological induction could be a potential future intervention strategy that warrants further research.

Identification of key pathways and genes in polycystic ovary syndrome via integrated bioinformatics analysis and prediction of small therapeutic molecules

“…The GO and pathway enrichment analysis was of great importance for interpreting the molecular mechanisms of the key cellular activities in PCOS. RPS5 [ 37 ], RBM3 [ 38 ], BAK1 [ 39 ], NDUFC2 [ 40 ], NDUFS4 [ 41 ], NDUFS5 [ 42 ], UQCRFS1 [ 43 ], COX6B1 [ 44 ], NDUFA13 [ 45 ], PRMT1 [ 46 ], RDX (radixin) [ 47 ], EPHB4 [ 48 ], SYNE2 [ 49 ], DNAH5 [ 50 ], NEDD4L [ 51 ], PDE4B [ 52 ] and CTNND1 [ 53 ] plays a critical role in the process of cardiovascular disease, but these genes might be linked with development of PCOS. Ostergaard et al [ 54 ], Zi et al [ 55 ], Kunej et al [ 56 ], Van der Schueren et al [ 57 ], Jin et al [ 58 ], Emdad et al [ 59 ], Liu et al [ 60 ], Scherag et al [ 61 ], Shi and Long [ 62 ], Sharma et al [ 63 ], Parente et al [ 64 ], Saint-Laurent et al [ 65 ] and Lee [ 66 ] demonstrated that over expression of COA3, PHB (prohibitin), UQCRC1, COX4I1, IFI27, MTDH (metadherin), S100A16, SDCCAG8, GLI2, NTN1, NLGN2, FGFR3 and PTPRN2 could cause obesity, but these genes might be involved in progression of PCOS.…”

Identification of Key Pathways and Genes in Polycystic Ovary Syndrome via Integrated Bioinformatics Analysis and Prediction of Small Therapeutic Molecules

“…The GO and pathway enrichment analysis was of great importance for interpreting the molecular mechanisms of the key cellular activities in PCOS. RPS5 [37], RBM3 [38], BAK1 [39], NDUFC2 [40], NDUFS4 [41], NDUFS5 [42], UQCRFS1 [43], COX6B1 [44], NDUFA13 [45], PRMT1 [46], RDX (radixin) [47], EPHB4 [48], SYNE2 [49], DNAH5 [50], NEDD4L [51], PDE4B [52] and CTNND1 [53] plays a critical role in the process of cardiovascular disease, but these genes might be linked with development of PCOS. Ostergaard et al [54], Zi et al [55], Kunej et al [56], Van der Schueren et al [57], Jin et al [58], Emdad et al [59], Liu et al [60], Scherag et al [61], Shi and Long [62], Sharma et al [63], Parente et al [64], Saint-Laurent et al [65] and Lee [66] demonstrated that over expression of COA3, PHB (prohibitin), UQCRC1, COX4I1, IFI27, MTDH (metadherin), S100A16, SDCCAG8, GLI2, NTN1, NLGN2, FGFR3 and PTPRN2 could cause obesity, but these genes might be involved in progression of PCOS.…”

Mechanisms of low-temperature rehabilitation technologies. Extreme aerocriotherapy

“…Показано, что RBM3 участвует в реализации эффектов нейропротекции, а представители БХШ рассматриваются как перспективные молекулы-прототипы новых лекарственных средств [30]. БХШ в нейрональной культуре снижает индуцированную оксидом азота гибель клеток, а понижение температуры корковых нейронов приводит к увеличению FGF21 и RBM3, что может предполагать наличие положительной связи и взаимодействия этих стрессбелков [31].…”