Analysis of FOS, BTG2, and NR4A in the function of renal medullary hypertension

Abstract

ABSTRACT. The aim of this study was to identify differentially expressed genes (DEGs) in renal medullary hypertension and reveal their pathogenic mechanisms. We downloaded the gene expression profile of GSE28360 from the Gene Expression Omnibus database. The profile included 14 samples (5 normal and 9 hypertension). The DEGs in normal and disease samples were distinguished with a false-discovery rate threshold of <0.05 and a fold-change value of >2 or <-2. We put the selected genes into the online program String 8.3 to obtain the protein-protein interaction network and selected the hub proteins. These hub proteins were then placed in the PANTHER database to determine hub protein-related pathways and explain their functions. Finally, we cleared up the singlenucleotide polymorphisms (SNPs) of the hub genes via combing with the National Center for Biotechnology SNP database. A total of 13 genes were identified as DEGs between normal and disease samples. Five selected hub proteins, B-cell translocation gene 2 (BTG2), FBJ murine osteosarcoma viral oncogene homolog (FOS), nuclear receptor subfamily 4, group A, member 1 (NR4A1), NR4A member 2 (NR4A2), and NR4A member 3 (NR4A3), were mainly related to angiogenesis and B-cell activation. After SNP analysis, 103, 103, 595, 150, and 493 SNPs were found to correspond to BTG2, FOS, NR4A1, NR4A2, and NR4A3, respectively. Our results suggest that pathways of angiogenesis and B-cell activation may involve in the progression of renal medulla hypertension.

Stress Reactivity, Susceptibility to Hypertension, and Differential Expression of Genes in Hypertensive Compared to Normotensive Patients

“…Using the PubMed database [ 69 ], we collected all the DEGs (of hypertensive compared with normotensive patients) that we could find ( Table 5 ). The total number of hypertension-related human DEGs found was 7865, as cited in the rightmost column of Table 5 [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”

“…In this work, we analyzed all the publicly available independent experimental RNA-Seq datasets—on transcriptomes from the tissues of hypertensive versus normotensive patients [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ], hypertensive versus normotensive animals [ 7 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 ], and domestic versus wild animals [ 72 , 176 , 177 , 178 , 179 , 180 , 181 , 182 , 183 , 184 , 185 , 186 , 187 , 188 , 189 , 190 , 191 , 192 , 193 ].…”

“…In this work, we analyzed all the publicly available independent experimental RNA-Seq datasets-on transcriptomes from the tissues of hypertensive versus normotensive patients [26][27][28][29][30][31][32][33][34][35][36][37][38][39], hypertensive versus normotensive animals [7,[40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55][56][57], and domestic versus wild animals [72,[176][177][178][179][180][181][182][183][184][185][186][187][188][189][190][191][192][193].…”

“…Parents of half of the hypertensive patients had hypertension, but all the known (>60) hypertension-related whole-genome human loci explained only 3% of this heritability of hypertension [ 25 ]. Maybe this is why mainstream transcriptome-profiling studies on hypertensive versus normotensive patients [ 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ] and animals [ 7 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 ] are focused on the differentially expressed genes (DEGs) that are specific to gender, age, and the stage of hypertension development. This is needed in predictive preventive personalized participatory (4P) medicine [ 58 ] to estimate where, how, why, and when hypertension might occur in a given patient depending on his/her genetic background.…”

Exosomal microRNA-150-5p from bone marrow mesenchymal stromal cells mitigates cerebral ischemia/reperfusion injury via targeting B-cell translocation gene 2

“…have elucidated that BTG2 is enriched in the renal medullary tissue samples of hypertensive patients, whereas the elevation of BTG2 leads to functional abnormalities and induces the occurrence of hypertensive disorders [37]. Furthermore, it has reported that the loss of BTG2 effectively facilitates the proliferation of cardiomyocyte in mouse with myocardial infarction [38].…”