UBIAD1 expression is associated with cardiac hypertrophy in spontaneously hypertensive rats

Abstract

The present study investigated the potential role of UbiA prenyltransferase domain-containing 1 (UBIAD1) in the pathogenesis of hypertensive cardiac hypertrophy. Spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) rats at 8, 16 and 28 weeks of age were used. Blood pressure was measured using a non-invasive tail cutoff system. Cardiac functional index was assessed by arterial catheterization. Myocardial structure and cell apoptosis were evaluated by hematoxylin and eosin staining, and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays, respectively. Myocardial expression of UBIAD1, coenzyme Q10 (CoQ10), endothelial nitric oxide synthase (eNOS) and atrial natriuretic peptide were evaluated by immunohistochemistry, western blotting and reverse transcription-quantitative polymerase chain reaction. Circulating and myocardial expression of nitric oxide (NO) were measured using the Griess method. SHRs exhibited increased blood pressure and cardiomyocyte apoptosis, as well as cardiac hypertrophy, compared with age-matched WKY rats. Myocardial expression of UBIAD1 was significantly decreased in SHRs in an age-dependent manner. Similarly, myocardial CoQ10 and eNOS expression were significantly reduced in SHR compared to age-matched WKY rats, and these expression levels additionally decreased further with aging. Serum and myocardial NO expression was additionally decreased in SHRs. Decreased UBIAD1 expression in SHR hearts was associated with decreased levels of CoQ10, eNOS and NO. Given the well-established role of UBIAD1 in the regulation of NO signaling, reduced expression of UBIAD1 in SHR hearts potentially contributed to the pathogenesis of hypertensive cardiac hypertrophy. Therefore, UBIAD1 may represent a potential therapeutic target for clinical treatment of hypertensive cardiac hypertrophy.

Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis

“…Expression of ERRFI1 190 , ALOX12 191 , SOCS5 192 , DDIT4 193 , DUSP4 194 , IL6ST 195 , DUSP1 196 , SMAD1 197 , NCL (nucleolin) 198 , METTL14 199 , FMOD (fibromodulin) 200 , CYGB (cytoglobin) 201 , UNC5A 202 and TAAR9 203 are believed to be associated with diabetic nephropathy. Genes include FAP (fibroblast activation protein alpha) 204 , EYA4 205 , BCL9 206 , IRF2BP2 207 , EGR3 208 , GADD45B 209 , DMD (dystrophin) 210 , LSR (lipolysis stimulated lipoprotein receptor) 211 , DLL4 212 , SUN2 213 , SOS1 214 , PIK3CA 215 , GAMT (guanidinoacetate N -methyltransferase) 216 , RBM47 217 , HSP90AA1 218 , GAB1 219 , S1PR1 220 , EDNRB (endothelin receptor type B) 221 , NFKBIA (NFKB inhibitor alpha) 222 , GJA1 223 , GADD45G 224 , PHLDA1 225 , CMPK2 226 , FIGN (fidgetin, microtubule severing factor) 227 , KCNJ2 228 , ABCC9 229 , DIRAS3 230 , EPHX1 231 , RAB4A 232 , UBIAD1 233 , CASQ2 234 , TTN (titin) 235 , KCNH1 236 , JPH2 237 , OXGR1 238 , UCHL1 239 , SERPINA3 240 , MMP28 241 , ADAMTS2 242 , P2RY1 243 , CSF2RA 244 , MYO1F …”

L-3-n-butylphthalide promotes restoration after an experimental animal model of intracerebral hemorrhage

“…With the deepening of research, more and more attention has been paid to the role of UBIAD1 in cell metabolism and maintaining internal environment stability 23 , 24 . UBIAD1 can also regulate the activity of eNOS and play a specific cardiovascular protective role 22 , 25 . These studies show that UBIAD1 and its catalytic products play an important role in regulating cell proliferation, apoptosis, and oxidative stress, and these mechanisms are closely related to the mechanism of cerebral ischemia-reperfusion and cerebral hemorrhage injury.…”

Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis

“…Expression of ERRFI1 [191], ALOX12 [192], SOCS5 [193], DDIT4 [194], DUSP4 [195], IL6ST [196], DUSP1 [197], SMAD1 [198], NCL (nucleolin) [199], METTL14 [200], FMOD (fibromodulin) [201], CYGB (cytoglobin) [202], UNC5A [203] and TAAR9 [204] are associated with prognosis in patients with diabetic nephropathy, but these genes might be novel target for T1DM. A previous study reported that FAP (fibroblast activation protein alpha) [205], EYA4 [206], BCL9 [207], IRF2BP2 [208], EGR3 [209], GADD45B [210], DMD (dystrophin) [211], LSR (lipolysis stimulated lipoprotein receptor) [212], DLL4 [213], SUN2 [214], SOS1 [215], PIK3CA [216], GAMT (guanidinoacetate N-methyltransferase) [217], RBM47 [218], HSP90AA1 [219], GAB1 [220], S1PR1 [221], EDNRB (endothelin receptor type B) [222], NFKBIA (NFKB inhibitor alpha) [223], GJA1 [224], GADD45G [225], PHLDA1 [226], CMPK2 [227], FIGN (fidgetin, microtubule severing factor) [228], KCNJ2 [229], ABCC9 [230], DIRAS3 [231], EPHX1 [232], RAB4A [233], UBIAD1 [234], CASQ2 [235], TTN (titin) [236], KCNH1 [237], JPH2 [238], OXGR1 [239], UCHL1 [240], SERPINA3 [241], MMP28 [242], ADAMTS2 [243], P2RY1 [244], CSF2RA [245], MYO1F [246], SELPLG (selectin P ligand) [247] and SAMHD1 [248] are expressed in cardiovascular disease, but these genes might be novel target for T1DM. MAOB (monoamine oxidase B) [249], VEGFC (vascular endothelial growth factor C) [250], DBP (D-box binding PAR bZIP transcription factor) [251], MYADM (myeloid associated differentiation marker) [252], NES (nestin) [253], SMURF1 [254], EDNRB (endothelin receptor type B) [255], MUC6 [25...…”