ABSTRACT
WRKY transcription factors are one of the largest families of transcription factors in higher plants and involved in regulating multiple and complex growth and development processes in plants. WRKY12 is a typical member of WRKY family. This article summarizes recent research progresses on the regulatory mechanism of WRKY12 in multiple growth and development processes, and analyzes the functional differences between WRKY12 and WRKY13. It provides a useful reference for further studying the molecular mechanism of WRKY12 in plant complex developments. It also provides clearer research ideas and reference strategies for exploring the self-regulation of other WRKY member and the mutual regulatory relationships between different WRKY family genes.
Subject(s)
Humans , Gene Expression Regulation, Plant , Phylogeny , Plant Development/genetics , Plant Proteins/metabolism , Plants/metabolism , Stress, Physiological , Transcription Factors/metabolismABSTRACT
<p><b>BACKGROUND</b>In China, the prevalence of chronic kidney disease has increased significantly. Many studies shows that the spectrum of kidney disease had changed in recent years. We retrospectively analyzed the pathological types of renal biopsy and its spectrum change at the General Hospital of the Chinese People's Liberation Army from December 1987 to December 2012, in order to offer new supporting evidences for further specifying the distribution of renal pathological types in China.</p><p><b>METHODS</b>According to the "Revised Protocol for the Histological Typing of Glomerulopathy" (WHO, 1995), pathological diagnosis of renal biopsy was classified, detection rate of each pathological type was summarized (i.e., percentage of total renal biopsy cases), study period was divided at an interval of 5 years, and age-stratified distribution change of main pathological types was analyzed.</p><p><b>RESULTS</b>The proportion of pathological types in 11 618 cases of renal biopsy was as follows: primary glomerulonephritis (PGN, 70.7%), secondary glomerulonephritis (SGN, 20.7%), tubular-interstitial nephropathy (4.0%), hereditary/rare nephropathy (0.3%), end-stage renal disease (0.9%), and unclassified renal disease (3.3%). Among PGN, there was IgA nephropathy (IgAN, 37.0%), membranous nephropathy (MN, 11.8%), mesangial proliferative glomerulonephritis (MsPGN, 8.9%), minimal change disease (MCD, 6.6%), and focal segmental glomerulosclerosis (3.9%). Among SGN there was lupus nephritis (LN, 5.5%), Henoch-Schönlein purpura glomerulonephritis (5.3%), hepatitis B virus-associated nephritis (HBVAN, 3.03%), diabetic nephropathy (2.2%), and hypertension/malignant hypertension-associated renal damage (1.9%). Pathological data were analyzed from 1987-1992 to 2008-2012 (after age adjustment). Detection rate of IgAN tended to rise (P < 0.001). Detection rates of MN and MCD rose significantly (P < 0.001), but detection rate of MsPGN dropped significantly (P < 0.001). Among SGN, detection rate of HBVAN tended to drop (P < 0.001).</p><p><b>CONCLUSION</b>In China, PGN was the most common glomerulopathy (mostly IgAN), LN was the most common SGN, and detection rate of MN and MCD rose significantly.</p>
Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Biopsy , Methods , China , Glomerulonephritis, Membranous , Diagnosis , Kidney , Pathology , Kidney Diseases , DiagnosisABSTRACT
<p><b>OBJECTIVE</b>To investigate high-concentration uric acid-induced endothelial dysfunction mediated by miR-155.</p><p><b>METHODS</b>Human umbilical vein endothelial cells (HUVECs) were incubated with 600 µmol/L uric acid for 24 and 48 h, and eNOS expression and NO content in the cell culture were measured. The target genes of miR-155 were predicted using on-line analysis software and validated by dual-luciferase system. Real-time PCR was used to detect the expression of miR-155 in endothelial cells incubated with high-concentration uric acid. The effect of miR-155 on endothelial dysfunction was assessed by transfection of its inhibitor into HUVECs.</p><p><b>RESULTS</b>The expression of eNOS and NO secretion decreased obviously in HUVECs incubated with 600 µmol/L uric acid. MicroRNA on-line analysis software and dual luciferase reporter experiments suggested that the level of eNOS translation was directly regulated by miR-155. The expression of miR-155 in endothelial cells was upregulated after stimulation with high-concentration uric acid, and was inhibited by transfection of miR-155 inhibitor. Expression of eNOS and secretion of NO were elevated in endothelial cells transfected with miR-155 inhibitor after incubation with high-concentration uric acid.</p><p><b>CONCLUSION</b>High-concentration uric acid can down-regulate eNOS expression via miR-155 to induce endothelial dysfunction.</p>
Subject(s)
Humans , Cells, Cultured , Down-Regulation , Human Umbilical Vein Endothelial Cells , Cell Biology , Metabolism , Hyperuricemia , Metabolism , Pathology , MicroRNAs , Metabolism , Nitric Oxide , Metabolism , Nitric Oxide Synthase Type III , Metabolism , Uric Acid , BloodABSTRACT
According to recent studies,cardiovascular disease,infection and malnutrition are the most common complications of maintenance hemodialysis (MHD),which also the main causes of death. Further studies illustrate that dialysis patients with micro-inflammatory state,which relate to patient uremia and hemodialysis,further more,closely related to the existing micro-inflammatory response to the above complications. Accordingly,to explore the mechanism in MHD patients with micro-inflammatory response,and to search for the effective micro-inflammation treatment,in addition,to enhance the quality of life of patients with MHD and survival rate has become a hot spot in recent years.