The role of Gadd45b in neurologic and neuropsychiatric disorders: An overview.

Growth arrest and DNA damage-inducible beta (Gadd45b) is directly intertwined with stress-induced DNA repair, cell cycle arrest, survival, and apoptosis. Previous research on Gadd45b has focused chiefly on non-neuronal cells. Gadd45b is extensively expressed in the nervous system and plays a critical role in epigenetic DNA demethylation, neuroplasticity, and neuroprotection, according to accumulating evidence. This article provided an overview of the preclinical and clinical effects of Gadd45b, as well as its hypothesized mechanisms of action, focusing on major psychosis, depression, autism, stroke, seizure, dementia, Parkinson's disease, and autoimmune diseases of the nervous system.

Lipid profiling differentiates the effect of ambient microenriched copper on a coral as an advanced tool for biomonitoring.

Copper can be beneficial or harmful to coral at environmentally relevant levels, making environmental monitoring a challenging. Membrane lipids make the cell a dynamic environment according to the circumstances; thus, the lipid profile should be indicative of an environmental/physiological state. To gain more insight into the copper effect on coral health and be a basis of biomonitoring, glycerophosphocholine profiling of coral exposed to microenriched copper levels was conducted in this study. The copper microenrichments resulted in a diacritical effect of decreasing carbonic anhydrase activity, following a supplementation effect, on coral lipid metabolism. Microdifferences in copper levels are critical to determine the coral metabolic state and were therefore included in this study. In addition, an excellent quantitative model correlating the coral lipid variation with the exposed copper levels or the induced physiological effect was obtained to demonstrate its performance for biomonitoring.

Lipid profiling of coral symbiosomes in response to copper-induced carbon limitation: A metabolic effect of algal symbionts on the host immune status.

Copper micropollutants are known to constrain coral's assimilation of carbonate, affecting the carbon available to algal symbionts and thus inducing a light stress. However, little is known regarding the physiological relevance of lipid metabolism in coral symbiotic algae in a carbon-limited state. Membrane lipids exhibit multiple physicochemical properties that are collectively responsible for the dynamic structure of cells depending on the physiological demands of the circumstances. To gain insight into lipid metabolism's importance in this regard, glycerophosphocholine (GPC) profiling of symbiosomes in coral (Seriatopora caliendrum) exposed to environmentally relevant copper levels (2.2-7.5 µg/L) for 4 days was performed in this study. Notably, reducing the number of 22:6-processing GPCs and increasing that of lyso-GPCs likely addressed the demands of metabolizing excess light energy, such as affecting the membrane dynamics to promote mitochondrial uncoupling. The decrease in 22:6-processing GPCs additionally protected cellular membranes from elevated oxidative stress, reducing their susceptibility to peroxidation and offsetting oxidized lipid-induced effects on membrane dynamics. The change in plasmanylcholines specifically localized within the symbiosome membrane also met the membrane requirements for responding to oxidative stress conditions. Moreover, increasing the 20:4-possessing plasmanylcholines and lysoplasmanylcholines and reducing the 22:6-possessing plasmanylcholines likely resulted in an imbalance of the immune reaction, influencing the coral-algae symbiosis given the role of such plasmanylcholines in cell signaling. In summary, carbon limitations induced by copper enrichment lead to a shift in the membrane lipid profile of coral symbiosomes, accommodating themselves to light stress conditions while compromising the symbiosis's stability.

miR­212 promotes renal interstitial fibrosis by inhibiting hypoxia­inducible factor 1­α inhibitor.

Renal interstitial fibrosis is one of the common causes, and a major pathological basis for the development of various types of chronic progressive renal to end­stage renal diseases. Therefore, it is important to clarify the underlying mechanisms of disease progression in order to develop effective strategies for the treatment and prevention of these pathologies. The aim of the present study was to investigate the association between microRNA (miR)­212 expression and the development of renal interstitial fibrosis, as well as analyzing the role of miR­212 in the disease. The expression of miR­212 was significantly increased in the peripheral blood of patients with renal interstitial fibrosis and in the kidney tissues of unilateral ureteral obstruction (UUO) mice. Angiotensin (Ang) II, TGF­ß1 and hypoxia were found to increase the expression of miR­212 and α smooth muscle actin (α­SMA) in NRK49F cells. Ang II stimulation induced the expression of miR­212 and α­SMA in NRK49F cells, while transfection of miR­212 mimics further upregulated the expression of α­SMA. miR­212 was also revealed to target hypoxia­inducible factor 1α inhibitor (HIF1AN) and to upregulate the expression of hypoxia­inducible factor 1α, α­SMA, connective tissue growth factor, collagen α­1(I) chain and collagen α­1(III) chain, whereas HIF1AN overexpression reversed the regulatory effects of miR­212. In UUO mice, miR­212 overexpression promoted the progression of renal interstitial fibrosis, whereas inhibiting miR­212 resulted in the opposite effect. These results indicated that high expression of miR­212 was closely associated with the occurrence of renal interstitial fibrosis, and that miR­212 may promote its development by targeting HIF1AN.

miR-19 promotes development of renal fibrosis by targeting PTEN-mediated epithelial-mesenchymal transition.

In recent years, it has been found that miRNA may play an important role in the field of gene regulation; miRNAs can participate in the regulation of various physiologic processes such as cell differentiation, proliferation, apoptosis, metabolism, and insulin secretion by regulation of target genes. The purpose of this study is to observe the relationship between the expression of miR-19 and renal fibrosis, to analyze the regulatory effect of miR-19 on renal tubular EMT, and to reveal its role and working mechanism in renal fibrosis. We found that the expression of miR-19 was significantly increased in peripheral blood of patients with renal fibrosis, in renal tissue of unilateral ureteral occlusion (UUO) mice, and in NRK-52E cells treated with TGF-ß1. Overexpression of miR-19 could decrease the expression of E-cadherin and increase the expression of α-SMA and fibronectin, while inhibition of miR-19 reverses TGF-ß1-induced EMT. Further studies revealed that miR-19 could inhibit its expression by binding to the 3'-UTR of PTEN. MiR-19 inhibitor or Akt inhibitor blocks phospho-Akt by TGF-ß1, and Akt inhibitors block miR-19 mimic-induced EMT. In UUO mice, overexpression of miR-19 promoted the development of renal fibrosis, while inhibition of miR-19 expression produced the opposite result. These results indicate that abnormal expression of miR-19 is associated with renal fibrosis. Moreover, miR-19 activates the Akt signaling pathway by targeting PTEN, and induces EMT in renal tubular epithelial cells, thereby promoting renal fibrosis.

Using lipidomic methodology to characterize coral response to herbicide contamination and develop an early biomonitoring model.

The use of omics technologies to profile an organism's systemic response to environmental changes can improve the effectiveness of biomonitoring. In cell physiology, the dynamic characteristics of membranes can be used to identify lipid profiles that detect environmental threats and assess the health problems associated with them. The efficacy of this approach was demonstrated by profiling glycerophosphocholines (GPCs, a major membrane lipid class) in the coral Seriatopora caliendrum after exposure to Irgarol 1051. A quantitative biomonitoring model for this photosystem II herbicide was developed by correlating variations in coral lipid profile with herbicide exposure levels and degree of photoinhibition. After 4 days of exposure, the predominant changes correlated with photoinhibition were an increase in lyso-GPCs and saturated GPCs and a decrease in phosphatidylcholines with unsaturated C18 chains or a polyunsaturated C22 chain. A time-course experiment showed that most of these lipid changes occurred opposite to the initial response and that the persistent changes can be attributed to photosynthetic shortages and the membrane accommodation of photoinhibition-induced oxidative conditions. These changes can help predict risk factors leading to coral bleaching. In this study, the application of a lipidomic methodology to characterize the adaptation of coral to ambient contamination serves as a basis for advancing environmental monitoring and assessment.