Medical Research Council Centre for Developmental and Biomedical Genetics, University of Sheffield, Sheffield S10 2TN, United Kingdom;
Published: February 2014
AI Article Synopsis
Article Abstract
The inflammatory response is integral to maintaining health by functioning to resist microbial infection and repair tissue damage. Large numbers of neutrophils are recruited to inflammatory sites to neutralize invading bacteria through phagocytosis and the release of proteases and reactive oxygen species into the extracellular environment. Removal of the original inflammatory stimulus must be accompanied by resolution of the inflammatory response, including neutrophil clearance, to prevent inadvertent tissue damage. Neutrophil apoptosis and its temporary inhibition by survival signals provides a target for anti-inflammatory therapeutics, making it essential to better understand this process. GM-CSF, a neutrophil survival factor, causes a significant increase in mRNA levels for the known anti-apoptotic protein serum and glucocorticoid-regulated kinase 1 (SGK1). We have characterized the expression patterns and regulation of SGK family members in human neutrophils and shown that inhibition of SGK activity completely abrogates the antiapoptotic effect of GM-CSF. Using a transgenic zebrafish model, we have disrupted sgk1 gene function and shown this specifically delays inflammation resolution, without altering neutrophil recruitment to inflammatory sites in vivo. These data suggest SGK1 plays a key role in regulating neutrophil survival signaling and thus may prove a valuable therapeutic target for the treatment of inflammatory disease.
Herpes simplex virus type 1 (HSV-1) is a common virus infecting the ocular tissue. It infects eye tissues, such as the eyelid, cornea, and conjunctiva. Corneal HSV-1 infection causes herpes simplex keratitis (HSK), which can induce vision loss.
Background: The occurrence of thoracic aortic dissection (TAD) is closely related to the transformation of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic phenotype. The role of SGK1 (serum- and glucocorticoid-regulated kinase 1) in VSMC phenotypic transformation and TAD occurrence is unclear.
Methods: Four-week-old male Sgk1 ( floxed) and Sgk1;Tagln (smooth muscle cell-specific knockout) mice were administered β-aminopropionitrile monofumarate for 4 weeks to model TAD.
Background: Ang-II (angiotensin II) impairs the function of the antihypertensive enzyme ACE2 (angiotensin-converting enzyme 2) by promoting its internalization, ubiquitination, and degradation, thus contributing to hypertension. However, few ACE2 ubiquitination partners have been identified, and their role in hypertension remains unknown.
Methods: Proteomics and bioinformatic analyses were used to identify ACE2 ubiquitination partners in the brain, heart, and kidney of hypertensive C57BL6/J mice of both sexes.
Objectives: Multiple sclerosis is a complex neurological disorder in which the immune system attacks the myelin sheath, leading to a range of symptoms. microRNA-155 plays a significant role in the pathogenesis of multiple sclerosis and neuropathic pain. Serum- and glucocorticoid-regulated kinase 3 (SGK3) protein is the target of microRNA-155.
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China; Beijing Key Laboratory for Metabolic Disorder-Related Cardiovascular Diseases, Beijing, 100069, China. Electronic address:
Background & Aims: Previous studies have established that hyperhomocysteinemia (HHcy) significantly contributes to the development of non-alcoholic steatohepatitis (NASH). Conversely, hydrogen sulfide (HS) has shown potential in mitigating NASH. Despite these findings, it remains uncertain whether HS can serve as a therapeutic agent against HHcy-induced liver damage.
