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Alberts Rudi,Chan Sze Chun,Meng Qian-Fang,He Shan,Rao Lang,Liu Xindong,Zhang Yongliang 대한면역학회 2022 Immune Network Vol.22 No.3
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has spread over the world causing a pandemic which is still ongoing since its emergence in late 2019. A great amount of effort has been devoted to understanding the pathogenesis of COVID-19 with the hope of developing better therapeutic strategies. Transcriptome analysis using technologies such as RNA sequencing became a commonly used approach in study of host immune responses to SARS-CoV-2. Although substantial amount of information can be gathered from transcriptome analysis, different analysis tools used in these studies may lead to conclusions that differ dramatically from each other. Here, we re-analyzed four RNA-sequencing datasets of COVID-19 samples including human bronchoalveolar lavage fluid, nasopharyngeal swabs, lung biopsy and hACE2 transgenic mice using the same standardized method. The results showed that common features of COVID-19 include upregulation of chemokines including CCL2, CXCL1, and CXCL10, inflammatory cytokine IL-1β and alarmin S100A8/S100A9, which are associated with dysregulated innate immunity marked by abundant neutrophil and mast cell accumulation. Downregulation of chemokine receptor genes that are associated with impaired adaptive immunity such as lymphopenia is another common feather of COVID-19 observed. In addition, a few interferon-stimulated genes but no type I IFN genes were identified to be enriched in COVID-19 samples compared to their respective control in these datasets. These features are in line with results from single-cell RNA sequencing studies in the field. Therefore, our re-analysis of the RNA-seq datasets revealed common features of dysregulated immune responses to SARS-CoV-2 and shed light to the pathogenesis of COVID-19.
Disturbed flow: p53 SUMOylation in the turnover of endothelial cells
Takabe, Wakako,Alberts-Grill, Noah,Jo, Hanjoong The Rockefeller University Press 2011 The Journal of cell biology Vol.193 No.5
<P>Disturbed blood flow induces apoptosis of vascular endothelial cells, which causes atherosclerosis. In this issue, Heo et al. (2011. <I>J. Cell Biol</I>. doi:10.1083/jcb.201010051) sheds light on p53’s role in this phenomenon. Disturbed flow induces peroxynitrite production, which activates protein kinase C ζ and it’s binding to the E3 SUMO (small ubiquitin-like modifier) ligase PIASy (protein inhibitor of activated STATy). This leads to p53 SUMOylation and its export to the cytosol, where it binds to the antiapoptotic protein Bcl-2 to induce apoptosis.</P>
Effects of Microgravity on Vestibular Development and Function in Rats: Genetics and Environment
Ronca, April-E.,Fritzsch, Bernd,Alberts, Jeffrey-R.,Bruce, Laura-L. The Korean Society for Integrative Biology 2000 Korean journal of biological sciences Vol.4 No.3
Our anatomical and behavioral studies of embryonic rats that developed in microgravity suggest that the vestibular sensory system, like the visual system, has genetically mediated precesses of development that establish crude connections between the periphery and the brain. Environmental stimuli also regulate connection formation including terminal branch formation and fine-tuning of synaptic contacts. Axons of vestibular sensory neurons from grabistatic as well as linear acceleration receptors reach their targets in both microgravity and norm81 gravity, suggesting that this is a genetically regulated component of development. However, microgravity exposure delays the development of terminal branches and synapses in gravistatic but not linear acceleration-sensitive neurons and also produces behavioral changes. These latter changes reflect environmentally controlled processes of development.
Rajeev Peravali,Rachael Bro,Elizabeth Bright,Patricia Mills,Dawn Petty,Justin Alberts 대한대장항문학회 2014 Annals of Coloproctolgy Vol.30 No.4
Purpose: DepoDur® is a single-dose extended-release morphine injection into the epidural space. It is not commonly used, but has many advantages over traditional analgesic regimens. We analyzed a number of these advantages in our case series in the context of the colorectal enhanced recovery program (ERP) and aimed to show that the ERP could be further enhanced by using DepoDur®. Methods: We conducted a prospective audit of all patients undergoing open and laparoscopic colorectal procedures where DepoDur® was used between July 2010 and April 2012. Validated pain scores were used, and primary outcome measures were resting and dynamic pain, mobilization, and need for additional analgesia. Results: Two hundred eighty patients were included in the case series. Good pain control was seen at 24 and 48 hours. Eighty-one percent of the patients required simple analgesia alone at 24 hours, and 62% required simple analgesia (paracetamol +/– nonsteroidal anti-inflammatory drugs) alone at 48 hours. Only a minority required additional oramorph and patient-controlled analgesia at 24 and 48 hours (19% at 24 hours and 38% at 48 hours). Seventy-nine percent of the patients were mobilized at 24 hours, and 88% of the patients were mobilized at 48 hours. Conclusion: DepoDur® is an effective alternative to conventional pain management techniques and may have a role in further enhancing the ERP.
Anti-Inflammatory and Antiatherogenic Role of BMP Receptor II in Endothelial Cells
Kim, Chan Woo,Song, Hannah,Kumar, Sandeep,Nam, Douglas,Kwon, Hyuk Sang,Chang, Kyung Hwa,Son, Dong Ju,Kang, Dong-Won,Brodie, Seth A.,Weiss, Daiana,Vega, J. David,Alberts-Grill, Noah,Griendling, Kathy,T American Heart Association, Inc. 2013 Arteriosclerosis, thrombosis, and vascular biology Vol.33 No.6
<P><B>Objective—</B></P><P>Atherosclerosis is an inflammatory disease with multiple underlying metabolic and physical risk factors. Bone morphogenic protein 4 (BMP4) expression is increased in endothelium in atherosclerosis-prone regions and is known to induce endothelial inflammation, endothelial dysfunction, and hypertension. BMP actions are mediated by 2 different types of BMP receptors (BMPRI and BMPRII). Here, we show a surprising finding that loss of BMPRII expression causes endothelial inflammation and atherosclerosis.</P><P><B>Approach and Results—</B></P><P>Using BMPRII siRNA and BMPRII<SUP>+/−</SUP> mice, we found that specific knockdown of BMPRII, but not other BMP receptors (Alk1, Alk2, Alk3, Alk6, ActRIIa, and ActRIIb), induced endothelial inflammation in a ligand-independent manner by mechanisms mediated by reactive oxygen species, nuclear factor-KappaB, and reduced nicotinamide adenine dinucleotide phosphate oxidases. Further, BMPRII<SUP>+/−</SUP>ApoE<SUP>−/−</SUP> mice developed accelerated atherosclerosis compared with BMPRII<SUP>+/+</SUP>ApoE<SUP>−/−</SUP> mice. Interestingly, we found that multiple proatherogenic stimuli, such as hypercholesterolemia, disturbed flow, prohypertensive angiotensin II, and the proinflammatory cytokine (tumor necrosis factor-α), downregulated BMPRII expression in endothelium, whereas antiatherogenic stimuli, such as stable flow and statin treatment, upregulated its expression in vivo and in vitro. Moreover, BMPRII expression was significantly diminished in human coronary advanced atherosclerotic lesions. Also, we were able to rescue the endothelial inflammation induced by BMPRII knockdown by overexpressing the BMPRII wild type, but not by the BMPRII short form lacking the carboxyl-terminal tail region.</P><P><B>Conclusions—</B></P><P>These results suggest that BMPRII is a critical, anti-inflammatory, and antiatherogenic protein that is commonly targeted by multiple pro- and antiatherogenic factors. BMPRII may be used as a novel diagnostic and therapeutic target in atherosclerosis.</P>