Cell StressPub Date : 2021-12-22eCollection Date: 2022-02-01DOI: 10.15698/cst2022.02.263
Mohammed K Hankir
{"title":"Building and breaking the gut barrier with bariatric surgery.","authors":"Mohammed K Hankir","doi":"10.15698/cst2022.02.263","DOIUrl":"https://doi.org/10.15698/cst2022.02.263","url":null,"abstract":"<p><p>Bariatric surgery has been proposed to improve glycemic control in morbidly obese patients by stabilising the gut barrier and alleviating endotoxemia-induced insulin resistance. Here, recent studies are highlighted which reveal site-specific and at times opposing effects of bariatric surgery on the gut barrier. Further understanding the underlying mechanisms may not only inform the development of novel gut-based drugs for the initial treatment of type 2 diabetes, but possibly also assist in the management of its eventual relapse.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"6 2","pages":"17-20"},"PeriodicalIF":6.4,"publicationDate":"2021-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8802433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39792362","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-12-21eCollection Date: 2022-01-01DOI: 10.15698/cst2022.01.262
Yushan Zhang, Chao Xu, Nelson I Agudelo Higuita, Resham Bhattacharya, Jennifer Holter Chakrabarty, Priyabrata Mukherjee
{"title":"Evaluation of I-TAC as a potential early plasma marker to differentiate between critical and non-critical COVID-19.","authors":"Yushan Zhang, Chao Xu, Nelson I Agudelo Higuita, Resham Bhattacharya, Jennifer Holter Chakrabarty, Priyabrata Mukherjee","doi":"10.15698/cst2022.01.262","DOIUrl":"10.15698/cst2022.01.262","url":null,"abstract":"<p><p>The COVID-19 pandemic has led to significant global health and economic consequences. There is an unmet need to define a molecular fingerprint of severity of the disease that may guide an early, rational and directed intervention preventing severe illness. We collected plasma from patients with moderate (nine cases), severe (22 cases) and critical (five cases) COVID-19 within three days of hospitalization (approximately one week after symptom onset) and used a cytokine antibody array to screen the 105 cytokines included in the array. We found that I-TAC, IP-10, ST2 and IL-1ra were significantly upregulated in patients with critical disease as compared to the non-critical (moderate and severe combined). ELISA further quantified I-TAC levels as 590.24±410.89, 645.35±517.59 and 1613.53±1010.59 pg/ml in moderate, severe and critical groups, respectively. Statistical analysis showed that I-TAC levels were significantly higher in patients with critical disease when compared with moderate (p = 0.04), severe (p = 0.03) or the combined non-critical (p = 0.02) group. Although limited by the low sample numbers, this study may suggest a role of I-TAC as a potential early marker to discriminate between critical and non-critical COVID-19 cases. Such knowledge is urgently needed for appropriate allocation of resources and to serve as a platform for future research towards early interventions that could mitigate disease severity and save lives.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"6 1","pages":"6-16"},"PeriodicalIF":6.4,"publicationDate":"2021-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8728569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10671009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-11-23eCollection Date: 2021-12-01DOI: 10.15698/cst2021.12.260
Clarissa Braun, Karl Katholnig, Christopher Kaltenecker, Monika Linke, Nyamdelger Sukhbaatar, Markus Hengstschläger, Thomas Weichhart
{"title":"p38 regulates the tumor suppressor PDCD4 via the TSC-mTORC1 pathway.","authors":"Clarissa Braun, Karl Katholnig, Christopher Kaltenecker, Monika Linke, Nyamdelger Sukhbaatar, Markus Hengstschläger, Thomas Weichhart","doi":"10.15698/cst2021.12.260","DOIUrl":"10.15698/cst2021.12.260","url":null,"abstract":"<p><p>Programmed cell death protein 4 (PDCD4) exerts critical functions as tumor suppressor and in immune cells to regulate inflammatory processes. The phosphoinositide 3-kinase (PI3K) promotes degradation of PDCD4 via mammalian target of rapamycin complex 1 (mTORC1). However, additional pathways that may regulate PDCD4 expression are largely ill-defined. In this study, we have found that activation of the mitogen-activated protein kinase p38 promoted degradation of PDCD4 in macrophages and fibroblasts. Mechanistically, we identified a pathway from p38 and its substrate MAP kinase-activated protein kinase 2 (MK2) to the tuberous sclerosis complex (TSC) to regulate mTORC1-dependent degradation of PDCD4. Moreover, we provide evidence that TSC1 and TSC2 regulate PDCD4 expression via an additional mechanism independent of mTORC1. These novel data extend our knowledge of how PDCD4 expression is regulated by stress- and nutrient-sensing pathways.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 12","pages":"176-182"},"PeriodicalIF":6.4,"publicationDate":"2021-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8645265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9401128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-10-29eCollection Date: 2021-11-01DOI: 10.15698/cst2021.11.258
Giusy Battilana, Francesca Zanconato, Stefano Piccolo
{"title":"Mechanisms of YAP/TAZ transcriptional control.","authors":"Giusy Battilana, Francesca Zanconato, Stefano Piccolo","doi":"10.15698/cst2021.11.258","DOIUrl":"https://doi.org/10.15698/cst2021.11.258","url":null,"abstract":"<p><p>Dysregulated gene expression is intrinsic to cell transformation, tumorigenesis and metastasis. Cancer-specific gene-expression profiles stem from gene regulatory networks fueled by genetic and epigenetic defects, and by abnormal signals of the tumor microenvironment. These oncogenic signals ultimately engage the transcriptional machinery on the cis -regulatory elements of a host of effector genes, through recruitment of transcription factors (TFs), co-activators and chromatin regulators. That said, whether gene-expression in cancer cells is the chaotic product of myriad regulations or rather a relatively ordered process orchestrated by few TFs (master regulators) has long remained enigmatic. Recent work on the YAP/TAZ co-activators has been instrumental to break new ground into this outstanding issue, revealing that tumor cells hijack growth programs that are active during development and regeneration through engagement of a small set of interconnected TFs and their nuclear partners.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 11","pages":"167-172"},"PeriodicalIF":6.4,"publicationDate":"2021-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8561301/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39716694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-10-15eCollection Date: 2021-11-01DOI: 10.15698/cst2021.11.259
Constantinos Demetriades, Julian Nüchel, Markus Plomann
{"title":"GRASPing the unconventional secretory machinery to bridge cellular stress signaling to the extracellular proteome.","authors":"Constantinos Demetriades, Julian Nüchel, Markus Plomann","doi":"10.15698/cst2021.11.259","DOIUrl":"https://doi.org/10.15698/cst2021.11.259","url":null,"abstract":"<p><p>Cellular adaptation to stress is a crucial homeostatic process for survival, metabolism, physiology, and disease. Cells respond to stress stimuli (e.g., nutrient starvation, growth factor deprivation, hypoxia, low energy, etc.) by changing the activity of signaling pathways, and interact with their environment by qualitatively and quantitatively modifying their intracellular, surface, and extracellular proteomes. How this delicate communication takes place is a hot topic in cell biological research, and has important implications for human disease.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 11","pages":"173-175"},"PeriodicalIF":6.4,"publicationDate":"2021-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8561302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39716693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-10-06eCollection Date: 2021-10-01DOI: 10.15698/cst2021.10.257
Emmanouela Kallergi, Vassiliki Nikoletopoulou
{"title":"Macroautophagy and normal aging of the nervous system: Lessons from animal models.","authors":"Emmanouela Kallergi, Vassiliki Nikoletopoulou","doi":"10.15698/cst2021.10.257","DOIUrl":"https://doi.org/10.15698/cst2021.10.257","url":null,"abstract":"<p><p>Aging represents a cumulative form of cellular stress, which is thought to challenge many aspects of proteostasis. The non-dividing, long-lived neurons are particularly vulnerable to stress, and, not surprisingly, even normal aging is highly associated with a decline in brain function in humans, as well as in other animals. Macroautophagy is a fundamental arm of the proteostasis network, safeguarding proper protein turnover during different cellular states and against diverse cellular stressors. An intricate interplay between macroautophagy and aging is beginning to unravel, with the emergence of new tools, including those for monitoring autophagy in cultured neurons and in the nervous system of different organisms <i>in vivo</i>. Here, we review recent findings on the impact of aging on neuronal integrity and on neuronal macroautophagy, as they emerge from studies in invertebrate and mammalian models.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 10","pages":"146-166"},"PeriodicalIF":6.4,"publicationDate":"2021-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8490955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39567324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-08-25eCollection Date: 2021-09-01DOI: 10.15698/cst2021.09.256
Ebony A Monson, Karla J Helbig
{"title":"Host upregulation of lipid droplets drives antiviral responses.","authors":"Ebony A Monson, Karla J Helbig","doi":"10.15698/cst2021.09.256","DOIUrl":"https://doi.org/10.15698/cst2021.09.256","url":null,"abstract":"<p><p>When a host cell is infected by a virus, it activates the innate immune response, setting off a cascade of signalling events leading to the production of an antiviral response. This immune response is typically robust and in general works well to clear viral infections, however, viruses have evolved evasion strategies to combat this, and therefore, a better understanding of how this response works in more detail is needed for the development of novel and effective therapeutics. Lipid droplets (LDs) are intracellular organelles and have historically been thought of simply as cellular energy sources, however, have more recently been recognised as critical organelles in signalling events. Importantly, many viruses are known to take over host cellular production of LDs, and it has traditionally been assumed the sole purpose of this is to supply energy for viral life cycle events. However, our recent work positions LDs as important organelles during the first few hours of an antiviral response, showing that they underpin the production of important antiviral cytokines following viral infection. Following infection of cells with either RNA viruses (Zika, Dengue, Influenza A) or a DNA (Herpes Simplex Virus-1) virus, LDs were rapidly upregulated, and this response was also replicated following stimulation with viral mimic agonists. This upregulation of LDs following infection was transient, and interestingly, did not follow the well described homeostatic mechanism of LD upregulation, instead being controlled by EGFR. The cell's ability to mount an effective immune response was greatly diminished when inhibiting EGFR, thus inhibiting LD upregulation during infection, also leading to an increase in viral replication. In this microreview, we extrapolate our recent findings and discuss LDs as an important organelle in the innate immune response.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 9","pages":"143-145"},"PeriodicalIF":6.4,"publicationDate":"2021-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39420927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-08-12eCollection Date: 2021-09-01DOI: 10.15698/cst2021.09.255
Suresh Kumar, Jingyue Jia, Vojo Deretic
{"title":"Atg8ylation as a general membrane stress and remodeling response.","authors":"Suresh Kumar, Jingyue Jia, Vojo Deretic","doi":"10.15698/cst2021.09.255","DOIUrl":"10.15698/cst2021.09.255","url":null,"abstract":"<p><p>The yeast Atg8 protein and its paralogs in mammals, mammalian Atg8s (mAtg8s), have been primarily appreciated for their participation in autophagy. However, lipidated mAtg8s, including the most frequently used autophagosomal membrane marker LC3B, are found on cellular membranes other than autophagosomes. Here we put forward a hypothesis that the lipidation of mAtg8s, termed 'Atg8ylation', is a general membrane stress and remodeling response analogous to the role that ubiquitylation plays in tagging proteins. Ubiquitin and mAtg8s are related in sequence and structure, and the lipidation of mAtg8s occurs on its C-terminal glycine, akin to the C-terminal glycine of ubiquitin. Conceptually, we propose that mAtg8s and Atg8ylation are to membranes what ubiquitin and ubiquitylation are to proteins, and that, like ubiquitylation, Atg8ylation has a multitude of downstream effector outputs, one of which is autophagy.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 9","pages":"128-142"},"PeriodicalIF":6.4,"publicationDate":"2021-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39420928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"PDLIM1: Structure, function and implication in cancer.","authors":"Jian-Kang Zhou, Xin Fan, Jian Cheng, Wenrong Liu, Yong Peng","doi":"10.15698/cst2021.08.254","DOIUrl":"https://doi.org/10.15698/cst2021.08.254","url":null,"abstract":"<p><p>PDLIM1, a member of the PDZ-LIM family, is a cytoskeletal protein and functions as a platform to form distinct protein complexes, thus participating in multiple physiological processes such as cytoskeleton regulation and synapse formation. Emerging evidence demonstrates that PDLIM1 is dysregualted in a variety of tumors and plays essential roles in tumor initiation and progression. In this review, we summarize the structure and function of PDLIM1, as well as its important roles in human cancers.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 8","pages":"119-127"},"PeriodicalIF":6.4,"publicationDate":"2021-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8335553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39314454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell StressPub Date : 2021-06-29eCollection Date: 2021-07-01DOI: 10.15698/cst2021.07.253
Juan Zapata-Muñoz, Beatriz Villarejo-Zori, Pablo Largo-Barrientos, Patricia Boya
{"title":"Towards a better understanding of the neuro-developmental role of autophagy in sickness and in health.","authors":"Juan Zapata-Muñoz, Beatriz Villarejo-Zori, Pablo Largo-Barrientos, Patricia Boya","doi":"10.15698/cst2021.07.253","DOIUrl":"10.15698/cst2021.07.253","url":null,"abstract":"<p><p>Autophagy is a critical cellular process by which biomolecules and cellular organelles are degraded in an orderly manner inside lysosomes. This process is particularly important in neurons: these post-mitotic cells cannot divide or be easily replaced and are therefore especially sensitive to the accumulation of toxic proteins and damaged organelles. Dysregulation of neuronal autophagy is well documented in a range of neurodegenerative diseases. However, growing evidence indicates that autophagy also critically contributes to neurodevelopmental cellular processes, including neurogenesis, maintenance of neural stem cell homeostasis, differentiation, metabolic reprogramming, and synaptic remodelling. These findings implicate autophagy in neurodevelopmental disorders. In this review we discuss the current understanding of the role of autophagy in neurodevelopment and neurodevelopmental disorders, as well as currently available tools and techniques that can be used to further investigate this association.</p>","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 7","pages":"99-118"},"PeriodicalIF":4.1,"publicationDate":"2021-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8283300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39221449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}