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A Role of GADD153 in ER Stress-induced Apoptosis in Recombinant Chinese Hamster Ovary Cells
Chaya Mohan,Madhavi Sathyamurthy,이균민 한국생물공학회 2012 Biotechnology and Bioprocess Engineering Vol.17 No.3
The imbalance between the folding capacity and the folding demand imposed on the endoplasmic reticulum (ER) of therapeutic protein-producing host cells results in a stressed ER. This initiates a series of cellular signaling events termed the unfolded protein response (UPR) aimed at restoring homeostasis. In order to alleviate ER stress and ER stress-induced apoptosis in recombinant Chinese hamster ovary (rCHO) cells, silencing of the growth arrest and DNA damage 153 gene (GADD153), the main pro-apoptotic factor of UPR, was attempted. The rCHO cells were cultured under four ER stress inducing conditions, including thapsigargin, brefeldin A, glucose deprivation, glucose and glutamine deprivation. In these conditions, the functions of stably GADD153-silenced clones were investigated. It was found that under exclusive ER stress-inducing conditions of thapsigargin and brefeldin A treatments, the GADD153-silenced clones showed a less incidence of apoptosis (about 38%) and less cell viability (about 58% non-viable cells) than the control cells. However, under nutrient deprivation, the beneficial effect of GADD153 silencing was not pronounced because nutrient deprivation led to a cascade of various events including GADD153-induced cell death. GADD153-overexpressing pool cells also substantiated the findings of GADD153 downregulation. Investigation of the underlying mechanism revealed that increased GADD153 expression results in an exaggerated production of reactive oxygen species (ROS) and that GADD153 silencing promotes translational attenuation facilitating cell recovery from stress. Taken together, this study suggests that GADD153 sensitizes cells to ER stress through mechanisms that involve enhanced oxidative injury and by manipulating the ER client protein load in rCHO cells. The imbalance between the folding capacity and the folding demand imposed on the endoplasmic reticulum (ER) of therapeutic protein-producing host cells results in a stressed ER. This initiates a series of cellular signaling events termed the unfolded protein response (UPR) aimed at restoring homeostasis. In order to alleviate ER stress and ER stress-induced apoptosis in recombinant Chinese hamster ovary (rCHO) cells, silencing of the growth arrest and DNA damage 153 gene (GADD153), the main pro-apoptotic factor of UPR, was attempted. The rCHO cells were cultured under four ER stress inducing conditions, including thapsigargin, brefeldin A, glucose deprivation, glucose and glutamine deprivation. In these conditions, the functions of stably GADD153-silenced clones were investigated. It was found that under exclusive ER stress-inducing conditions of thapsigargin and brefeldin A treatments, the GADD153-silenced clones showed a less incidence of apoptosis (about 38%) and less cell viability (about 58% non-viable cells) than the control cells. However, under nutrient deprivation, the beneficial effect of GADD153 silencing was not pronounced because nutrient deprivation led to a cascade of various events including GADD153-induced cell death. GADD153-overexpressing pool cells also substantiated the findings of GADD153 downregulation. Investigation of the underlying mechanism revealed that increased GADD153 expression results in an exaggerated production of reactive oxygen species (ROS) and that GADD153 silencing promotes translational attenuation facilitating cell recovery from stress. Taken together, this study suggests that GADD153 sensitizes cells to ER stress through mechanisms that involve enhanced oxidative injury and by manipulating the ER client protein load in rCHO cells.
Efficient Energy and Position Aware Routing Protocol for Wireless Sensor Networks
( Chaya Shivalingagowda ),( Dr. P. V. Y. Jayasree ),( Dinesh. K. Sah ) 한국인터넷정보학회 2020 KSII Transactions on Internet and Information Syst Vol.14 No.5
Reliable and secure data transmission in the application environment assisted by the wireless sensor network is one of the major challenges. Problem like blind forwarding and data inaccessibility affect the efficiency of overall infrastructure performance. This paper proposes routing protocol for forwarding and error recovery during packet loss. The same is achieved by energy and hops distance-based formulation of the routing mechanism. The reachability of the intermediate node to the source node is the major factor that helps in improving the lifetime of the network. On the other hand, intelligent hop selection increases the reliability over continuous data transmission. The number of hop count is factor of hop weight and available energy of the node. The comparison over the previous state of the art using QualNet-7.4 network simulator shows the effectiveness of proposed work in terms of overall energy conservation of network and reliable data delivery. The simulation results also show the elimination of blind forwarding and data inaccessibility.
Mohan, Chaya,Park, Soon Hye,Chung, Joo Young,Lee, Gyun Min John Wiley & Sons 2007 Biotechnology and bioengineering Vol.98 No.3
<P>Protein disulfide isomerase (PDI), one of the ER-resident molecular chaperones, forms and isomerizes disulfide bonds. This study attempts to investigate the effect of PDI expression level on specific productivity (q) of recombinant Chinese hamster ovary (rCHO) cells producing thrombopoietin (TPO) and antibody (Ab). To regulate the PDI expression level, the Tet-Off system was introduced in TPO and Ab producing CHO cells, and stable Tet-Off cells (TPO-Tet-Off and Ab-Tet-Off) were screened using the luciferase assay. The doxycycline-regulated PDI expression system in Tet-Off rCHO cells (Tet-TPO-PDI and Tet-Ab-PDI) was established by the cotransfection of pTRE-PDI and pTK-Hyg expression vector into TPO-Tet-Off and Ab-Tet-Off cells, respectively. Subsequent screening was done by Western blot analysis of PDI and an enzyme-linked immunosorbent assay of the secreted TPO and antibody. We cultured two Tet-TPO-PDI and two Tet-Ab-PDI clones, and all these clones showed an average of 2.5-fold increase in PDI expression when compared to the basal level. In both these cell lines the PDI expression was tightly controlled by various concentrations of doxycycline. The q of TPO (q<SUB>TPO</SUB>) was unaffected but that of antibody producing cells was increased by 15–27% due to the PDI expression level. Biotechnol. Bioeng. 2007;98:611–615. © 2007 Wiley Periodicals, Inc.</P>
Mohan, Chaya,Lee, Gyun Min Wiley Subscription Services, Inc., A Wiley Company 2010 Biotechnology and bioengineering Vol.107 No.2
<P>To enhance specific antibody (Ab) productivity (q<SUB>Ab</SUB>) of recombinant Chinese hamster ovary (rCHO) cells, post-translational limitations in the endoplasmic reticulum during antibody production should be relieved. Previously, we reported that overexpression of protein disulfide isomerase (PDI), which catalyzes disulfide bond exchanges and assists in protein folding of newly synthesized proteins, enhanced q<SUB>Ab</SUB> of rCHO cells by about 27% (Mohan et al., 2007, Biotechnol Bioeng 98:611–615) . Since the rate limiting step in disulfide bond formation is found to be the regeneration of oxidized PDI, the oxidation state of PDI, as well as the amount of PDI, might be important. Endoplasmic reticulum oxidoreductase (ERO1L) maintains PDI in an oxidized state so that disulfide bond formation occurs. Here, PDI and its helper protein, ERO1L were overexpressed in rCHO cells producing an Ab in an attempt to ease the bottleneck in disulfide bond formation, and hence, Ab folding and secretion. Transient expression of ERO1L alone and with PDI resulted in enhanced q<SUB>Ab</SUB> by 37% and 55%, respectively. In contrast, under stable inducible co-overexpression of PDI and ERO1L, the q<SUB>Ab</SUB> was unaffected or negatively affected by varying degrees, depending on the individual expression levels of these genes. In stable clones with altered oxidation state of PDI due to co-overexpression of PDI and ERO1L, secretion of Ab was hindered and PDI-associated retention of Ab was seen in the cells. Under transient gene expression, secretion of Ab was not compromised. The data presented here suggests a possible mechanism of PDI/ERO1L interaction with the target Ab and shows how the expression levels of these proteins could affect the q<SUB>Ab</SUB> of this Ab-producing rCHO cell line. Biotechnol. Bioeng. 2010;107: 337–346. © 2010 Wiley Periodicals, Inc.</P>
Intraosseous ameloblastoma masquerading as exophytic growth: a case report
Sanjay CJ,Chaya M David,Rachna Kaul,Ramnarayan BK,Prashanth Ramachandra 대한구강악안면방사선학회 2011 Imaging Science in Dentistry Vol.41 No.2
Intraosseous ameloblastoma is the most common and simple type of ameloblastoma prevalent among odontogenic tumors. Clinico-radiographically intraosseous ameloblastoma presents as slow, painless swelling or expansion of the jaws and described as multilocular expansile radiolucency that occurs most frequently in mandibular molar/ramus area. This article describes a case of follicular ameloblastoma involving 45 year old male which is different from the usual presentation, which includes-exophytic growth, different location and without expansion of the cortex.
Intraosseous ameloblastoma masquerading as exophytic growth: a case report
CJ, Sanjay,David, Chaya.M,Kaul, Rachna,BK, Ramnarayan,Ramachandra, Prashanth Korean Academy of Oral and Maxillofacial Radiology 2011 Imaging Science in Dentistry Vol.41 No.2
Intraosseous ameloblastoma is the most common and simple type of ameloblastoma prevalent among odontogenic tumors. Clinico-radiographically intraosseous ameloblastoma presents as slow, painless swelling or expansion of the jaws and described as multilocular expansile radiolucency that occurs most frequently in mandibular molar/ramus area. This article describes a case of follicular ameloblastoma involving 45 year old male which is different from the usual presentation, which includes-exophytic growth, different location and without expansion of the cortex.