Ever since the first report that mutations in methyl-CpG-binding protein 2 (MeCP2) causes Rett syndrome (RTT), a severe neurological disorder in females world-wide, there has been a keen interest to gain a comprehensive understanding of this protein. While the classical model associated with MeCP2 function suggests its role in gene suppression via recruitment of co-repressor complexes and histone deacetylases to methylated CpG-sites, recent discoveries have brought to light its role in transcription activation, modulation of RNA splicing, and chromatin compaction. Various post-translational modifications (PTMs) of MeCP2 further increase its functional versatility. Involvement of MeCP2 in pathologies other than RTT, such as tumorigenesis however, remains poorly explored and understood. This review provides a survey of the literature implicating MeCP2 in breast, colon and prostate cancer.
{"title":"Functional assessment of MeCP2 in Rett syndrome and cancers of breast, colon, and prostate.","authors":"Somnath Pandey, Kevin Pruitt","doi":"10.1139/bcb-2016-0154","DOIUrl":"https://doi.org/10.1139/bcb-2016-0154","url":null,"abstract":"Ever since the first report that mutations in methyl-CpG-binding protein 2 (MeCP2) causes Rett syndrome (RTT), a severe neurological disorder in females world-wide, there has been a keen interest to gain a comprehensive understanding of this protein. While the classical model associated with MeCP2 function suggests its role in gene suppression via recruitment of co-repressor complexes and histone deacetylases to methylated CpG-sites, recent discoveries have brought to light its role in transcription activation, modulation of RNA splicing, and chromatin compaction. Various post-translational modifications (PTMs) of MeCP2 further increase its functional versatility. Involvement of MeCP2 in pathologies other than RTT, such as tumorigenesis however, remains poorly explored and understood. This review provides a survey of the literature implicating MeCP2 in breast, colon and prostate cancer.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"52 1","pages":"368-378"},"PeriodicalIF":0.0,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86648659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shuidong Feng, Ji-Hua Yang, C. Yao, Sisi Yang, Ze-Mei Zhu, Di Wu, H. Ling, Liang Zhang
Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides without protein-coding potential. Although these molecules were initially considered as "junk products" of transcription without biological relevance, recent advances in research have shown that lncRNA plays an important role, not only in cellular processes such as proliferation, differentiation, and metabolism, but also in the pathological processes of cancers, diabetes, and neurodegenerative diseases. In this review, we focus on the potential regulatory roles of lncRNA in diabetes and the complications associated with diabetes.
{"title":"Potential regulatory mechanisms of lncRNA in diabetes and its complications.","authors":"Shuidong Feng, Ji-Hua Yang, C. Yao, Sisi Yang, Ze-Mei Zhu, Di Wu, H. Ling, Liang Zhang","doi":"10.1139/bcb-2016-0110","DOIUrl":"https://doi.org/10.1139/bcb-2016-0110","url":null,"abstract":"Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides without protein-coding potential. Although these molecules were initially considered as \"junk products\" of transcription without biological relevance, recent advances in research have shown that lncRNA plays an important role, not only in cellular processes such as proliferation, differentiation, and metabolism, but also in the pathological processes of cancers, diabetes, and neurodegenerative diseases. In this review, we focus on the potential regulatory roles of lncRNA in diabetes and the complications associated with diabetes.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"163 1","pages":"361-367"},"PeriodicalIF":0.0,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76893868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yeying Wang, B. Hai, Xiaoqun Niu, Li Ai, Yu Cao, Ran Li, Yongxia Li
Obstructive sleep apnea (OSA) is a breathing disorder during sleep, with a most prominent character of chronic intermittent hypoxia (CIH), which induces the generation of reactive oxygen species (ROS) that damages multiple tissues and causes metabolic disorders. In this study, we established a rat model of varying OSA with different grades of CIH (12.5% O2, 10% O2, 7.5% O2, and 5% O2) for 12 weeks, and found that CIH stimulated insulin secretion, reduced the insulin:proinsulin ratio in pancreatic tissue, and caused pancreatic tissue lesions and cell apoptosis in a dose-dependent manner. Moreover, CIH promoted the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and activated mitogen-activated protein kinase (MAPK) family members, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, depending on the O2 concentration. In summary, CIH disturbed insulin secretion, and caused inflammation, lesions, and cell apoptosis in pancreatic tissue via the MAPK signaling pathway, which may be of great significance for clinical treatment of OSA and type 2 diabetes mellitus (T2DM).
{"title":"Chronic intermittent hypoxia disturbs insulin secretion and causes pancreatic injury via the MAPK signaling pathway.","authors":"Yeying Wang, B. Hai, Xiaoqun Niu, Li Ai, Yu Cao, Ran Li, Yongxia Li","doi":"10.1139/bcb-2016-0167","DOIUrl":"https://doi.org/10.1139/bcb-2016-0167","url":null,"abstract":"Obstructive sleep apnea (OSA) is a breathing disorder during sleep, with a most prominent character of chronic intermittent hypoxia (CIH), which induces the generation of reactive oxygen species (ROS) that damages multiple tissues and causes metabolic disorders. In this study, we established a rat model of varying OSA with different grades of CIH (12.5% O2, 10% O2, 7.5% O2, and 5% O2) for 12 weeks, and found that CIH stimulated insulin secretion, reduced the insulin:proinsulin ratio in pancreatic tissue, and caused pancreatic tissue lesions and cell apoptosis in a dose-dependent manner. Moreover, CIH promoted the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and activated mitogen-activated protein kinase (MAPK) family members, extracellular regulated protein kinase (ERK), c-Jun N-terminal kinase (JNK), and P38, depending on the O2 concentration. In summary, CIH disturbed insulin secretion, and caused inflammation, lesions, and cell apoptosis in pancreatic tissue via the MAPK signaling pathway, which may be of great significance for clinical treatment of OSA and type 2 diabetes mellitus (T2DM).","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"5 1","pages":"415-420"},"PeriodicalIF":0.0,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90179265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Linker histones (H1s) are a primary component of metazoan chromatin, fulfilling numerous functions, both in vitro and in vivo, including stabilizing the wrapping of DNA around the nucleosome, promoting folding and assembly of higher order chromatin structures, influencing nucleosome spacing on DNA, and regulating specific gene expression. However, many molecular details of how H1 binds to nucleosomes and recognizes unique structural features on the nucleosome surface remain undefined. Numerous, confounding studies are complicated not only by experimental limitations, but the use of different linker histone isoforms and nucleosome constructions. This review summarizes the decades of research that has resulted in several models of H1 association with nucleosomes, with a focus on recent advances that suggest multiple modes of H1 interaction in chromatin, while highlighting the remaining questions.
{"title":"Linker histones: novel insights into structure-specific recognition of the nucleosome.","authors":"Amber R. Cutter, J. Hayes","doi":"10.1139/bcb-2016-0097","DOIUrl":"https://doi.org/10.1139/bcb-2016-0097","url":null,"abstract":"Linker histones (H1s) are a primary component of metazoan chromatin, fulfilling numerous functions, both in vitro and in vivo, including stabilizing the wrapping of DNA around the nucleosome, promoting folding and assembly of higher order chromatin structures, influencing nucleosome spacing on DNA, and regulating specific gene expression. However, many molecular details of how H1 binds to nucleosomes and recognizes unique structural features on the nucleosome surface remain undefined. Numerous, confounding studies are complicated not only by experimental limitations, but the use of different linker histone isoforms and nucleosome constructions. This review summarizes the decades of research that has resulted in several models of H1 association with nucleosomes, with a focus on recent advances that suggest multiple modes of H1 interaction in chromatin, while highlighting the remaining questions.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"29 1","pages":"171-178"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89399525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The phospho-transfer mechanism of yeast phosphoglycerate kinase (PGK) has been probed through formation of trifluoromagnesate (MgF3-) and tetrafluoroaluminate (AlF4-) transition state analogue complexes and analyzed using 19F, 1H waterLOGSY and 1H chemical shift perturbation NMR spectroscopy. We observed the first 19F NMR spectroscopic evidence for the formation of metal fluoride transition state analogues of yeast PGK and also observed significant changes to proton chemical shifts of PGK in the presence, but not in the absence, of fluoride upon titration of ligands, providing indirect evidence of the formation of a closed ternary transition state. WaterLOGSY NMR spectroscopy experiments using an uncompetitive model were used in an attempt to measure ligand binding affinities within the transition state analogue complexes.
{"title":"MgF3- and AlF4- transition state analogue complexes of yeast phosphoglycerate kinase.","authors":"N. McCormick, S. Forget, R. Syvitski, D. Jakeman","doi":"10.1139/bcb-2016-0067","DOIUrl":"https://doi.org/10.1139/bcb-2016-0067","url":null,"abstract":"The phospho-transfer mechanism of yeast phosphoglycerate kinase (PGK) has been probed through formation of trifluoromagnesate (MgF3-) and tetrafluoroaluminate (AlF4-) transition state analogue complexes and analyzed using 19F, 1H waterLOGSY and 1H chemical shift perturbation NMR spectroscopy. We observed the first 19F NMR spectroscopic evidence for the formation of metal fluoride transition state analogues of yeast PGK and also observed significant changes to proton chemical shifts of PGK in the presence, but not in the absence, of fluoride upon titration of ligands, providing indirect evidence of the formation of a closed ternary transition state. WaterLOGSY NMR spectroscopy experiments using an uncompetitive model were used in an attempt to measure ligand binding affinities within the transition state analogue complexes.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"10 1","pages":"295-303"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88662161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O. Lisakovska, I. Shymanskyy, A. Mazanova, A. Khomenko, M. Veliky
The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-κB)/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D3. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg/kg body weight, 30 days) induces chronic liver injury in female Wistar rats. Specifically, increased hepatocellular necrosis and caspase-3-dependent apoptosis were observed. Prednisolone enhanced iNOS protein expression, NO generation, and tyrosine nitration in liver cells. Despite unchanged hepatic level of the NF-κB/p65 protein, prednisolone increased inhibitory κB-α (IκB-α) degradation, nuclear translocation, and phosphorylation of NF-κB/p65 at Ser311, indicating that NF-κB activation can be involved in the induction of iNOS/NO. All changes were associated with a 2.9-fold decrease in the serum content of 25-hydroxyvitamin D3 and significant reduction of hepatic vitamin D3 receptor (VDR) expression that points reliably to vitamin D3 deficiency and failures in VDR signaling. Vitamin D3 co-administration (100 IU/rat, 30 days) prevented glucocorticoid-evoked abnormalities in hepatic tissue. In conclusion, prednisolone-induced liver disturbances were associated with the impairment of NF-κB/iNOS/NO responses that can be ameliorated by vitamin D3 treatment through VDR-mediated mechanisms.
本研究旨在确定强的松龙诱导的肝细胞损伤是否伴有与核因子κB (NF-κB)/诱导型NO合成酶(iNOS)激活相关的过量一氧化氮(NO)水平，并评估维生素D3治疗的疗效。组织病理学检查、肝转氨酶(丙氨酸转氨酶和天冬氨酸转氨酶)活性和细胞死亡实验一致表明，强的松龙(5 mg/kg体重，30天)诱导雌性Wistar大鼠慢性肝损伤。具体而言，观察到肝细胞坏死和caspase-3依赖性凋亡增加。强的松龙增强肝细胞iNOS蛋白表达、NO生成和酪氨酸硝化。尽管肝脏中NF-κB/p65蛋白水平不变，但强的松龙增加了抑制κB-α (i -κB -α)降解、核易位和NF-κB/p65在311位点的磷酸化，表明NF-κB活化可能参与了iNOS/NO的诱导。所有这些变化都与血清25-羟基维生素D3含量降低2.9倍和肝脏维生素D3受体(VDR)表达显著降低有关，这可靠地表明维生素D3缺乏和VDR信号传导失败。维生素D3联合给药(100 IU/大鼠，30天)可防止糖皮质激素引起的肝组织异常。综上所述，强的松龙引起的肝脏紊乱与NF-κB/iNOS/NO反应的损害有关，而维生素D3治疗可以通过vdr介导的机制改善这种损害。
{"title":"Vitamin D3 protects against prednisolone-induced liver injury associated with the impairment of the hepatic NF-κB/iNOS/NO pathway.","authors":"O. Lisakovska, I. Shymanskyy, A. Mazanova, A. Khomenko, M. Veliky","doi":"10.1139/bcb-2016-0070","DOIUrl":"https://doi.org/10.1139/bcb-2016-0070","url":null,"abstract":"The study was carried out to define whether prednisolone-induced damage to hepatic cells is accompanied by excessive nitric oxide (NO) levels associated with nuclear factor kappa B (NF-κB)/inducible NO synthase (iNOS) activation and evaluate the efficacy of the treatment with vitamin D3. Histopathological examination, activities of liver transaminases (alanine aminotransferase and aspartate aminotransferase), and cell death assays consistently showed that prednisolone (5 mg/kg body weight, 30 days) induces chronic liver injury in female Wistar rats. Specifically, increased hepatocellular necrosis and caspase-3-dependent apoptosis were observed. Prednisolone enhanced iNOS protein expression, NO generation, and tyrosine nitration in liver cells. Despite unchanged hepatic level of the NF-κB/p65 protein, prednisolone increased inhibitory κB-α (IκB-α) degradation, nuclear translocation, and phosphorylation of NF-κB/p65 at Ser311, indicating that NF-κB activation can be involved in the induction of iNOS/NO. All changes were associated with a 2.9-fold decrease in the serum content of 25-hydroxyvitamin D3 and significant reduction of hepatic vitamin D3 receptor (VDR) expression that points reliably to vitamin D3 deficiency and failures in VDR signaling. Vitamin D3 co-administration (100 IU/rat, 30 days) prevented glucocorticoid-evoked abnormalities in hepatic tissue. In conclusion, prednisolone-induced liver disturbances were associated with the impairment of NF-κB/iNOS/NO responses that can be ameliorated by vitamin D3 treatment through VDR-mediated mechanisms.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"81 1","pages":"213-222"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76702936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Streltsova, A. V. Klinkova, Anastasia A Kuchukova, A. Y. Kadin, L. Kanevskiy, E. Kovalenko
Alcohol consumption affects the human immune system, causing a variety of disorders. However, the mechanisms of development of these changes are not fully understood. We hypothesized that ethanol may influence the expression of MICA and MICB, stress-induced molecules capable of regulating the activity of cytotoxic lymphocytes through the interaction with receptor NKG2D, which substantially affects the functionality of cellular immunity. We analyzed the effects of ethanol on MICA/B expression in tumor cell lines and human leukocytes. In the cell line models, ethanol caused different changes in the surface expression of MICA/B; in particular, it induced the translocation of intracellular proteins MICA/B to the cell surface and shedding of MICA (in soluble and microparticle-associated forms) from the plasma membrane. The observed results are not linked with cell death in cultures, taking place only under higher doses of ethanol. Ethanol at physiologically relevant concentrations (and higher) stimulated expression of MICA/B genes in different cell types. The effect of ethanol was more pronounced in hepatocyte line HepG2 compared with hematopoietic cell lines K562, Jurkat, and THP-1. Among the tested leukocytes, the most sensitive to ethanol action were T cells activated ex vivo with IL-2, in which the increase of MICA/B mRNA expression was registered with the smallest dose of ethanol (0.125%). In human monocytes, ethanol may lead to elevations in surface MICA/B levels. Presumably, changes in MICA/B expression caused by ethanol can affect the functions of NKG2D-positive cytotoxic lymphocytes, modulating immune reactions at excessive alcohol consumption.
{"title":"Ethanol-dependent expression of the NKG2D ligands MICA/B in human cell lines and leukocytes.","authors":"M. Streltsova, A. V. Klinkova, Anastasia A Kuchukova, A. Y. Kadin, L. Kanevskiy, E. Kovalenko","doi":"10.1139/bcb-2016-0120","DOIUrl":"https://doi.org/10.1139/bcb-2016-0120","url":null,"abstract":"Alcohol consumption affects the human immune system, causing a variety of disorders. However, the mechanisms of development of these changes are not fully understood. We hypothesized that ethanol may influence the expression of MICA and MICB, stress-induced molecules capable of regulating the activity of cytotoxic lymphocytes through the interaction with receptor NKG2D, which substantially affects the functionality of cellular immunity. We analyzed the effects of ethanol on MICA/B expression in tumor cell lines and human leukocytes. In the cell line models, ethanol caused different changes in the surface expression of MICA/B; in particular, it induced the translocation of intracellular proteins MICA/B to the cell surface and shedding of MICA (in soluble and microparticle-associated forms) from the plasma membrane. The observed results are not linked with cell death in cultures, taking place only under higher doses of ethanol. Ethanol at physiologically relevant concentrations (and higher) stimulated expression of MICA/B genes in different cell types. The effect of ethanol was more pronounced in hepatocyte line HepG2 compared with hematopoietic cell lines K562, Jurkat, and THP-1. Among the tested leukocytes, the most sensitive to ethanol action were T cells activated ex vivo with IL-2, in which the increase of MICA/B mRNA expression was registered with the smallest dose of ethanol (0.125%). In human monocytes, ethanol may lead to elevations in surface MICA/B levels. Presumably, changes in MICA/B expression caused by ethanol can affect the functions of NKG2D-positive cytotoxic lymphocytes, modulating immune reactions at excessive alcohol consumption.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"16 1","pages":"280-288"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73783650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Josefina Duran-Bedolla, J. Téllez-Sosa, H. Valdovinos-Torres, N. Pavón, M. Buelna-Chontal, Ángel T. Tello-López, R. Argotte-Ramos, Mario H. Rodríguez, M. C. Rodríguez
For malaria transmission, Plasmodium parasites must develop in the mosquito vector. Oxidative stress in the insect midgut, triggered by environmental changes (e.g., pH and temperature), influences the cellular signaling involved in differentiation from gametocytes to mobile ookinetes for the purpose of parasite survival. Oxidative stress activates the homeostatic response to stress characterized by the phosphorylation eIF2α, the attenuation of protein synthesis, and the transcription of genes participating in the unfolded protein response and antioxidant processes, forming a part of an integrated stress response (ISR). We hypothesized that ISR operates during the differentiation of gametocytes to ookinetes to assure Plasmodium survival. Using in-vitro conditions resembling the mosquito midgut conditions, we cultured Plasmodium berghei gametocytes to ookinetes and evaluated the redox balance by detecting reactive oxygen species and superoxide dismutase activity. Additionally, we evaluated the phosphorylation of eIF2α, the attenuation of the global protein synthesis, and the gene expression of cellular stress markers (e.g., endoplasmic reticulum chaperones and antioxidant molecules, measured by reverse-transcription quantitative polymerase chain reaction), finding that these processes were all taking place, probably to improve survival during the differentiation of Plasmodium berghei ookinetes.
{"title":"Cellular stress associated with the differentiation of Plasmodium berghei ookinetes.","authors":"Josefina Duran-Bedolla, J. Téllez-Sosa, H. Valdovinos-Torres, N. Pavón, M. Buelna-Chontal, Ángel T. Tello-López, R. Argotte-Ramos, Mario H. Rodríguez, M. C. Rodríguez","doi":"10.1139/bcb-2016-0028","DOIUrl":"https://doi.org/10.1139/bcb-2016-0028","url":null,"abstract":"For malaria transmission, Plasmodium parasites must develop in the mosquito vector. Oxidative stress in the insect midgut, triggered by environmental changes (e.g., pH and temperature), influences the cellular signaling involved in differentiation from gametocytes to mobile ookinetes for the purpose of parasite survival. Oxidative stress activates the homeostatic response to stress characterized by the phosphorylation eIF2α, the attenuation of protein synthesis, and the transcription of genes participating in the unfolded protein response and antioxidant processes, forming a part of an integrated stress response (ISR). We hypothesized that ISR operates during the differentiation of gametocytes to ookinetes to assure Plasmodium survival. Using in-vitro conditions resembling the mosquito midgut conditions, we cultured Plasmodium berghei gametocytes to ookinetes and evaluated the redox balance by detecting reactive oxygen species and superoxide dismutase activity. Additionally, we evaluated the phosphorylation of eIF2α, the attenuation of the global protein synthesis, and the gene expression of cellular stress markers (e.g., endoplasmic reticulum chaperones and antioxidant molecules, measured by reverse-transcription quantitative polymerase chain reaction), finding that these processes were all taking place, probably to improve survival during the differentiation of Plasmodium berghei ookinetes.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"80 1","pages":"310-317"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90858640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohd Afiq Hazlami Habib, Gan Chee Yuen, Fazilah Othman, Nurul Nabilah Zainudin, A. Latiff, M. Ismail
The natural rubber latex extracted from the bark of Hevea brasiliensis plays various important roles in today's modern society. Following ultracentrifugation, the latex can be separated into 3 layers: C-serum, lutoids, and rubber particles. Previous studies have shown that a large number of proteins are present in these 3 layers. However, a complete proteome for this important plant is still unavailable. Protein sequences have been recently translated from the completed draft genome database of H. brasiliensis, leading to the creation of annotated protein databases of the following H. brasiliensis biosynthetic pathways: photosynthesis, latex allergens, rubberwood formation, latex biosynthesis, and disease resistance. This research was conducted to identify the proteins contained within the latex by way of de novo sequencing from mass spectral data obtained from the 3 layers of the latex. Peptides from these proteins were fragmented using collision-induced dissociation, higher-energy collisional dissociation, and electron-transfer dissociation activation methods. A large percentage of proteins from the biosynthetic pathways (63% to 100%) were successfully identified. In addition, a total of 1839 unique proteins were identified from the whole translated draft genome database (AnnHBM).
{"title":"Proteomics analysis of latex from Hevea brasiliensis (clone RRIM 600).","authors":"Mohd Afiq Hazlami Habib, Gan Chee Yuen, Fazilah Othman, Nurul Nabilah Zainudin, A. Latiff, M. Ismail","doi":"10.1139/bcb-2016-0144","DOIUrl":"https://doi.org/10.1139/bcb-2016-0144","url":null,"abstract":"The natural rubber latex extracted from the bark of Hevea brasiliensis plays various important roles in today's modern society. Following ultracentrifugation, the latex can be separated into 3 layers: C-serum, lutoids, and rubber particles. Previous studies have shown that a large number of proteins are present in these 3 layers. However, a complete proteome for this important plant is still unavailable. Protein sequences have been recently translated from the completed draft genome database of H. brasiliensis, leading to the creation of annotated protein databases of the following H. brasiliensis biosynthetic pathways: photosynthesis, latex allergens, rubberwood formation, latex biosynthesis, and disease resistance. This research was conducted to identify the proteins contained within the latex by way of de novo sequencing from mass spectral data obtained from the 3 layers of the latex. Peptides from these proteins were fragmented using collision-induced dissociation, higher-energy collisional dissociation, and electron-transfer dissociation activation methods. A large percentage of proteins from the biosynthetic pathways (63% to 100%) were successfully identified. In addition, a total of 1839 unique proteins were identified from the whole translated draft genome database (AnnHBM).","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"20 1","pages":"232-242"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82406171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Adrian Taylor, L. Schenkel, Maiya K. Yokich, M. Bakovic
It was hypothesized that choline supplementation in insulin resistant (IR) CTP:phosphoethanolamine cytidylyltransferase deficient (Pcyt2+/-) mice would ameliorate muscle function by remodeling glucose and fatty acid (FA) metabolism. Pcyt2+/- mice either received no treatment or were allowed access to 2 mg/mL choline in drinking water for 4 weeks. Skeletal muscle was harvested from choline treated and untreated mice. Lipid analysis and metabolic gene expression and signaling pathways were compared between untreated Pcyt2+/- mice, treated Pcyt2+/- mice, and Pcyt2+/+ mice. The major positive effect of choline supplementation on IR muscle was the reduction of glucose utilization for FA and triglyceride (TAG) synthesis and increased muscle glucose storage as glycogen. Choline reduced the expression of genes for FA and TAG formation (Scd1, Fas, Srebp1c, Dgat1/2), upregulated the genes for FA oxidation (Cpt1, Pparα, Pgc1α), and had minor effects on phospholipid and lipolysis genes. Pcyt2+/- muscle had reduced insulin signaling (IRS1), autophagy (LC3), and choline transport (CTL1) proteins that were restored by choline treatment. Additionally, choline activated AMPK and Akt while inhibiting mTORC1 phosphorylation. These data established that choline supplementation could restore muscle glucose metabolism by reducing lipogenesis and improving mitochondrial and intracellular signaling for protein and energy metabolism in insulin resistant Pcyt2 deficient mice.
{"title":"Adaptations to excess choline in insulin resistant and Pcyt2 deficient skeletal muscle.","authors":"Adrian Taylor, L. Schenkel, Maiya K. Yokich, M. Bakovic","doi":"10.1139/bcb-2016-0105","DOIUrl":"https://doi.org/10.1139/bcb-2016-0105","url":null,"abstract":"It was hypothesized that choline supplementation in insulin resistant (IR) CTP:phosphoethanolamine cytidylyltransferase deficient (Pcyt2+/-) mice would ameliorate muscle function by remodeling glucose and fatty acid (FA) metabolism. Pcyt2+/- mice either received no treatment or were allowed access to 2 mg/mL choline in drinking water for 4 weeks. Skeletal muscle was harvested from choline treated and untreated mice. Lipid analysis and metabolic gene expression and signaling pathways were compared between untreated Pcyt2+/- mice, treated Pcyt2+/- mice, and Pcyt2+/+ mice. The major positive effect of choline supplementation on IR muscle was the reduction of glucose utilization for FA and triglyceride (TAG) synthesis and increased muscle glucose storage as glycogen. Choline reduced the expression of genes for FA and TAG formation (Scd1, Fas, Srebp1c, Dgat1/2), upregulated the genes for FA oxidation (Cpt1, Pparα, Pgc1α), and had minor effects on phospholipid and lipolysis genes. Pcyt2+/- muscle had reduced insulin signaling (IRS1), autophagy (LC3), and choline transport (CTL1) proteins that were restored by choline treatment. Additionally, choline activated AMPK and Akt while inhibiting mTORC1 phosphorylation. These data established that choline supplementation could restore muscle glucose metabolism by reducing lipogenesis and improving mitochondrial and intracellular signaling for protein and energy metabolism in insulin resistant Pcyt2 deficient mice.","PeriodicalId":9524,"journal":{"name":"Canadian journal of biochemistry and cell biology = Revue canadienne de biochimie et biologie cellulaire","volume":"36 1","pages":"223-231"},"PeriodicalIF":0.0,"publicationDate":"2017-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79373841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：