Pub Date : 2017-01-01Epub Date: 2017-12-12DOI: 10.4172/2168-9296.1000190
Michelle R Garcia
The mechanistic events of female infertility have been investigated for over 50 years and despite progress many causes of infertility remain elusive. However, over half of idiopathic infertility issues have been attributed to a defective ovarian tissue responsible for the maintenance of a conceptus, the corpus luteum (CL). Many CL defects are attributed, in part, to abnormal vascularization (angiogenesis), which occurs primarily during the developmental stage of the luteal lifespan. A few well-established angiogenic growth promotants have been implicated in luteal angiogenic processes but the mechanisms of the process are still under investigation. Recent evidence supports a role for the adipokine hormone leptin as a probable component in the angiogenic and developmental processes of a CL. Leptin expression is present during the developmental and maturation stages of the luteal lifespan and stimulates the expression of angiogenic hormones in the CL. Induced leptin deficient CL have a higher occurrence of abnormal, underdeveloped gross morphology and an increase in the number of large diameter vessels and large luteal cells. Leptin replacement therapy in leptin deficient CL accelerates tissue development, increasing overall tissue mass and forming a structure that resembled a mature CL during the early stages of development. Collectively, the evidence supports the supposition that leptin is involved in the angiogenic and developmental processes of luteal tissue.
{"title":"Leptin Contributes to the Development of the Corpus Luteum.","authors":"Michelle R Garcia","doi":"10.4172/2168-9296.1000190","DOIUrl":"https://doi.org/10.4172/2168-9296.1000190","url":null,"abstract":"The mechanistic events of female infertility have been investigated for over 50 years and despite progress many causes of infertility remain elusive. However, over half of idiopathic infertility issues have been attributed to a defective ovarian tissue responsible for the maintenance of a conceptus, the corpus luteum (CL). Many CL defects are attributed, in part, to abnormal vascularization (angiogenesis), which occurs primarily during the developmental stage of the luteal lifespan. A few well-established angiogenic growth promotants have been implicated in luteal angiogenic processes but the mechanisms of the process are still under investigation. Recent evidence supports a role for the adipokine hormone leptin as a probable component in the angiogenic and developmental processes of a CL. Leptin expression is present during the developmental and maturation stages of the luteal lifespan and stimulates the expression of angiogenic hormones in the CL. Induced leptin deficient CL have a higher occurrence of abnormal, underdeveloped gross morphology and an increase in the number of large diameter vessels and large luteal cells. Leptin replacement therapy in leptin deficient CL accelerates tissue development, increasing overall tissue mass and forming a structure that resembled a mature CL during the early stages of development. Collectively, the evidence supports the supposition that leptin is involved in the angiogenic and developmental processes of luteal tissue.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2168-9296.1000190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35793607","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}
Pub Date : 2017-01-01DOI: 10.4172/2168-9296.1000179
A. Berezin
The “obesity paradox” phenomenon is referred to as a U-shaped curve between long-term prognosis and body mass index in heart failure patients. There is a large body of evidence regarding the regulatory role of visceral adipose tissue-related adipocytokines in activity of endogenous repair system. The reparation of myocardium and endothelium may strongly enhance by differentiation and mobbing of endothelial progenitor cells (EPCs). They improve angiogenesis and collateral vessel growth, as well as counteract vascular injury. It has suggested that several metabolic factors frequently associated with HF may increase the number of circulating EPCs, which mediate repair processes and collaborate with obese. In contrast, decreased number and/or weak functionality of EPCs relate with altered endogenous repair system and may negatively contribute in HF development. Finally, moving across recently received evidence “obesity paradox” could be elucidated as a result of interplaying of trigging repair systems and ability of EPCs to response on challenges enhancing reparative potency in target organs, i.e. myocardium, vascular wall and endothelium.
{"title":"\"Obesity Paradox\" in Heart Failure: The Possible Role of Progenitor Endothelial Cell Dysfunction","authors":"A. Berezin","doi":"10.4172/2168-9296.1000179","DOIUrl":"https://doi.org/10.4172/2168-9296.1000179","url":null,"abstract":"The “obesity paradox” phenomenon is referred to as a U-shaped curve between long-term prognosis and body mass index in heart failure patients. There is a large body of evidence regarding the regulatory role of visceral adipose tissue-related adipocytokines in activity of endogenous repair system. The reparation of myocardium and endothelium may strongly enhance by differentiation and mobbing of endothelial progenitor cells (EPCs). They improve angiogenesis and collateral vessel growth, as well as counteract vascular injury. It has suggested that several metabolic factors frequently associated with HF may increase the number of circulating EPCs, which mediate repair processes and collaborate with obese. In contrast, decreased number and/or weak functionality of EPCs relate with altered endogenous repair system and may negatively contribute in HF development. Finally, moving across recently received evidence “obesity paradox” could be elucidated as a result of interplaying of trigging repair systems and ability of EPCs to response on challenges enhancing reparative potency in target organs, i.e. myocardium, vascular wall and endothelium.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78385835","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}
Pub Date : 2017-01-01DOI: 10.4172/2168-9296.1000188
Odontuya Davaadorj, H. Akatsuka, Yoshiki Yamaguchi, Chisa Okada, Masatoshi Ito, N. Fukunishi, Y. Sekijima, H. Ohnota, K. Kawai, Takahiro Suzuki, Takehito Sato, Yasuyuki Suzuki
Sialidosis type I patient-derived induced pluripotent stem cells (iPSCs) were generated from blood mononuclear cells. During embryoid body-like 3D culture, aggregates of patient-derived iPSCs were irregular in shape and had increased vacuoles filled with lipid droplets and cellular components such as damaged mitochondria. Retinal pigment epithelial cells induced from patient-derived iPSCs showed impaired autophagy flux with decreased formation of LC3 puncta. Sialidosis patient-derived iPSCs could provide a useful tool for investigating the mechanism of the autophagy/ lysosome-mediated degradation system.
{"title":"Impaired Autophagy in Retinal Pigment Epithelial Cells Induced from iPS Cells obtained from a Patient with Sialidosis","authors":"Odontuya Davaadorj, H. Akatsuka, Yoshiki Yamaguchi, Chisa Okada, Masatoshi Ito, N. Fukunishi, Y. Sekijima, H. Ohnota, K. Kawai, Takahiro Suzuki, Takehito Sato, Yasuyuki Suzuki","doi":"10.4172/2168-9296.1000188","DOIUrl":"https://doi.org/10.4172/2168-9296.1000188","url":null,"abstract":"Sialidosis type I patient-derived induced pluripotent stem cells (iPSCs) were generated from blood mononuclear cells. During embryoid body-like 3D culture, aggregates of patient-derived iPSCs were irregular in shape and had increased vacuoles filled with lipid droplets and cellular components such as damaged mitochondria. Retinal pigment epithelial cells induced from patient-derived iPSCs showed impaired autophagy flux with decreased formation of LC3 puncta. Sialidosis patient-derived iPSCs could provide a useful tool for investigating the mechanism of the autophagy/ lysosome-mediated degradation system.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75944755","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}
Pub Date : 2016-08-31DOI: 10.4172/2168-9296.1000177
M. Barandalla, S. Colleoni, G. Lazzari
Human Embryonic Stem Cells (hESCs) potentially offer a unique in vitro model to study how an adverse environment during the early developmental stages post-fertilization can affect the physiology of the undifferentiated embryonic stem cells existing in the early embryo and predispose to long term effects on the offspring, according to the Developmental Origins of Health and Disease (DOHaD) concept. A number of unfavourable conditions can affect the development of the early embryo inducing oxidative stress both in vivo, for instance in gestational diabetes and in vitro, when embryos are derived from Assisted Reproductive Technologies (ART). Therefore, the aim of this study was the development of a novel in vitro model to analyse the effects of oxidative stress and the antioxidant response against Reactive Oxygen Species (ROS) in embryonic stem cells in comparison with somatic cells, fibroblasts and endothelial cells. To this purpose we designed an in vitro protocol based on hydrogen peroxide (H2O2) treatment of 72 h, in order to better resemble the period of embryonic development from the early cleavages to the blastocyst stage. We demonstrate that H2O2 treatment induces the modification of crucial oxidative stress biomarkers like ROS and lipid peroxidation levels, and mobilizes several antioxidant enzymes through NFkβ translocation. Moreover we show differences between somatic and embryonic cells in their antioxidant response towards H2O2 induced damage. Therefore this study presents a promising in vitro model to investigate the effects of oxidative stress conditions on early human embryonic cells.
{"title":"Differential Response of Human Embryonic Stem and Somatic Cells to Non-Cytotoxic Hydrogen Peroxide Exposure: An Attempt to Model In Vitro the Effects of Oxidative Stress on the Early Embryo.","authors":"M. Barandalla, S. Colleoni, G. Lazzari","doi":"10.4172/2168-9296.1000177","DOIUrl":"https://doi.org/10.4172/2168-9296.1000177","url":null,"abstract":"Human Embryonic Stem Cells (hESCs) potentially offer a unique in vitro model to study how an adverse environment during the early developmental stages post-fertilization can affect the physiology of the undifferentiated embryonic stem cells existing in the early embryo and predispose to long term effects on the offspring, according to the Developmental Origins of Health and Disease (DOHaD) concept. A number of unfavourable conditions can affect the development of the early embryo inducing oxidative stress both in vivo, for instance in gestational diabetes and in vitro, when embryos are derived from Assisted Reproductive Technologies (ART). Therefore, the aim of this study was the development of a novel in vitro model to analyse the effects of oxidative stress and the antioxidant response against Reactive Oxygen Species (ROS) in embryonic stem cells in comparison with somatic cells, fibroblasts and endothelial cells. To this purpose we designed an in vitro protocol based on hydrogen peroxide (H2O2) treatment of 72 h, in order to better resemble the period of embryonic development from the early cleavages to the blastocyst stage. We demonstrate that H2O2 treatment induces the modification of crucial oxidative stress biomarkers like ROS and lipid peroxidation levels, and mobilizes several antioxidant enzymes through NFkβ translocation. Moreover we show differences between somatic and embryonic cells in their antioxidant response towards H2O2 induced damage. Therefore this study presents a promising in vitro model to investigate the effects of oxidative stress conditions on early human embryonic cells.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88874796","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}
Pub Date : 2016-08-31DOI: 10.4172/2168-9296.1000176
R. Kaushik, M. Dige, P. Rout
NADPH oxidase (NOX) proteins are membrane-associated, multi-unit enzymes that catalyze the reduction of oxygen using NADPH as an electron donor. The present study was carried out to analyse expression profile of ENOX2 gene in heat stress susceptible (HSS) and heat stress tolerant (HST) individuals in response to heat stress. The genomic DNA was isolated from blood. The total RNA was isolated from different tissues such as liver, spleen and kidney. High Resolution Melting (HRM) genotyping exhibited two different genotypes in four goat breeds. The relative expression pattern of ENOX2 gene in liver, spleen and kidney showed 7.40 10.01 and 3.92 fold higher expression than control. Barbari, Jamunapari, Jakhrana and Sirohi exhibited 8.11, 10.97, 5.65 and 5.87 higher fold expression than control. Heat stress-susceptible (HSS) and heat stress-tolerant (HST) individuals exhibited 12.45 and 5.41 fold ENOX2 gene expressions than control in response to long term heat stress.
{"title":"Molecular Characterization and Expression Profiling of ENOX2 Gene in Response to Heat Stress in Goats","authors":"R. Kaushik, M. Dige, P. Rout","doi":"10.4172/2168-9296.1000176","DOIUrl":"https://doi.org/10.4172/2168-9296.1000176","url":null,"abstract":"NADPH oxidase (NOX) proteins are membrane-associated, multi-unit enzymes that catalyze the reduction of oxygen using NADPH as an electron donor. The present study was carried out to analyse expression profile of ENOX2 gene in heat stress susceptible (HSS) and heat stress tolerant (HST) individuals in response to heat stress. The genomic DNA was isolated from blood. The total \u0000RNA \u0000was isolated from different tissues such as liver, spleen and kidney. High Resolution Melting (HRM) genotyping exhibited two different genotypes in four goat breeds. The relative expression pattern of ENOX2 gene in liver, spleen and kidney showed 7.40 10.01 and 3.92 fold higher expression than control. Barbari, Jamunapari, Jakhrana and Sirohi exhibited 8.11, 10.97, 5.65 and 5.87 higher fold expression than control. Heat stress-susceptible (HSS) and heat stress-tolerant (HST) individuals exhibited 12.45 and 5.41 fold ENOX2 \u0000 gene \u0000expressions than control in response to long term heat stress.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89597263","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}
Pub Date : 2016-07-17DOI: 10.4172/2168-9296.1000E140
K. Coskun, L. Tutar, Yusuf Tutar
Heat Shock Protein 70 (Hsp70) is a molecular chaperone having a major role in protein quality control under normal and stressful conditions. It prevents the aggregation, helps substrate protein folding, protein degradation, transportation, and regulation [1,2]. Hsp70 has two domains; substrate binding domain (SBD) and nucleotide binding domain (NBD). NBD binds to ATP and performs ATP hydrolysis in order to fold substrate proteins to their native structure. Native structure helps substrate protein to properly function. SBD contains hydrophobic amino acid residues, and this hydrophobic cavity helps unfolded substrate proteins to fold their native structure. Thus, exposed part of the folded proteins may not interact with each other and cause aggregation. The biological activity of Hsp70 family is based on ATP hydrolysis and hydrolysis rate is changed by some of the associated cochaperone proteins [1,3,4].
{"title":"Current Drug Design Studies for Hsp70 in Oncological Applications","authors":"K. Coskun, L. Tutar, Yusuf Tutar","doi":"10.4172/2168-9296.1000E140","DOIUrl":"https://doi.org/10.4172/2168-9296.1000E140","url":null,"abstract":"Heat Shock Protein 70 (Hsp70) is a molecular chaperone having a major role in protein quality control under normal and stressful conditions. It prevents the aggregation, helps substrate protein folding, protein degradation, transportation, and regulation [1,2]. Hsp70 has two domains; substrate binding domain (SBD) and nucleotide binding domain (NBD). NBD binds to ATP and performs ATP hydrolysis in order to fold substrate proteins to their native structure. Native structure helps substrate protein to properly function. SBD contains hydrophobic amino acid residues, and this hydrophobic cavity helps unfolded substrate proteins to fold their native structure. Thus, exposed part of the folded proteins may not interact with each other and cause aggregation. The biological activity of Hsp70 family is based on ATP hydrolysis and hydrolysis rate is changed by some of the associated cochaperone proteins [1,3,4].","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76724105","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}
Pub Date : 2016-07-07DOI: 10.4172/2168-9296.1000175
Heedoo Lee, Duo Zhang, J. Minhas, Yang Jin
Extracellular vesicles (EVs) are a group of heterogeneous, nano-sized structures surrounded by lipid bilayer membranes that are released by cells. Depending on their size and mechanisms of formation, EVs are often referred to as exosomes, microvesicles (MVs) and apoptotic bodies (AB). EVs are evolutionally conserved vesicles that mediate intercellular communications and cross-talk, via transferring proteins, lipids and nucleic acids. Accumulating evidence suggests that EVs exert essential physiological and pathological functions on both their mother and recipient cells. Therefore, growing interests focus on the potentials of EVs to serve as novel targets for the development of therapeutic and diagnostic strategies. Currently, extensive reports are yielded from cancer research. However, besides malignancy, EVs may also serve as crucial regulators in other devastating conditions, such as the acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). The generation, regulation and function of EVs in ARDS/ALI are largely unexplored. In this mini review, we will briefly review the current understanding of EVs and their known physiological/pathological functions in the pathogenesis of ARDS/ALI. Previously, only scattered reports have been published in this field. We believe that further investigations focusing on EVs and their compositions will shed light on novel insights in the research of ARDS/ALI.
{"title":"Extracellular Vesicles Facilitate the Intercellular Communications in the Pathogenesis of Lung Injury.","authors":"Heedoo Lee, Duo Zhang, J. Minhas, Yang Jin","doi":"10.4172/2168-9296.1000175","DOIUrl":"https://doi.org/10.4172/2168-9296.1000175","url":null,"abstract":"Extracellular vesicles (EVs) are a group of heterogeneous, nano-sized structures surrounded by lipid bilayer membranes that are released by cells. Depending on their size and mechanisms of formation, EVs are often referred to as exosomes, microvesicles (MVs) and apoptotic bodies (AB). EVs are evolutionally conserved vesicles that mediate intercellular communications and cross-talk, via transferring proteins, lipids and nucleic acids. Accumulating evidence suggests that EVs exert essential physiological and pathological functions on both their mother and recipient cells. Therefore, growing interests focus on the potentials of EVs to serve as novel targets for the development of therapeutic and diagnostic strategies. Currently, extensive reports are yielded from cancer research. However, besides malignancy, EVs may also serve as crucial regulators in other devastating conditions, such as the acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). The generation, regulation and function of EVs in ARDS/ALI are largely unexplored. In this mini review, we will briefly review the current understanding of EVs and their known physiological/pathological functions in the pathogenesis of ARDS/ALI. Previously, only scattered reports have been published in this field. We believe that further investigations focusing on EVs and their compositions will shed light on novel insights in the research of ARDS/ALI.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78945806","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}
Pub Date : 2016-07-07DOI: 10.4172/2168-9296.1000174
M. Lopez-Diaz
It is widely recognized by the scientific community that there is a serious health problem in developed societies due to the increased prevalence in neurodegenerative diseases. Diseases such as Parkinson ́s, Alzheimer ́s, ALS, etc., require more than one therapeutic approach depending on the pathogenesis of the disease, among them, regenerative therapy of the nervous tissues is needed in an urgent and safe way.
{"title":"Neurodegenerative Diseases: In Vitro Culture of Neural Progenitor and Neural Stem Cells Challenges and Hopes","authors":"M. Lopez-Diaz","doi":"10.4172/2168-9296.1000174","DOIUrl":"https://doi.org/10.4172/2168-9296.1000174","url":null,"abstract":"It is widely recognized by the scientific community that there is a serious health problem in developed societies due to the increased prevalence in neurodegenerative diseases. Diseases such as Parkinson ́s, Alzheimer ́s, ALS, etc., require more than one therapeutic approach depending on the pathogenesis of the disease, among them, regenerative therapy of the nervous tissues is needed in an urgent and safe way.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75623470","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}
Pub Date : 2016-06-15DOI: 10.4172/2168-9296.1000173
A. Berezin
Heart failure (HF) remains to be a serious public and health problem, which associate with higher morbidity, mortality and disability. Although there are high-quality developed clinical recommendations regarding prevention and treatment of HF, patients with HF have experienced the poor clinical outcomes. Currently transfer of drugs using extracellular vesicles (EVs) into target cells in vivo is promising methods for attenuation of cardiac remodeling and ischemia. The mini review is presented data confirming the role of specific novel delivery drug systems released wide spectrum of biological active molecules based on EVs’ releasing in HF. The use of EV systems might allow localized and sustained cytokine release and consequently a prolonged biological effect with induction of tissue regeneration and revascularization in HF.
{"title":"Utilization of Novel Delivery Drug Systems Based on Release of Extracellular Vesicles in Heart Failure","authors":"A. Berezin","doi":"10.4172/2168-9296.1000173","DOIUrl":"https://doi.org/10.4172/2168-9296.1000173","url":null,"abstract":"Heart failure (HF) remains to be a serious public and health problem, which associate with higher morbidity, mortality and disability. Although there are high-quality developed clinical recommendations regarding prevention and treatment of HF, patients with HF have experienced the poor clinical outcomes. Currently transfer of drugs using extracellular vesicles (EVs) into target cells in vivo is promising methods for attenuation of cardiac remodeling and ischemia. The mini review is presented data confirming the role of specific novel delivery drug systems released wide spectrum of biological active molecules based on EVs’ releasing in HF. The use of EV systems might allow localized and sustained cytokine release and consequently a prolonged biological effect with induction of tissue regeneration and revascularization in HF.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90489426","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}
Pub Date : 2016-05-21DOI: 10.4172/2168-9296.1000172
M. A. Alam
A growing body of evidence suggests that mutations in MTHFR gene are involved in cardiovascular diseases (CVD) - cardiac development, atherosclerosis, myocardial infarction, heart failure, hypertension, aneurysms- and several other disease- cancers, neurological and metabolic disorders. Genetic variations in other genes are added risk for CVD- a leading cause of morbidity and mortality around the globe. Accumulating data over the decade has enhanced our understanding of MTHFR deficiency and diseases associated risk. The frequency of MTHFR 677 C→T and 1298 A→C gene mutations varies substantially in different regions of the world among different racial and ethnic groups. In particular, 677C→T and 1298 A→C variant are associated with clinical manifestation of almost all noncommunicable diseases. This review describes the roles of MTHFR gene mutation in CVD and prospective therapies for heart disease treatment.
{"title":"Methylenetetrahydrofolate Reductase Gene Polymorphisms and Cardiovascular Diseases","authors":"M. A. Alam","doi":"10.4172/2168-9296.1000172","DOIUrl":"https://doi.org/10.4172/2168-9296.1000172","url":null,"abstract":"A growing body of evidence suggests that mutations in MTHFR gene are involved in cardiovascular diseases (CVD) - cardiac development, atherosclerosis, myocardial infarction, heart failure, hypertension, aneurysms- and several other disease- cancers, neurological and metabolic disorders. Genetic variations in other genes are added risk for CVD- a leading cause of morbidity and mortality around the globe. Accumulating data over the decade has enhanced our understanding of MTHFR deficiency and diseases associated risk. The frequency of MTHFR 677 C→T and 1298 A→C gene mutations varies substantially in different regions of the world among different racial and ethnic groups. In particular, 677C→T and 1298 A→C variant are associated with clinical manifestation of almost all noncommunicable diseases. This review describes the roles of MTHFR gene mutation in CVD and prospective therapies for heart disease treatment.","PeriodicalId":9775,"journal":{"name":"Cell & developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86286216","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}
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