ABSTRACT
The sirtuin proteins constitute class III histone deacetylases (HDACs). These evolutionarily conserved NAD(+)-dependent enzymes form an important component in a variety of cellular and biological processes with highly divergent as well as convergent roles in maintaining metabolic homeostasis, safeguarding genomic integrity, regulating cancer metabolism and also inflammatory responses. Amongst the seven known mammalian sirtuin proteins, SIRT1 has gained much attention due to its widely acknowledged roles in promoting longevity and ameliorating age-associated pathologies. The contributions of other sirtuins in the field of aging are also gradually emerging. Here, we summarize some of the recent discoveries in sirtuins biology which clearly implicate the functions of sirtuin proteins in the regulation of premature cellular senescence and accelerated aging. The roles of sirtuins in various cellular processes have been extrapolated to draw inter-linkage with anti-aging mechanisms. Also, the latest findings on sirtuins which might have potential effects in the process of aging have been reviewed.
Subject(s)
Animals , Humans , Aging, Premature , Genetics , Longevity , Genetics , Sirtuin 1 , Genetics , MetabolismABSTRACT
Objective To study the effects of marrow mesenchymal stem cells on heart functions and ventricular remodeling after myocardial infarction in rats. Methods Myocardial infarction model was established by ligation of the left anterior descending coronary artery (LAD) in adult SD rats. 4 and 8 weeks after MMSCs implantation, he-modynamic evaluations, left ventricular weight/body weight ratio and heart weight/body weight ratio were determined. HE staining was performed for counting microvasculars and Van Gieson staining was used for measurements and calculation of the myocardial fibrillar collagen. Then we investigated the migration and evolution of MSCs in vivo by fluorescent microscope. Results HR was significantly decreased in transplantation MMSCs group. Eight weeks after transplantation, body weight in transplantation MMSCs group reached that of control group. At the same time, SBP, DBP and MBP were significantly increased in transplantation MMSCs group. HR was significantly decreased in transplantation MMSCs group. Secondly, left ventricular weight/body weight ratio and heart weight/body weight ratio were significantly decreased 4 weeks after transplantation MMSCs. Then the ratio was significantly decreased 8 weeks after transplantation MMSCs. Thirdly density of microvasculars was increased at the boundary of infarction site in the animals transplanted MMSCs. Finally, total volume of the myocardial fibrillar collagen was reduced in the MMSCs treated groups after MI. Conclusion Transplanting MMSCs can improve the ventricular remodeling and heart functions in acute MI rat models.
ABSTRACT
Objective To study the effects of marrow mesenchymal stem cells on heart functions and ventricular remodeling after myocardial infarction in rats. Methods Myocardial infarction model was established by ligation of the left anterior descending coronary artery (LAD) in adult SD rats. 4 and 8 weeks after MMSCs implantation,hemodynamic evaluations,left ventricular weight/body weight ratio and heart weight/body weight ratio were determined. HE staining was performed for counting microvasculars and Van Gieson staining was used for measurements and calculation of the myocardial fibrillar collagen. Then we investigated the migration and evolution of MSCs in vivo by fluorescent microscope. Results HR was significantly decreased in transplantation MMSCs group. Eight weeks after transplantation,body weight in transplantation MMSCs group reached that of control group. At the same time,SBP,DBP and MBP were significantly increased in transplantation MMSCs group. HR was significantly decreased in transplantation MMSCs group. Secondly,left ventricular weight/body weight ratio and heart weight/bodyweight ratio were significantly decreased 4 weeks after transplantation MMSCs. Then the ratio was significantly decreased 8 weeks after transplantation MMSCs. Thirdly density of microvasculars was increased at the boundary of infarction site in the animals transplanted MMSCs. Finally,total volume of the myocardial fibrillar collagen was reduced in the MMSCs treated groups after MI. Conclusion Transplanting MMSCs can improve the ventricular remodeling and heart functions in acute MI rat models.
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Epigenetics refers to non-coding sequence changes such as DNA methylation, histone modifications, chromosome remodeling and non-coding RNA regulation.Histone modifications include acetylation, phosphorylation, methylation, ubiquitination and ADP ribosylation.The combinations of different histone modifications, known as "histone code", are dynamic during development and differentiation and play important roles in the regulation of gene expressions in spatial-temporal manners.The modification on a particular residue in a histone affects not only the modifications at different residues in its own protein but also other histones.The histone modifications is a complicated network and the regulation remains elusive.
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Hutchinson-Gilford progeria syndrome (HGPS) is an early onset severe premature aging disorder due to a point mutation in LMNA gene which encodes nuclear lamin A/C. The mutation activates a cryptic splice site within exon 11 of LMNA, resulting in a 50-amino acid in-frame deletion in prelamin A. However, it is not clear how the mutation in a structural protein under the nuclear envelope could give rise to premature aging phenotypes. Recent studies showed that various abnormalities have been found in nuclear structures and functions of HGPS cells, mainly including progerin accumulation and nuclear morphology abnormalities, altered nuclear mechanical properties, changes of histone methylation patterns and epigenetic control, gene misregulation, p53 signalling activation, and increased genomic instability. Two hypotheses recently emerged in the explanation of the pathogenic mechanisms contributing to HGPS. No effective clinical intervention has been developed so far for HGPS. Several fascinating therapeutic strategies have recently been provided, such as farnesyltransferase inhibitors, antisense oligonucleotides and RNA interference. HGPS has been considered to be a model for studying the mechanisms responsible for normal aging. This study will help to elucidate the physiological functions of lamin A and nuclear envelope, together with their roles in normal aging process and diseases.
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Institutions and management for some key processes in medical equipment management are described. Desired effect is achieved in practice. Good and efficicent medical equipment management is one of the important factors to guarantee medical quality in hospital. Medical equipment management should be improved with the equipment development.
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Cell aging,the fundamental unit of biological decay,is responsible for senile disease. With the development of research,the mechanism of cell aging has been investigated in molecular level. Two hypotheses have emerged to explain the reason that lamins contribute to cell aging,one is the mechanical stress hypothesis,the other is the gene expression hypothesis. The latter proposes that mutations in A-type lamins lead to abnormal tissue-specific gene regulation. In recent years,the molecular mechanisms of lamins causing cell aging primarily include gene mutation,Zmpste24 mutation,CAAX mutation and other mutations. These mutations in the gene that encode nuclear lamins cause nuclear lamina damage directly and result in cell aging,which have been associated with several degenerative disorders.