Coronary artery bypass grafting (CABG) is one of the most efficient procedures for patients with advanced coronary artery disease. From all the blood vessels with the potential to be used in this procedure, the internal thoracic artery (ITA) and the saphenous vein (SV) are the most commonly applied as aortocoronary conduits. Nevertheless, in order to evaluate the graft patency and efficiency effectively, basic knowledge should be constantly expanding at the molecular level as well, as the understanding of predictive factors is still limited. In this study, we have employed the expressive microarray approach, validated with Real-Time Quantitative Polymerase Chain Reaction (RT-qPCR), to analyze the transcriptome of both venous and arterial grafts. Searching for potential molecular factors, we analyzed differentially expressed gene ontologies involved in bone development and morphogenesis, for the possibility of discovery of new markers for the evaluation of ITA and SV segment quality. Among three ontological groups of interest-"endochondral bone morphogenesis", "ossification", and "skeletal system development"-we found six genes common to all of them. BMP6, SHOX2, COL13A1, CSGALNACT1, RUNX2, and STC1 showed differential expression patterns in both analyzed vessels. STC1 and COL13A1 were upregulated in ITA samples, whereas others were upregulated in SV. With regard to the Runx2 protein function in osteogenic phenotype regulation, the RUNX2 gene seems to be of paramount importance in assessing the potential of ITA, SV, and other vessels used in the CABG procedure. Overall, the presented study provided valuable insight into the molecular background of conduit characterization, and thus indicated genes that may be the target of subsequent studies, also at the protein level. Moreover, it has been suggested that RUNX2 may be recognized as a molecular marker of osteogenic changes in human blood vessels.
- MeSH
- Aorta, Thoracic metabolism MeSH
- Biomarkers MeSH
- Gene Regulatory Networks MeSH
- Coronary Artery Bypass * MeSH
- Humans MeSH
- Morphogenesis genetics MeSH
- Gene Expression Profiling MeSH
- Saphenous Vein metabolism MeSH
- Computational Biology methods MeSH
- Bone Development genetics MeSH
- Gene Expression Regulation, Developmental * MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
Mammalian cumulus-oocyte complexes (COCs) reach full developmental capability during folliculogenesis and oogenesis. It is well recognized that only gametes achieving MII stage after in vivo or in vitro maturation (IVM) are successfully fertilized by a single spermatozoon. Although the process of oocyte nuclear and/or cytoplasmic maturation in pigs is well determined, there exist many differences that promote these processes in vivo and in vitro. Therefore, this study aimed to investigate the differences in RNA expression profiles between porcine oocytes before and after IVM using microarray and real-time quantitative polymerase chain reaction (RT-qPCR) assays. Experiments were performed on oocytes isolated from 55 pubertal crossbred Landrace gilts. The oocytes were analyzed both before and after IVM and only Brilliant Cresyl Blue (BCB)-positive gametes were used for subsequent microarray analysis (Affymetrix) and RT-qPCR analysis. The microarray assay, which measures expression of 12,258 transcripts, revealed 419 differentially expressed transcripts in porcine oocytes, from which 379 were downregulated and 40 were upregulated before IVM compared to those analyzed after IVM. After DAVID analysis, we found eight different transcripts, including IHH, BMP1, WWTR1, CHRDL1, KLF10, EIF2AK3, MMP14, and STC1. Their expression is related to the "bone development" ontology group and was further subjected to hierarchical clusterization. Using RT-qPCR analysis, we confirmed the results of the microarray assay, showing increased expression of the eight genes in oocytes before IVM compared to oocytes after maturation in vitro. It has been suggested that "bone development" belongs to one ontological group involving genes substantially upregulated in porcine oocytes before IVM. We suggest that the gamete mRNA expression profile before IVM may comprise stored transcripts, which are templates for protein biosynthesis following fertilization. We also hypothesize that these mRNAs may be a specific "fingerprint" of folliculogenesis and oogenesis in pigs.
- MeSH
- Transcriptional Activation MeSH
- Down-Regulation MeSH
- Gene Expression physiology MeSH
- Gene Ontology MeSH
- In Vitro Oocyte Maturation Techniques MeSH
- Real-Time Polymerase Chain Reaction MeSH
- RNA, Messenger biosynthesis genetics MeSH
- Oocytes cytology metabolism MeSH
- Oogenesis genetics MeSH
- Swine genetics growth & development MeSH
- RNA Precursors MeSH
- Oligonucleotide Array Sequence Analysis methods MeSH
- Gene Expression Profiling MeSH
- Transcriptome physiology MeSH
- Up-Regulation MeSH
- Bone Development genetics physiology MeSH
- Gene Expression Regulation, Developmental * MeSH
- Animals MeSH
- Check Tag
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- MeSH
- Child MeSH
- Genetic Predisposition to Disease MeSH
- Bone Density genetics MeSH
- Humans MeSH
- Adolescent MeSH
- Osteoporosis * genetics prevention & control MeSH
- Polymorphism, Genetic MeSH
- Bone Development genetics MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Adolescent MeSH
- Publication type
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Somatic mutations in receptor tyrosine kinase FGFR3 cause excessive cell proliferation, leading to cancer or skin overgrowth. Remarkably, the same mutations inhibit chondrocyte proliferation and differentiation in developing bones, resulting in skeletal dysplasias, such as hypochondroplasia, achondroplasia, SADDAN and thanatophoric dysplasia. A similar phenotype is observed in Noonan syndrome, Leopard syndrome, hereditary gingival fibromatosis, neurofibromatosis type 1, Costello syndrome, Legius syndrome and cardiofaciocutaneous syndrome. Collectively termed RASopathies, the latter syndromes are caused by germline mutations in components of the RAS/ERK MAP kinase signaling pathway. This article considers the evidence suggesting that FGFR3 activation in chondrocytes mimics the activation of major oncogenes signaling via the ERK pathway. Subsequent inhibition of chondrocyte proliferation in FGFR3-related skeletal dysplasias and RASopathies is proposed to result from activation of defense mechanisms that originally evolved to safeguard mammalian organisms against cancer.
- MeSH
- Cell Differentiation genetics MeSH
- Chondrocytes cytology metabolism MeSH
- Genes, ras genetics MeSH
- Humans MeSH
- Bone Neoplasms genetics pathology MeSH
- Cell Proliferation MeSH
- Receptor, Fibroblast Growth Factor, Type 3 genetics metabolism MeSH
- Signal Transduction MeSH
- Bone Development genetics MeSH
- Bone Diseases, Developmental genetics pathology MeSH
- Germ-Line Mutation MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
The MYB family of transcription activators has been associated with a high proliferation rate and an undifferentiated state of cells in a number of tissues. Recently emerging data suggest that these molecules may also play a role in differentiation. In this study, the pattern of expression of c-MYB was followed during postnatal stages of mouse molar odontogenesis using immunohistochemistry on serial sections. Along with an abundance of the c-MYB protein in proliferating zones, we confirmed the presence of this protein in differentiated ameloblasts, odontoblasts, and osteoblasts. In addition, c-MYB was also found in cementoblasts and alveolar fibroblasts. These findings suggest integration of c-MYB into regulatory networks during hard-tissue differentiation and mineralization.
- MeSH
- Ameloblasts metabolism MeSH
- Cell Differentiation genetics MeSH
- Connective Tissue Cells metabolism MeSH
- Genes, myc genetics MeSH
- In Situ Nick-End Labeling MeSH
- Molar cytology growth & development metabolism MeSH
- Mice MeSH
- Odontogenesis genetics MeSH
- Alveolar Process cytology growth & development metabolism MeSH
- Proto-Oncogene Proteins c-myb * analysis genetics metabolism MeSH
- Bone Development genetics physiology MeSH
- Gene Expression Regulation, Developmental genetics physiology MeSH
- Dental Cementum metabolism MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Osteoporóza je onemocnění s významnou složkou genetickou a s řadou možných rizikových situací pro svůj vznik a vývoj v průběhu celého života. Proto také prevence osteoporózy musí začínat již v dětství, pokračovat v dospívání – kdy je třeba dosáhnout maximální možné vrcholové kostní hmoty – a trvat až do konce života. Základem je vždy adekvátní přísun vápníku, vitaminu D a dostatek pohybu. Je třeba monitorovat rizikové faktory – přidružené choroby i rizikové léky. Je třeba dispenzarizovat ohrožené jedince a provádět screening a monitoraci pomocí měření DXA, je třeba registrovat zlomeniny. Ve vyšším věku je potřeba hodnotit a omezovat riziko pádů.
Osteoporosis is a disease with a significant genetic component and a number of possible risk situations due to its origin and development throughout life. Therefore, osteoporosis prevention must begin as early as childhood, continue in adulthood – when the maximum possible peak bone mass needs to be achieved – and last for the rest of a person‘s life. Adequate calcium and vitamin D intake and enough exercise are always essential. Risk factors including associated diseases and risk medications need to be monitored. Surveillance of individuals at risk and screening and monitoring by use of DXA measurement are required and fractures must be registered. The risk of falls needs to be evaluated and reduced in an advanced age.
- MeSH
- Absorptiometry, Photon utilization MeSH
- Child MeSH
- Humans MeSH
- Osteoporosis prevention & control MeSH
- Mass Screening MeSH
- Osteoporosis, Postmenopausal MeSH
- Aged MeSH
- Calcium, Dietary MeSH
- Vitamin D therapeutic use MeSH
- Bone Development physiology genetics MeSH
- Check Tag
- Child MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- MeSH
- Precursor Cell Lymphoblastic Leukemia-Lymphoma drug therapy complications metabolism MeSH
- Child MeSH
- Congresses as Topic MeSH
- Humans MeSH
- Bone Diseases, Metabolic genetics MeSH
- Osteogenesis Imperfecta therapy MeSH
- Parathyroid Hormone metabolism therapeutic use MeSH
- Bone Development physiology genetics drug effects MeSH
- Check Tag
- Child MeSH
- Humans MeSH
