Chumaeva N.,University of Helsinki |
Chumaeva N.,Institute of Cell Biophysics |
Hintsanen M.,University of Helsinki |
Juonala M.,University of Turku |
And 2 more authors.
BMC Cardiovascular Disorders | Year: 2010
Background: The syndrome of vital exhaustion (VE), characterized by fatigue and irritability, may contribute to an increased risk of atherosclerosis. The aim of the study was to explore sex differences in the interactions of VE with endothelial dysfunction and VE with reduced carotid elasticity, the important contributors to the development of early atherosclerosis, on preclinical atherosclerosis.Methods: The participants were 1002 women and 719 men aged 24-39 examined in the Cardiovascular Risk in Young Finns study. Vital exhaustion was measured using the Maastricht Questionnaire. Preclinical atherosclerosis was assessed by carotid intima-media thickness (IMT), endothelial function was measured by brachial flow-mediated dilatation (FMD), and arterial elasticity by carotid artery compliance (CAC) using ultrasound techniques.Results: We found a significant CAC x VE interaction for IMT only for the men. Our results imply that high VE level significantly related to high IMT levels among the men with low CAC, but not among the women with low CAC or among the women or men with high CAC. No significant FMD x VE interactions for IMT for the women or men were found.Conclusions: High VE may exert an effect on IMT for men with impaired arterial elasticity. The results suggest that high vitally exhausted men with reduced arterial elasticity are at increased risk of atherosclerosis in early life and imply men's decreased stress coping in relation to stressful psychological coronary risk factors. © 2010 Chumaeva et al; licensee BioMed Central Ltd.
Khubutiya M.S.,Sklifosovsky Research Institute for Emergency Medicine |
Vagabov A.V.,Sklifosovsky Research Institute for Emergency Medicine |
Temnov A.A.,Sklifosovsky Research Institute for Emergency Medicine |
Sklifas A.N.,Institute of Cell Biophysics
Cytotherapy | Year: 2014
The purpose of this review is to systematize data from many studies and observations of proliferative, anti-apoptotic and anti-inflammatory effects of mesenchymal stromal cell (MSC) paracrine factors and their biologic effects in models of acute organ injury. © 2014 International Society for Cellular Therapy.
Xie J.,Tsinghua University |
Wang C.,Chongqing University |
Huang D.-Y.,University of Washington |
Zhang Y.,Tsinghua University |
And 4 more authors.
Journal of Biomechanics | Year: 2013
The anterior cruciate ligament (ACL) is known to have a poor self-healing ability. In contrast, the medial collateral ligament (MCL) can heal relatively well and restore the joint function. Transforming growth factor-beta1 (TGF-Β1) is considered to be an important chemical mediator in the wound healing of the ligaments. While the role of TGF-Β1-induced expressions of the lysyl oxidases (LOXs) and matrix metalloproteinases (MMPs), which respectively facilitate the extracellular matrix (ECM) repair and degradation, is poorly understood. In this study, we used equibiaxial stretch chamber to mimic mechanical injury of ACL and MCL fibroblasts, and aimed to determine the intrinsic differences between ACL and MCL by characterizing the differential expressions of LOXs and MMPs in response to TGF-Β1 after mechanical injury. By using semi-quantitative PCR, quantitative real-time PCR, western blot and zymography, we found TGF-Β1 induced injured MCL to express more LOXs than injured ACL (up to 1.85-fold in LOX, 2.21-fold in LOXL-1, 1.71-fold in LOXL-2, 2.52-fold in LOXL-3 and 3.32-fold in LOXL-4). Meanwhile, TGF-Β1 induced injured ACL to express more MMPs than injured MCL fibroblasts (up to 2.33-fold in MMP-1, 2.45-fold in MMP-2, 1.89-fold in MMP-3 and 1.50-fold in MMP-12). The further protein results were coincident with the gene expressions above. The different expressions of LOXs and MMPs inferred the intrinsic differences between ACL and MCL, and the intrinsic differences could help to explain their differential healing abilities. © 2012 Elsevier Ltd.
Vekshin N.L.,Institute of Cell Biophysics
Biologicheskie Membrany | Year: 2010
Protomitohondria (PRM) from liver cells of junior (1 month old) and adult (9 month old) rats were isolated using centrifugation and filtration through millipore filters with pore size of 0.10-0.45 μm and characterized by means of photometry and fluorometry. PRM are young mitochondrial organelles, precursors of mature mitochondria (MH), in specialized animal cells. Having hundreds of times smaller volume, PRM do not differ much from MH either in young or in adult rats. However, during maturation of PRM to MH, an increase in the content of flavins and cytochromes is noticeable in young animals. The number of PRM of various sizes in young and adult rats differs. In addition, there are strong differences in the intensity of fluorescence of the probe ANS in PRM and MH of younger and older animals, suggesting a different number of binding sites. The obtained data suggest that the total transformation of PRM to MH in cells of young animals takes place, similarly with the transformation in cells of adult rats.
Frolova M.S.,Institute of Cell Biophysics |
Vekshin N.L.,Institute of Cell Biophysics
Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology | Year: 2014
It is known that one of the reasons leading to the development of neuroligical disorders, such as Parkinson's disease, is the damage of the mitochondrial NADH dehydrogenase. We suggest that it happens when NADH dehydrogenase loses connection with its coenzyme flavine mononucleotide (FMN) in the active center. This process is blocked by the enzyme substrate NADH or by the reaction product NAD. In this work we have developed a method based on fluorescence spectroscopy to monitor the stability of FMN in isolated rat liver mitochondria. It was observed that this process is strongly blocked by adenine analogs ATP, ADP, and AMP. Adenine, adenosine, NADPH, nicotine amide, and nicotine acid did not prevent the FMN loss. The obtained data could be used as a basis for construction of synthetic analogues of adenosine phosphates for the treatment of mitochondrial diseases. © 2014 Pleiades Publishing, Ltd.