Institute of Cell Biophysics

Moscow oblast, Russia

Institute of Cell Biophysics

Moscow oblast, Russia

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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.

Lunin S.M.,Institute of Cell Biophysics | Novoselova E.G.,Institute of Cell Biophysics
Expert Opinion on Therapeutic Targets | Year: 2010

Importance of the field: Inflammatory diseases are characterized by severe immune imbalances, leading to excessive or inappropriate release of mediators, which, in turn, result in massive damage to organs and systems. Effective means to control inappropriate immune reactions are often life-critical needs. Available data on the role of thymus-derived hormones in inflammation show their great potential. Areas covered in this review: The review aims to systematize information for the last two decades on immune system regulation by thymic peptide hormones, with a primary focus on the role of these hormones in the systemic inflammatory response and inflammatory diseases. Anti-inflammatory potential of three thymic hormones thymulin, thymosin-alpha, and thymopoietin is discussed, reviewing recently published clinical and experimental studies. What the reader will gain: Our analysis revealed the regulation of inflammatory processes via thymic hormones that could be prospective for therapeutic application. This regulation may be mediated through thymic hormone effects on peripheral immune cell activities and bidirectional coupling between thymic hormones and the hypothalamicpituitaryadrenal axis. Take-home message: In view of the role of thymic hormones in immune and neuroendocrine systems, they could be suitable as therapeutic agents for inflammation. © 2010 Informa UK Ltd.

Lunin S.M.,Institute of Cell Biophysics | Glushkova O.V.,Institute of Cell Biophysics | Khrenov M.O.,Institute of Cell Biophysics | Novoselova T.V.,Institute of Cell Biophysics | And 3 more authors.
Immunobiology | Year: 2013

Modulation of autoimmune inflammation by the thymic peptides thymulin and thymopentin was studied in mice with acute experimental autoimmune encephalomyelitis (EAE), which resembles multiple sclerosis in humans. EAE was induced in NZW mice by a single immunisation with myelin basic protein coupled with adjuvants. Visible signs of pathology appeared on days 12-14 after the immunisation, peaked on days 20-25, were retained up to day 45, and then reverted. A biphasic cytokine response was also detected. In the " early" phase, which started at day 35, increased levels of interferon-gamma and interleukin-6 in the blood were observed; during the " delayed" phase, which started at day 48, the levels of plasma interleukin-17 and tumour necrosis factor-alpha were also raised. In addition, the phosphorylation of NF-kappaB signalling proteins and the production of heat shock protein Hsp72 were significantly increased in splenic lymphocytes from EAE-bearing mice. When applied intraperitoneally every other day for 30 days, either thymulin or thymopentin (15. μg per 100. g of body weight) significantly reduced the disease severity compared to untreated EAE mice. The effect of thymulin but not thymopentin remained after its withdrawal. Thymulin reduced the cytokine response in both the early and the delayed phases, whereas thymopentin only reduced the " early phase cytokines" (IL-6 and interferon-gamma). Both peptides significantly reduced the level of phosphorylation of the NF-kappaB signalling protein IKK and the production of Hsp72 protein. The data presented here indicate the presence of time-dependent immune responses in EAE-bearing mice, which may be associated with the Th1 and Th17 subpopulations of T-cells. Thymulin and thymopentin demonstrated different patterns of activity, most likely via mechanisms involved in NF-kappa B signalling and Hsp72 expression. © 2012 Elsevier GmbH.

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.

Frolova M.S.,Institute of Cell Biophysics | Vekshin N.L.,Institute of Cell Biophysics
Journal of Fluorescence | Year: 2014

It is known that one of the reasons, leading to the development of neuromuscular diseases, including Parkinson's disease, is damage of the mitochondrial NADH-dehydrogenase. Perhaps, it happens when NADH-dehydrogenase loses connection with its coenzyme - flavine mononucleotide (FMN) that occurs at various influences on the enzyme. Previously, we have developed a method, based on fluorescence spectroscopy, to monitor the rate of exit of FMN from isolated mitochondria to solution. Also, we obtained the data that this process is blocked by the enzyme substrate - NADH or by the product - NAD. Recently, we found that this process is strongly blocked by adenine analogs of NAD, contained phosphates: ATP, ADP, and AMP. Adenosine phosphates are able to stabilize the FMN molecule in NADH-dehydrogenase. Using fluorescence spectroscopy and photocolorimetry, we have tested also other natural purine compounds - cAMP, cGMP, GMP, GDP, GTP, IMP, inosine, guanine, and caffeine. It is found that such derivatives of guanine as GMP, GDP, and GTP can prevent the release of FMN into solution. Guanine, cGMP, cAMP and caffeine did not prevent this process. The obtained data allow understand the mechanism of mitochondrial diseases, involving damage of mitochondrial NADH-dehydrogenase, and may help in development of medicines for treatment of these diseases. © 2014 Springer Science+Business Media New York.

Novoselova E.G.,Institute of Cell Biophysics | Lunin S.M.,Institute of Cell Biophysics | Khrenov M.O.,Institute of Cell Biophysics | Parfenyuk S.B.,Institute of Cell Biophysics | And 3 more authors.
Immunobiology | Year: 2015

To explore the effect of the spaceflight environment on immunity in animals, C57/BL6 mice flown on a 30-day space high-orbit satellite mission (BION-M1) were analyzed. Cytokine response in mice was measured in tandem with the following parameters: the synthesis of inducible forms of the heat shock proteins HSP72 and HSP90α; activity of the NF-κB, IFR3, and SAPK/JNK signalling pathways; and TLR4 expression. In addition, apoptosis in the thymus was measured by caspase-3 and ph-p53/p53 ratio testing. In response to flight environment exposure, mice had a reduction in spleen and thymus masses and decreased splenic and thymic lymphocyte counts. Plasma concentration of IL-6 and IFN-γ but not TNF-α was decreased in C57BL6 mice. The NF-κB activity in splenic lymphocytes through the canonical pathway involving IκB degradation was significantly increased at 12. h after landing. One week after landing, however, the activity of NF-κB was markedly decreased below even the control values. Non-canonical NF-κB activity increased during the whole observation period. The activities of SAPK/JNK and IRF-3 were invariable at 12. h but significantly increased 7 days after landing. The expression of Hsp72 and Hsp90α was somewhat increased 12. h (Hsp72) and 7 days (Hsp90α). TLR4 expression in splenic cells was significantly increased only at 12. h, returning to normal 7 days after landing. To assess the apoptosis in thymus lymphocytes, caspase-3 and levels of p53 protein along with its phosphorylated form were measured in thymic lymphocytes. The results indicated that the high-orbit spaceflight environment caused an increase in the level of p53 but more notably in the activated, phosphorylated form of the p53 protein. The calculated ratio of the active to inactive forms of the protein (ph-53/p53) 12. h after landing increased by more than twofold, indicating the apparent induction of apoptosis in thymus cells. Interestingly, 7 days after the landing, this ratio was not restored, but rather increased: the specified ratio was four times higher compared to the ground-based control. Measurements of caspase-3 in thymic cells indicated more expressive increase in apoptosis. Taken together, the results of the present study indicate that spaceflight induces an imbalance in the immunity of mice, showing variation in signalling, apoptosis and stress response that are not restored by 7 days after landing. These changes are distinguished from classic stress-related alterations usually caused by conventional stressors. © 2014 Elsevier GmbH.

PubMed | Institute of Cell Biophysics
Type: | Journal: International journal of radiation biology | Year: 2017

To clarify whether extremely low-level microwaves (MW) alone or in combination with p38 inhibitor affect immune cell responses to inhalation exposure of mice to low-level toluene.The cytokine profile, heat shock proteins expression, and the activity of several signal cascades, namely, NF-B, SAPK/JNK, IRF-3, p38 MAPK, and TLR4 were measured in spleen lymphocytes of mice treated to air-delivered toluene (0.6mg/mA single exposure to air-delivered low-level toluene induced activation of NF-B, SAPK/JNK, IFR-3, p38 MAPK and TLR4 pathways. Furthermore, air toluene induced the expression of Hsp72 and enhanced IL-1, IL-6, and TNF- in blood plasma, which is indicative of a pro-inflammatory response. Exposure to MW alone also resulted in the enhancement of the plasma cytokine values (e.g. IL-6, TNF-, and IFN-) and activation of the NF-B, MAPK p38, and especially the TLR4 pathways in splenic lymphocytes. Paradoxically, pre-exposure to MW partially recovered or normalized the lymphocyte parameters in the toluene-exposed mice, while the p38 inhibitor XI additionally increased protective activity of microwaves by down regulating MAPKs (JNK and p38), IKK, as well as expression of TLR4 and Hsp90-.The results suggest that exposure to low-intensity MW at specific conditions may recover immune parameters in mice undergoing inhalation exposure to low-level toluene via mechanisms involving cellular signaling.

PubMed | Institute of Cell Biophysics
Type: | Journal: International immunopharmacology | Year: 2016

The aim of this study was to compare immune imbalances in pre-diabetic and diabetic mice and to evaluate the efficacy of several agents in improving the immunity of mice with type 1 diabetes. Pre-diabetic and diabetic models generated by a single or double alloxan injection were monitored for plasma glucose and pancreas immunohistochemistry. To study the immunity in pre-diabetic and diabetic Balb/C male mice; the levels of cytokines; synthesis of inducible heat shock proteins HSP72 and HSP90; activity of the NF-B, IFR3, SAPK/JNK, and TLR4 pathways; and apoptosis levels in thymuses were measured. Pre-diabetes resulted in a decrease in IL-4, IL-5 and IL-10 in plasma; in diabetic mice, plasma IFN-gamma, IL-6, TNF-alpha, and IL-10 were decreased. The NF-B alternative pathway activity and TLR4 expression were significantly increased only in pre-diabetic mice, whereas SAPK/JNK activation was observed at both stages of diabetes. Other measured parameters also showed distinct altered patterns in the immunity of pre-diabetic and diabetic mice. Treatment with an inhibitor of NF-B, thymulin, or a diet with an antioxidant improved or normalized the immune balance in diabetic mice and also notably decreased pancreatic cell damage in pre-diabetic mice.

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