Effect of nitrate on gene and protein expression of nitric oxide synthase enzymes in insulin-sensitive tissues of type 2 diabetic male rats

2021 ◽  
Vol 21 ◽  
Author(s):  
Majid Shokri ◽  
Sajad Jeddi ◽  
Hassan Faridnouri ◽  
Vajiheh Khorasani ◽  
Khosrow Kashfi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Expression ◽  
Mrna Level ◽  
Diabetic Rats ◽  
Metabolic Effects ◽  
Male Rats ◽  
Epididymal Adipose Tissue ◽  
Protein Levels ◽  
Gene And Protein Expression

Background and Objective: Decreased nitric oxide (NO) bioavailability contributes to the pathophysiology of type 2 diabetes mellitus (T2DM). This study aims to determine the effects of nitrate (NO3–) on gene and protein expression of NO synthase (NOS) enzymes in the liver, soleus muscle (SM), and epididymal adipose tissue (eAT) of rats with T2DM. Methods: Twenty-eight male rats were divided into 4 groups: Control, diabetes, control+NO3–, and diabetes+NO3– (n = 7/each group). NO3– was administered for 6 months, and mRNA and protein levels of NOS enzymes were measured at the end of the study. Results: mRNA and protein levels of inducible NOS (iNOS) were higher in the liver (475% and 73%), SM (271% and 43%), and eAT (543% and 24%) of rats with T2DM. In the case of the endothelial NOS (eNOS), diabetic rats had lower mRNA and protein levels in the liver (26% and 24%) and SM (60% and 62%) and lower mRNA level (30%) in eAT. mRNA and protein levels of neural NOS (nNOS) were lower in SM (69% and 73%) and eAT (25% and 31%) of rats with T2DM. NO3– administration restored disrupted iNOS and eNOS expressions to their near normal values in all the studied tissues; NO3– also increased nNOS mRNA and protein levels in SM and eAT but decreased nNOS protein level in the liver. Conclusion: Long-term NO3– administration restored disrupted expression of NOS enzymes in the liver, SM, and eAT of rats with T2DM; these findings partly explain the beneficial metabolic effects of nitrate in T2DM.

scholarly journals Berberine Protects against Palmitate-Induced Endothelial Dysfunction: Involvements of Upregulation of AMPK and eNOS and Downregulation of NOX4

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Ming Zhang ◽  
Chun-Mei Wang ◽  
Jing Li ◽  
Zhao-Jie Meng ◽  
Sheng-Nan Wei ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Protein Expression ◽  
Umbilical Vein ◽  
Mrna Level ◽  
Critical Factor ◽  
Cardiovascular Complications ◽  
Protein Levels ◽  
Underlying Mechanisms ◽  
Umbilical Vein Endothelial Cells

Endothelial dysfunction is a critical factor during the initiation of cardiovascular complications in diabetes. Berberine can ameliorate endothelial dysfunction induced by diabetes. However, the underlying mechanisms remain unclear. The aim of this study was to investigate the protective effect and mechanism of berberine on palmitate-induced endothelial dysfunction in human umbilical vein endothelial cells (HUVECs). The cell viability of HUVECs was determined by MTT assays. Nitric oxide (NO) level and production of reactive oxygen species (ROS) were determined in supernatants or in the cultured HUVECs. The mRNA level of endothelial nitric oxide synthase (eNOS) was measured by RT-PCR, and the protein levels of eNOS, p-eNOS, Akt, p-Akt, AMPK, p-AMPK, and NADPH oxidase (NOX4) were analyzed. The results demonstrated that berberine significantly elevated NO levels and reduced the production of ROS. The expressions of eNOS were significantly increased, while NOX4 protein expression was decreased in berberine-treated HUVECs. Moreover, berberine upregulated the protein expression of AMPK and p-AMPK in palmitate-treated HUVECs, but had no effect on the levels of Akt. Therefore, berberine ameliorates palmitate-induced endothelial dysfunction by upregulating eNOS expression and downregulating expression of NOX4. This regulatory effect of berberine may be related to the activation of AMPK.

scholarly journals PO-078 Effects of aerobic and resistance training on cardiac diastolic dysfunction in type 2 diabetic rats

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Shunchang Li ◽  
Derun Gao ◽  
Ismail Laher ◽  
Quansheng Su
Keyword(s):  
Diabetes Mellitus ◽  
Resistance Training ◽  
Protein Expression ◽  
Diastolic Dysfunction ◽  
Aerobic Training ◽  
Diabetic Rats ◽  
Collagen I ◽  
Male Rats ◽  
Type I

Objective To compare the effects of two types of physical training on cardiac diastolic dysfunction in type 2 diabetes mellitus and investigate the role of passive tension regulators—titin and collagen. Methods Sprague-Dawley (SD) male rats were divided into two groups: control and diabetes. Each group was subdivided into three subgroups: sedentary rats, rats submitted to aerobic trained and rats submitted to resistance training. Diabetic rats were induced by high-fat diet combined with low-dose injections of streptozocin (STZ). Aerobic trained rats ran on a treadmill at 21m/min for 60 min per day, while resistance trained rats climbed a ladder with incremental loads. The train period lasted for 8 weeks. Results All diabetic rats had increased fasting blood glucose (FBG) and left ventricular end diastolic pressure (LVEDP), a lower down stroke of the pressure curve (dp/dt min), longer exponential time constants of relaxation (Tau) in relation to control rats, while the protein expression of titin was decreased significantly, and the expression of collagen I, TGFβ1 were increased slightly, the ratio of type I and III collagen was raised in diabetic rats. Both types of training promoted a decrease in FBG and HOMA-IR in diabetic rats. Aerobic exercise trained diabetic rats had significant higher –dp/dtmin, and shorter Tau, but -dp/dtmin and Tau in resistance exercise trained diabetic rats had no significant been improved, even more aggravation. Moreover, aerobic training increased the protein expression of titin and HSP27, and the amount of co-localization of titin and HSP27 elevated, the protein expression of collagen I, TGFβ1 were decreased, and the ratio of type I and type III got close to normal. Resistance training further decreased the expression of titin, collagen I, and TGFβ1, collagen volume fraction (CVF) was increased significantly, and the ratio of type I and III collagen was disturbed, but the co-localization of titin and HSP27 elevated slightly. Conclusions Aerobic training ameliorates cardiac diastolic dysfunction in diabetes and this improvement may be related to increase titin repaired by HSP27, while resistance training aggravates the cardiac diastolic dysfunction in early diabetes mellitus and it could be caused by worsening myocardial interstitial fibrosis.

scholarly journals Acidified Nitrite Accelerates Wound Healing in Type 2 Diabetic Male Rats: A Histological and Stereological Evaluation

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 1872
Author(s):  
Hamideh Afzali ◽  
Mohammad Khaksari ◽  
Sajad Jeddi ◽  
Khosrow Kashfi ◽  
Mohammad-Amin Abdollahifar ◽  
...  
Keyword(s):  
Wound Healing ◽  
Fibrous Tissue ◽  
Diabetic Rats ◽  
Male Rats ◽  
Numerical Density ◽  
Basal Cells ◽  
Diabetic Wound Healing ◽  
Diabetic Wounds ◽  
Endothelial Growth Factor

Impaired skin nitric oxide production contributes to delayed wound healing in type 2 diabetes (T2D). This study aims to determine improved wound healing mechanisms by acidified nitrite (AN) in rats with T2D. Wistar rats were assigned to four subgroups: Untreated control, AN-treated control, untreated diabetes, and AN-treated diabetes. AN was applied daily from day 3 to day 28 after wounding. On days 3, 7, 14, 21, and 28, the wound levels of vascular endothelial growth factor (VEGF) were measured, and histological and stereological evaluations were performed. AN in diabetic rats increased the numerical density of basal cells (1070 ± 15.2 vs. 936.6 ± 37.5/mm3) and epidermal thickness (58.5 ± 3.5 vs. 44.3 ± 3.4 μm) (all p < 0.05); The dermis total volume and numerical density of fibroblasts at days 14, 21, and 28 were also higher (all p < 0.05). The VEGF levels were increased in the treated diabetic wounds at days 7 and 14, as was the total volume of fibrous tissue and hydroxyproline content at days 14 and 21 (all p < 0.05). AN improved diabetic wound healing by accelerating the dermis reconstruction, neovascularization, and collagen deposition.

Abstract 15295: Molecular Mechanism of Chronic Sildenafil-Caused Regression of Heart Failure: Effects on the Express of Cardiac SR Ca2+-ATPase, Subtype of β-Adrenergic Receptors and Nitric Oxide Synthase Isoforms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Heng-Jie Cheng ◽  
Tiankai Li ◽  
Che Ping Cheng
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Male Rats ◽  
Protein Levels ◽  
Myocyte Function ◽  
Oxide Synthase ◽  
Β Adrenergic Receptors

Background: Sildenafil (SIL), a selective inhibitor of PDE5 has been shown to exert profound beneficial effects in heart failure (HF). Recently we further found that SIL caused regression of cardiac dysfunction in a rat model with isoproterenol (ISO)-induced progressive HF. However, the molecular basis is unclear. We hypothesized that reversal of HF-induced detrimental alterations on the expressions of cardiac SR Ca 2+ -ATPase (SERCA2a), β-adrenergic receptors (AR) and nitric oxide synthase (NOS) isoforms by SIL may play a key role for its salutary role in HF. Methods: Left ventricular (LV) and myocyte function and the protein levels of myocyte β 1 - and β 3 - AR, SERCA2a, phospholamban (PLB) and three NOS were simultaneously evaluated in 3 groups of male rats (6/group): HF , 3 months (M) after receiving ISO (170 mg/kg sq for 2 days); HF/SIL , 2 M after receiving ISO, SIL (70 μg/kg/day sq via mini pump) was initiated and given for 1 M; and Controls (C). Results: Compared with controls, ISO-treated rats progressed to severe HF at 3 M after ISO followed by significantly decreased LV contractility (E ES , HF: 0.7 vs C: 1.2 mmHg/μl) and slowed LV relaxation, reductions in the peak velocity of myocyte shortening (77 vs 136 μm/sec), relengthening (62 vs 104 μm/sec) and [Ca 2+ ] iT (0.15 vs 0.24) accompanied by a diminished myocyte inotropic response to β-AR agonist, ISO (10 -8 M). These abnormalities were associated with concomitant significant decreases in myocyte protein levels of β 1 -AR (0.23 vs 0.64), SERCA2a (0.46 vs 0.80), PLB Ser16 /PLB ratio (0.24 vs 0.40) and eNOS (0.28 vs 0.46), but significantly increases in protein levels of β 3 -AR (0.29 vs 0.10) and iNOS (0.18 vs 0.08) with relatively unchanged nNOS. Chronic SIL prevented the HF-induced decreases in LV and myocyte contraction, relaxation, peak [Ca 2+ ] iT , and restored normal myocyte contractile response to ISO stimulation. With SIL, protein levels of myocyte β 1 - and β 3 -AR, SERCA2a were restored close to control values, but eNOS was significantly elevated than controls (0.77). Conclusions: Chronic SIL prevents HF-caused downregulation of cardiac β 1 -AR and reverse contrast changes between iNOS and β 3 -AR with SERCA 2a and eNOS expression, leading to the preservation of LV and myocyte function, [Ca 2+ ] iT , and β-adrenergic reserve.

scholarly journals PO-086 Exercise enhances cardiac antioxidant capacity in diabetic rats through the Keap1/Nrf2 signaling pathway

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Shiqiang Wang
Keyword(s):  
Oxidative Stress ◽  
Blood Glucose ◽  
Protein Expression ◽  
Signaling Pathway ◽  
Diabetic Rats ◽  
Heart Weight ◽  
Stress Injury ◽  
Myocardial Oxidative Stress ◽  
Nrf2 Signaling Pathway ◽  
Gene And Protein Expression

Objective To investigate the effects of exercise on the myocardial oxidative stress injury of diabetic rats, and discussed the role of Keap1/Nrf2 signaling pathway in this process Methods  Tyep 2 diabetic rat model was established by streptozotocin injection through abdominal cavity and high fat diet. The all the diabetic rats were divided into three groups: control group (NC), diabetes group(T2DM) and diabetes exercise group, NC and T2DM group were kept quiet for 8 weeks, T2DME group was trained for 8 weeks. After the exercise, weight, heart weight and blood were measured. MDA, T-SOD and GSH-PX enzyme were measured by biochemical method. Ho-1, Keap1, Nrf2 gene and protein expression were detected by RT-PCR and WesternBlotting. Results Compared with NC group, the weight of rats in the T2DM group significantly decreased [(528+/-71g vs 362+/-33g), P<0.05], HWI  significantly increased [(2.845+/-0.22 vs 3.841+/-0.21, P <0.05], blood glucose was significantly increased [(6.4±3.8 vs 26±7.5mmol/L), P <0.01],T-SOD and GSH-PX activity decreased significantly (P<0.05), Ho-1 protein expression increased (P<0.01), Keap1 and Nrf2 showed no significant changes, and Nrf2 nuclear transposition decreased (P<0.05). Compared with the T2DM group, no significant change in body weight and heart weight in the T2DME group, with significant decrease in HWI[（3.841±0.21 vs 3.235±0.23），P＜0.05], with significant decrease in blood glucose [（26.0±7.5 vs 21.0±6.8），P＜0.05]. Ho-1 gene and protein expression increased significantly（P＜0.05and P＜0.01）, with no significant change of Keap1, while Nrf2 expression increased significantly (P < 0.05), and Nrf2 nuclear transposition increased significantly (P < 0.01). Conclusions Exercise activates the myocardial Keap1/Nrf2 signaling pathway in rats, promotes the expression of downstream antioxidant enzymes, increases cardiac antioxidant capacity, and resists diabetic myocardial oxidative stress injury.

Simulated microgravity effects on the rat carotid and femoral arteries: role of contractile protein expression and mechanical properties of the vessel wall

2007 ◽  
Vol 102 (4) ◽  
pp. 1595-1603 ◽  
Author(s):  
Sunup Hwang ◽  
Stanislav A. Shelkovnikov ◽  
Ralph E. Purdy
Keyword(s):  
Carotid Artery ◽  
Protein Expression ◽  
Femoral Artery ◽  
Vessel Wall ◽  
Male Rats ◽  
Force Analysis ◽  
Western Blots ◽  
Active Length ◽  
Femoral Arteries ◽  
Protein Levels

The goal of this study was to determine the effects of microgravity on myofilament protein expression and both passive and active length-force relationships in carotid and femoral arteries. Microgravity was simulated by 20-day hindlimb unweighting (HU) in Wistar male rats, and carotid and femoral artery segments were isolated from both HU and control (CTL) rats for Western blot and length-force analysis. Western blots revealed that HU significantly decreased myosin light chain-20 (MLC-20) protein levels in both carotid and femoral arteries and decreased myosin heavy chain (MHC) in femoral artery. α-Actin levels were not altered by HU treatment in either artery. Length-force analysis demonstrated that HU did not change either passive or active length-force relationships in the femoral artery. HU-treated arterial rings developed significantly less force to 100 mM K+ than CTL, but optimal lengths were identical. In the carotid artery, length-active force curves were identical for both CTL and HU; however the length-passive force curve for HU-treated rings exhibited a steeper slope than CTL, suggesting decreased compliance of the artery wall. In conclusion, our data suggest that the HU-induced decreases in both MLC-20 and MHC in femoral artery are responsible for the decreased contraction to 100 mM K+ in HU-treated femoral artery rings. In the carotid artery, the HU-induced decrease in vessel wall compliance may counter any decrease in contractility caused by the decreased MLC-20 levels.

Abstract P153: Downregulation of Neuronal Nitric Oxide Synthase Within the Paraventricular Nucleus in Insulin Dependent Diabetic Akita Mice

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Neeru M Sharma ◽  
Paras K Mishra ◽  
Kaushik P Patel
Keyword(s):  
Nitric Oxide ◽  
Paraventricular Nucleus ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Ang Ii ◽  
Protein Levels ◽  
Catalytically Active ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
Akita Mice

Activation of both renin-angiotensin- system (RAS) and sympathetic system are the primary etiologic events in the development of hypertension in diabetes mellitus (DM). However, the precise mechanisms for sympathetic activation in DM have not been elucidated. Our previous studies have demonstrated that neuronal nitric oxide (nNOS) expression and nitric oxide (NO) mediated inhibition of sympathetic nerve activity (SNA) is markedly reduced in the paraventricular nucleus (PVN) of streptozotocin-induced diabetic rats. We have further demonstrated that Angiotensin II (Ang II) via Ang II type 1 receptors (AT 1 R) modulates the expression of nNOS in the PVN, which augments sympathetic outflow. Here we hypothesized that DM-linked hypertension and cardiovascular dysregulation is due to the reduction in nNOS with the PVN. To test the hypothesis, we used Ins2 +/- Akita (a spontaneous, insulin dependent genetic diabetic murine model) which showed an increase in systolic blood pressure at the age of 14 weeks compared to corresponding C57BL/6J (WT) mice with concomitant decreased expression of nNOS (0.75±0.05 WT vs. 0.43±0.11* Akita) in the PVN. Further, Akita mice had increased expression of ACE (angiotensin converting enzyme) (WT 0.34±0.04 vs. Akita 0.58±0.05*) and AT 1 R (WT 0.29±0.09 vs. Akita 0.49±0.03*) and decreased expression of ACE2 (0.27±0.03 WT vs. 0.17±0.05* Akita) and Mas receptor (WT 0.77±0.07 vs. Akita 0.46±0.02*), suggesting an imbalance in the excitatory and protective arms of RAS. Moreover, we found increased protein levels of PIN (a protein inhibitor of nNOS, known to dissociate catalytically active nNOS dimers to monomers) (WT 0.71±0.09 vs. Akita 1.75±0.08) with 72 percent decrease in dimer/monomer ratio of nNOS (WT 0.19±0.0 vs. Akita 0.11±0.04) in the PVN of Akita mice. Taken together, our studies suggest that accumulation of PIN, mediated by activation of the excitatory arm of RAS, leads to a decrease in the active dimeric form of nNOS resulting in reduced NO causing an over-activation of the sympathetic drive, leading to hypertension in DM. 1

scholarly journals Comparison of the Effects of Glibenclamide on Metabolic Parameters, GLUT1 Expression, and Liver Injury in Rats With Severe and Mild Streptozotocin-Induced Diabetes Mellitus

Medicina ◽  
2012 ◽  
Vol 48 (10) ◽  
pp. 78 ◽  
Author(s):  
Jelizaveta Sokolovska ◽  
Sergejs Isajevs ◽  
Olga Sugoka ◽  
Jelena Sharipova ◽  
Natalia Paramonova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Protein Expression ◽  
Diabetic Rats ◽  
Metabolic Parameters ◽  
Gene And Protein Expression ◽  
Glut1 Expression ◽  
Mild Diabetes ◽  
Streptozotocin Induced Diabetes ◽  
Glut1 Gene

Background and Objective. Glucose transport via GLUT1 protein could be one of additional mechanisms of the antidiabetic action of sulfonylureas. Here, the GLUT1 gene and the protein expression was studied in rats in the course of severe and mild streptozotocin-induced diabetes mellitus and under glibenclamide treatment. Material and Methods. Severe and mild diabetes mellitus was induced using different streptozotocin doses and standard or high fat chow. Rats were treated with glibenclamide (2 mg/kg daily, per os for 6 weeks). The therapeutic effect of glibenclamide was monitored by measuring several metabolic parameters. The GLUT1 mRNA and the protein expression in the kidneys, heart, and liver was studied by means of real-time R T-PCR and immunohistochemistry. Results. The glibenclamide treatment decreased the blood glucose concentration and increased the insulin level in both models of severe and mild diabetes mellitus. Severe diabetes mellitus provoked an increase in both GLUT1 gene and protein expression in the kidneys and the heart, which was nearly normalized by glibenclamide. In the kidneys of mildly diabetic rats, an increase in the GLUT1 gene expression was neither confirmed on the protein level nor influenced by the glibenclamide treatment. In the liver of severely diabetic rats, the heart and the liver of mildly diabetic rats, the GLUT1 gene and the protein expression was changed independently of each other, which might be explained by abortive transcription, and pre- and posttranslational modifications of gene expression. Conclusions. The GLUT1 expression was found to be affected by the glucose and insulin levels and can be modulated by glibenclamide in severely and mildly diabetic rats. Glibenclamide can prevent the liver damage caused by severe hyperglycemia.

scholarly journals The expression of cytokines in the milk somatic cells, blood leukocytes and serum of goats infected with small ruminant lentivirus

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Justyna Jarczak ◽  
Danuta Słoniewska ◽  
Jarosław Kaba ◽  
Emilia Bagnicka
Keyword(s):  
Protein Expression ◽  
Small Ruminant ◽  
Somatic Cells ◽  
Immunological Response ◽  
Dairy Goats ◽  
Blood Leukocytes ◽  
Protein Levels ◽  
Tnf Α ◽  
Gene And Protein Expression ◽  
Milk Somatic Cells

Abstract Background The present study aimed to determine the expression of cytokines, which is associated with the immunological response of dairy goats against small ruminant lentivirus (SRLV). The study was conducted on 26 dairy goats in their second to sixth lactation, which were divided by breed and parity into two groups: SRLV naturally infected (N = 13) and non-infected (N = 13) animals. All goats in the study were asymptomatic. The milk and blood samples, which served as studied material were taken on days 7, 30, 120 and 240 of the lactation. The gene and protein expression of several cytokines was studied using Real-Time PCR and ELISA methods. Results INF-β and INF-γ expression was down-regulated in the milk somatic cells (MSC) of SRLV-infected goats. However, an increased concentration of INF-β was observed in the MSC in SRLV-infected goats, while INF-γ expression was not observed in both SRLV-infected and non-infected animals The SRLV-infected goats also displayed decreased expression of IL-1α, IL-1β, IL-6 and INF-γ genes in the blood leukocytes,with IL-1α, IL-1β and IL-6 protein levels also being decreased in the sera. TNF-α was the only gene that demonstrated increased expression in both the MSC and the blood of infected animals; however, no such overexpression was observed at the protein level. Conclusions SRLV probably influences the immune system of infected animals by deregulating of the expression of cytokines. Further, epigenetic studies may clarify the mechanisms by which SRLV regulates the gene and protein expression of the host.

scholarly journals Sensory Neuropeptides and their Receptors Participate in Mechano-Regulation of Murine Macrophages

2019 ◽  
Vol 20 (3) ◽  
pp. 503 ◽  
Author(s):  
Dominique Muschter ◽  
Anna-Sophie Beiderbeck ◽  
Tanja Späth ◽  
Christian Kirschneck ◽  
Agnes Schröder ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Level ◽  
Cyclic Stretch ◽  
Murine Bone Marrow ◽  
Raw264.7 Macrophages ◽  
Neurokinin Receptor ◽  
Calcitonin Gene ◽  
Gene And Protein Expression ◽  
Sensory Neuropeptides ◽  
Comparable Activity

This study aimed to analyze if the sensory neuropeptide SP (SP) and the neurokinin receptor 1 (NK1R) are involved in macrophage mechano-transduction, similar to chondrocytes, and if alpha-calcitonin gene-related peptide (αCGRP) and the CGRP receptor (CRLR/Ramp1) show comparable activity. Murine RAW264.7 macrophages were subjected to a cyclic stretch for 1–3 days and 4 h/day. Loading and neuropeptide effects were analyzed for gene and protein expression of neuropeptides and their receptors, adhesion, apoptosis, proliferation and ROS activity. Murine bone marrow-derived macrophages (BMM) were isolated after surgical osteoarthritis (OA) induction and proliferation, apoptosis and osteoclastogenesis were analyzed in response to loading. Loading induced NK1R and CRLR/Ramp1 gene expression and altered protein expression in RAW264.7 macrophages. SP protein and mRNA level decreased after loading whereas αCGRP mRNA expression was stabilized. SP reduced adhesion in loaded RAW264.7 macrophages and both neuropeptides initially increased the ROS activity followed by a time-dependent suppression. OA induction sensitized BMM to caspase 3/7 mediated apoptosis after loading. Both sensory neuropeptides, SP and αCGRP, and their receptors are involved in murine macrophage mechano-transduction affecting neuropeptide impact on adhesion and ROS activity. OA induction altered BMM apoptosis in response to loading indicate that OA-associated biomechanical alterations might affect the macrophage population.

Sign in / Sign up

Export Citation Format

Share Document