Association between monocyte chemoattractant protein-1 and blood pressure in smokers

Komiyama, Maki; Takanabe, Rieko; Ono, Koh; Shimada, Sawahiko; Wada, Hiromichi; Satoh‐Asahara, Noriko; Morimoto, Tatsuya; Shimatsu, Akira; Takahashi, Yuko; Hasegawa, Koji

doi:10.1177/0300060517723415

Cited by 20 publications

(16 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Serum levels of the oxidative stress marker MCP-1 were increased in our heavy smokers, which is in accordance with other reports [45,46]. Accumulation of Reactive Oxygen Species (ROS) can directly induce formation of osteoclasts from mononuclear cells [47,48] and also by upregulation of MCP-1, a strong inducer of osteoclast fusion and osteoclastogenesis [22,23,24].…”

Section: Discussionsupporting

confidence: 91%

Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty

Ehnert¹,

Aspera-Werz²,

Ihle³

et al. 2019

JCM

View full text Add to dashboard Cite

Numerous studies have described a correlation between smoking and reduced bone mass. This not only increases fracture risk but also impedes reconstruction/fixation of bone. An increased frequency of complications following surgery is common. Here, we investigate the effect of smoking on the clinical outcome following total joint arthroplasty (TJA). 817 patients receiving primary or revision (including clinical transfers) TJA at our level-one trauma center have been randomly interviewed twice (pre- and six months post-surgery). We found that 159 patients developed complications (infections, disturbed healing, revisions, thrombosis, and/or death). Considering nutritional status, alcohol and cigarette consumption as possible risk factors, OR was highest for smoking. Notably, mean age was significantly lower in smokers (59.2 ± 1.0a) than non-smokers (64.6 ± 0.8; p < 0.001). However, the number of comorbidities was comparable between both groups. Compared to non-smokers (17.8 ± 1.9%), the complication rate increases with increasing cigarette consumption (1–20 pack-years (PY): 19.2 ± 2.4% and >20 PY: 30.4 ± 3.6%; p = 0.002). Consequently, mean hospital stay was longer in heavy smokers (18.4 ± 1.0 day) than non-smokers (15.3 ± 0.5 day; p = 0.009) or moderate smokers (15.9 ± 0.6 day). In line with delayed healing, bone formation markers (BAP and CICP) were significantly lower in smokers than non-smokers 2 days following TJA. Although, smoking increased serum levels of MCP-1, OPG, sRANKL, and Osteopontin as well as bone resorption markers (TRAP5b and CTX-I) were unaffected. In line with an increased infection rate, smoking reduced 25OH vitamin D3 (immune-modulatory), IL-1β, IL-6, TNF-α, and IFN-γ serum levels. Our data clearly show that smoking not only affects bone formation after TJA but also suppresses the inflammatory response in these patients. Thus, it is feasible that therapies favoring bone formation and immune responses help improve the clinical outcome in smokers following TJA.

show abstract

Section: Discussionsupporting

confidence: 91%

Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty

Ehnert¹,

Aspera-Werz²,

Ihle³

et al. 2019

JCM

View full text Add to dashboard Cite

show abstract

“…Even after using medical treatment and lifestyle modifications, it is still hard to achieve the goal of reducing blood glucose to an optimal level 4 , 5 ) . In T2DM, atherosclerosis plays an important role in cardiovascular disease complications, and vascular inflammation due to hyperglycemia is one of the mechanisms of atherosclerosis 6 – 10 ) .…”

Section: Introductionmentioning

confidence: 99%

Canagliflozin Prevents Diabetes-Induced Vascular Dysfunction in ApoE-Deficient Mice

Rahadian

Fukuda

Salim

et al. 2020

JAT

View full text Add to dashboard Cite

Recent studies have demonstrated that selective sodium-glucose cotransporter 2 inhibitors (SGLT2is) reduce cardiovascular events, although their mechanism remains obscure. We examined the effect of canagliflozin, an SGLT2i, on atherogenesis and investigated its underlying mechanism. Method: Canagliflozin (30 mg/kg/day) was administered by gavage to streptozotocin-induced diabetic apolipoprotein E-deficient (ApoE /) mice. Sudan IV staining was performed at the aortic arch. Immunostaining, quantitative RT-PCR, and vascular reactivity assay were performed using the aorta. In vitro experiments using human umbilical vein endothelial cells (HUVECs) were also performed. Result: Canagliflozin decreased blood glucose (P 0.001) and total cholesterol (P 0.05) levels. Sudan IV staining showed that 12-week canagliflozin treatment decreased atherosclerotic lesions (P 0.05). Further, 8-week canagliflozin treatment ameliorated endothelial dysfunction, as determined by acetylcholine-induced vasodilation (P 0.05), and significantly reduced the expressions of inflammatory molecules such as ICAM-1 and VCAM-1 in the aorta at the RNA and protein levels. Canagliflozin also reduced the expressions of NADPH oxidase subunits such as NOX2 and p22phox in the aorta and reduced urinary excretion of 8-OHdG, suggesting a reduction in oxidative stress. Methylglyoxal, a precursor of advanced glycation end products, increased the expressions of ICAM-1 and p22phox in HUVECs (P 0.05, both). Methylglyoxal also decreased the phosphorylation of eNOS Ser1177 and Akt but increased the phosphorylation of eNOS Thr495 and p38 MAPK in HUVECs. Conclusion: Canagliflozin prevents endothelial dysfunction and atherogenesis in diabetic ApoE / mice. Antiinflammatory and antioxidative potential due to reduced glucose toxicity to endothelial cells might be its underlying mechanisms. using medical treatment and lifestyle modifications, it is still hard to achieve the goal of reducing blood glucose to an optimal level 4, 5). In T2DM, atherosclerosis plays an

show abstract

“…This is consistent with cross-sectional results showing a strong correlation between MCP-1 and BP in smokers. 36 Surprisingly, a significant increased hypertension risk associated with MCP-1 was seen among women with normal BMI (<25 kg/m 2 ; HR = 3.45) and diastolic BP (<80 mmHg; HR = 1.29) at baseline ( Supplemental Table 2 ). We anticipated that the pro-inflammatory nature of obesity would potentially work synergistically with pro-inflammatory biomarkers to increase hypertension risk, which was not observed in our present study.…”

Section: Discussionmentioning

confidence: 93%

The association between serum inflammatory biomarkers and incident hypertension among postmenopausal women in the Buffalo OsteoPerio Study

et al. 2020

View full text Add to dashboard Cite

Several serum inflammatory biomarkers have been associated with blood pressure and hypertension prevalence in cross-sectional studies. Few of these associations have been evaluated prospectively. We examined associations for 10 serum inflammatory biomarkers with incident hypertension among 471 postmenopausal women (mean age = 65) in the Buffalo OsteoPerio Study. Concentrations of C-reactive protein, interleukin (IL)-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-α, monocyte chemoattractant protein (MCP)-1, adiponectin, and leptin were measured using multiplexed sandwich immunoassays on fasting serum samples collected at baseline (1997–2001). Incident hypertension (195 cases) was defined as physician-diagnosed hypertension and treatment with medication identified on annual mailed health surveys during follow-up (mean 10 years). Cox regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) between log-transformed biomarkers (per 1-SD) and hypertension. When adjusted for age, leptin was significantly associated with hypertension risk (HR=1.55, 95% CI: 1.04, 2.29), however, the association was attenuated and not significant after adjustment for demographic and lifestyle factors, including BMI. Significant (P<0.10) interactions were observed for smoking (never, ever) with CRP (HR: Never, 1.31; Ever, 0.91; P=0.06) and MCP-1 (HR: Never, 0.59; Ever, 5.11; P=0.004); for BMI (<25, ≥25) with MCP-1(HR: <25, 3.45; ≥25, 0.95; P=0.07); for systolic BP with IL-10 (HR: <120, 0.85; 120–139, 1.11; P=0.07); and for diastolic BP with MCP-1 (HR: <80, 1.29; 80–89, 0.84; P=0.03) and with adiponectin (HR: <80, 0.86; 80–89, 1.50; P=0.03). This study adds needed understanding on prospective associations between several serum inflammatory biomarkers and hypertension risk in older postmenopausal women, among whom hypertension burden is substantial.

show abstract

Association between monocyte chemoattractant protein-1 and blood pressure in smokers

Cited by 20 publications

References 36 publications

Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty

Smoking Dependent Alterations in Bone Formation and Inflammation Represent Major Risk Factors for Complications Following Total Joint Arthroplasty

Canagliflozin Prevents Diabetes-Induced Vascular Dysfunction in ApoE-Deficient Mice

The association between serum inflammatory biomarkers and incident hypertension among postmenopausal women in the Buffalo OsteoPerio Study

Contact Info

Product

Resources

About