scholarly journals Adipocytes as an Important Source of Serum S100B and Possible Roles of This Protein in Adipose Tissue

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Carlos Alberto Gonçalves ◽  
Marina Concli Leite ◽  
Maria Cristina Guerra
Keyword(s):  
Adipose Tissue ◽  
Brain Injury ◽  
Brain Damage ◽  
Current Knowledge ◽  
Biological Significance ◽  
Serum Levels ◽  
Serum S100b ◽  
Definitive Evidence ◽  
Astroglial Activation

Adipocytes contain high levels of S100B and in vitro assays indicate a modulated secretion of this protein by hormones that regulate lipolysis, such as glucagon, adrenaline, and insulin. A connection between lipolysis and S100B release has been proposed but definitive evidence is lacking. Although the biological significance of extracellular S100B from adipose tissue is still unclear, it is likely that this tissue might be an important source of serum S100B in situations related, or not, to brain damage. Current knowledge does not preclude the use of this protein in serum as a marker of brain injury or astroglial activation, but caution is recommended when discussing the significance of changes in serum levels where S100B may function as an adipokine, a neurotrophic cytokine, or an alarmin.

Diagnostic values of proenkephalin and S100B protein in traumatic brain injury

2017 ◽  
Vol 41 (3) ◽  
Author(s):  
Anil Yalcin ◽  
Ahmet Baydin ◽  
Özgür Korhan Tuncel ◽  
Ali Kemal Erenler ◽  
Cengiz Çokluk ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Calcium Binding ◽  
Statistical Significance ◽  
Serum Levels ◽  
Clinical Findings ◽  
Serum S100b ◽  
Diagnostic Values ◽  
Single Lesion

AbstractBackground:The primary aim of this study was to investigate the diagnostic values of serum S100 calcium-binding protein B (S100B) and proenkephalin (P-ENK) levels in brain damage caused by traumatic brain injury (TBI).Methods:We prospectively collected serum blood samples of 58 adult patients admitted to our emergency department due to TBI. Serum S100B and P-ENK levels were measured and compared according to clinical findings and outcomes of the patients.Results:When patients with brain injury were compared to controls, statistical significance was determined in both S100B and P-ENK levels. According to the receiver operating characteristic (ROC) analysis, cut-off values for serum S100B and P-ENK levels for the differential diagnosis of patients with and without brain damage were found to be 785.944 ng/mL and 2.445 ng/mL, respectively. There was a statistical significance in both S100B and P-ENK levels when patients who were discharged and those who died were compared.Conclusions:Serum S100B and P-ENK levels are found to be elevated in patients with TBI when compared to controls. Additionally, serum levels of both markers are found to be elevated in patients with multiple lesions when compared to patients with a single lesion. Serum S100B and P-ENK levels may also be used as predictors of mortality in patients with TBI.

scholarly journals Astrocytes and the Warning Signs of Intracerebral Hemorrhagic Stroke

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Annalisa Scimemi
Keyword(s):  
Risk Factors ◽  
Brain Injury ◽  
Brain Damage ◽  
Hemorrhagic Stroke ◽  
Current Knowledge ◽  
Warning Signs ◽  
Brain Hemorrhage ◽  
Medical Practices ◽  
The Us ◽  
The Brain

Two decades into the two thousands, intracerebral hemorrhagic stroke (ICH) continues to reap lives across the globe. In the US, nearly 12,000 people suffer from ICH every year. Half of them survive, but many are left with permanent physical and cognitive disabilities, the severity of which depends on the location and broadness of the brain region affected by the hemorrhage. The ongoing efforts to identify risk factors for hemorrhagic stroke have been instrumental for the development of new medical practices to prevent, aid the recovery and reduce the risk of recurring ICH. Recent efforts approach the study of ICH from a different angle, providing information on how we can limit brain damage by manipulating astrocyte receptors. These results provide a novel understanding of how astrocytes contribute to brain injury and recovery from small ICH. Here, we discuss current knowledge on the risk factors and molecular pathology of ICH and the functional properties of astrocytes and their role in ICH. Last, we discuss candidate astrocyte receptors that may prove to be valuable therapeutic targets to treat ICH. Together, these findings provide basic and clinical scientists useful information for the future development of strategies to improve the detection of small ICH, limit brain damage, and prevent the onset of more severe episodes of brain hemorrhage.

scholarly journals What Is in a Cat Scratch? Growth of Bartonella henselae in a Biofilm

2021 ◽  
Vol 9 (4) ◽  
pp. 835
Author(s):  
Udoka Okaro ◽  
Sierra George ◽  
Burt Anderson
Keyword(s):  
Biofilm Formation ◽  
Current Knowledge ◽  
Bartonella Henselae ◽  
Biological Significance ◽  
Mammalian Host ◽  
Cat Scratch Disease ◽  
Cat Flea ◽  
Clinical Presentations

Bartonella henselae (B. henselae) is a gram-negative bacterium that causes cat scratch disease, bacteremia, and endocarditis, as well as other clinical presentations. B. henselae has been shown to form a biofilm in vitro that likely plays a role in the establishment and persistence of the bacterium in the host. Biofilms are also known to form in the cat flea vector; hence, the ability of this bacterium to form a biofilm has broad biological significance. The release of B. henselae from a biofilm niche appears to be important in disease persistence and relapse in the vertebrate host but also in transmission by the cat flea vector. It has been shown that the BadA adhesin of B. henselae is critical for adherence and biofilm formation. Thus, the upregulation of badA is important in initiating biofilm formation, and down-regulation is important in the release of the bacterium from the biofilm. We summarize the current knowledge of biofilm formation in Bartonella species and the role of BadA in biofilm formation. We discuss the evidence that defines possible mechanisms for the regulation of the genes required for biofilm formation. We further describe the regulation of those genes in the conditions that mimic both the arthropod vector and the mammalian host for B. henselae. The treatment for persistent B. henselae infection remains a challenge; hence, a better understanding of the mechanisms by which this bacterium persists in its host is critical to inform future efforts to develop drugs to treat such infections.

scholarly journals Subcutaneous Adipose Tissue Cell-derived Cytokines Are Early Markers of Impaired Glucose Tolerance in Severe Obesity

2021 ◽  
Author(s):  
Vittoria D'Esposito ◽  
Maria Rosaria Ambrosio ◽  
Domenico Liguoro ◽  
Giuseppe Perruolo ◽  
Manuela Lecce ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Severe Obesity ◽  
Serum Levels ◽  
Tolerance Test ◽  
Tissue Cell ◽  
Oral Glucose ◽  
Mrna Levels

Abstract Background Excessive adiposity provides an inflammatory environment. However, in people with severe obesity, how systemic and local adipose tissue (AT)-derived cytokines contribute to worsening glucose tolerance is not clear. Methods 92 severely obese (SO) individuals undergoing bariatric surgery were enrolled and subjected to detailed clinical phenotyping. Following an Oral Glucose Tolerance Test, participants were included in three groups, based on the presence of normal glucose tolerance (NGT), impaired glucose tolerance (IGT) or Type 2 Diabetes (T2D). Serum and subcutaneous AT (SAT) biopsies were obtained and Mesenchymal Stem Cells (MSCs) were isolated, characterized and differentiated in adipocytes in vitro. TNFA and PPARG mRNA levels were determined by qRT-PCR. Circulating, adipocyte- and MSC-released cytokines, chemokines and growth factors were assessed by multiplex ELISA. Results Serum levels of IL-9, IL-13 and MIP-1β were increased in SO individuals with T2D, as compared with those with either IGT or NGT. At variance, SAT samples obtained from SO individuals with IGT displayed levels of TNFA which were 3-fold higher compared to those with NGT, but not different from those with T2D. Elevated levels of TNFα were also found in differentiated adipocytes, isolated from the SAT specimens of individuals with IGT and T2D, compared to those with NGT. Consistent with the pro-inflammatory milieu, IL-1β and IP-10 secretion was significantly higher in adipocytes from individuals with IGT and T2D. Moreover, increased levels of TNFα, both mRNA and secreted protein, were detected in MSCs obtained from IGT and T2D, compared to NGT SO individuals. Exposure of T2D and IGT–derived MSCs to quercetin reduced TNFα levels and was paralleled by a significant decrease of the secretion of inflammatory cytokines. Conclusion In severe obesity, enhanced SAT-derived inflammatory phenotype is an early step in the progression toward T2D and may be, at least in part, attenuated by quercetin.

Adipocytes and preadipocytes promote the proliferation of colon cancer cells in vitro

2007 ◽  
Vol 292 (3) ◽  
pp. G923-G929 ◽  
Author(s):  
Sadahiro Amemori ◽  
Akifumi Ootani ◽  
Shigehisa Aoki ◽  
Takehiro Fujise ◽  
Ryo Shimoda ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Adipose Tissue ◽  
Cancer Cells ◽  
Cell Lines ◽  
Elevated Serum ◽  
Collagen Gel ◽  
Serum Levels ◽  
Colon Cancer Cells ◽  
Trophic Effect

Obesity, a risk factor for colon cancer, is associated with elevated serum levels of leptin, a protein produced by adipocytes. The aim of the present study was to clarify the effects of adipose tissue on colon cancer proliferation by using cultured cell lines. To achieve this, colon cancer cells (CACO-2, T84, and HT29) were cocultured with adipose tissue, isolated mature adipocytes, and isolated preadipocytes in a three-dimensional collagen gel culture system. The adipocytes and preadipocytes used were isolated from C57BL/6J and leptin-deficient ob/ob mice. Proliferation of the cancer cells was evaluated by nuclear bromodeoxyuridine uptake. The adipose tissue, mature adipocytes, and preadipocytes isolated from C57BL/6J mice significantly increased the proliferation of the colon cancer cells. This trophic effect of mature adipocytes on the cancer cell lines was observed only for cells from lean littermates and not for those from ob/ob mice. In contrast, the trophic effect of preadipocytes was not abolished in ob/ob mice, and this finding was supported by the result that leptin had a trophic effect on cancer cells. In conclusion, adipocytes were able to enhance the proliferation of colon cancer cells in vitro, partly via leptin, suggesting that adipose tissues, including mature adipocytes and preadipocytes, may promote the growth of colorectal cancer.

scholarly journals Influence of Acute and Chronic Exercise on Abdominal Fat Lipolysis: An Update

2020 ◽  
Vol 11 ◽  
Author(s):  
Claire Laurens ◽  
Isabelle de Glisezinski ◽  
Dominique Larrouy ◽  
Isabelle Harant ◽  
Cedric Moro
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Acute Exercise ◽  
Current Knowledge ◽  
Weight Maintenance ◽  
Preventive Measure ◽  
Whole Body ◽  
Physiological Control ◽  
Exercise Induced

Exercise is a powerful and effective preventive measure against chronic diseases by increasing energy expenditure and substrate mobilization. Long-duration acute exercise favors lipid mobilization from adipose tissue, i.e., lipolysis, as well as lipid oxidation by skeletal muscles, while chronic endurance exercise improves body composition, facilitates diet-induced weight loss and long-term weight maintenance. Several hormones and factors have been shown to stimulate lipolysis in vitro in isolated adipocytes. Our current knowledge supports the view that catecholamines, atrial natriuretic peptide and insulin are the main physiological stimuli of exercise-induced lipolysis in humans. Emerging evidences indicate that contracting skeletal muscle can release substances capable of remote signaling to organs during exercise. This fascinating crosstalk between skeletal muscle and adipose tissue during exercise is currently challenging our classical view of the physiological control of lipolysis, and provides a conceptual framework to better understand the pleotropic benefits of exercise at the whole-body level.

scholarly journals Carnosine Protects against Cerebral Ischemic Injury by Inhibiting Matrix-Metalloproteinases

2021 ◽  
Vol 22 (14) ◽  
pp. 7495
Author(s):  
Eun-Hye Kim ◽  
Eun-Sun Kim ◽  
Donggeun Shin ◽  
Donghyun Kim ◽  
Sungbin Choi ◽  
...  
Keyword(s):  
Brain Injury ◽  
Matrix Metalloproteinases ◽  
Brain Damage ◽  
Infarct Volume ◽  
Treatment Options ◽  
Gelatin Zymography ◽  
Enzyme Assays ◽  
Ischemic Brain ◽  
Cerebral Ischemic

Stroke is one of the leading causes of death and disability worldwide. However, treatment options for ischemic stroke remain limited. Matrix-metalloproteinases (MMPs) contribute to brain damage during ischemic strokes by disrupting the blood-brain barrier (BBB) and causing brain edemas. Carnosine, an endogenous dipeptide, was found by us and others to be protective against ischemic brain injury. In this study, we investigated whether carnosine influences MMP activity. Brain MMP levels and activity were measured by gelatin zymography after permanent occlusion of the middle cerebral artery (pMCAO) in rats and in vitro enzyme assays. Carnosine significantly reduced infarct volume and edema. Gelatin zymography and in vitro enzyme assays showed that carnosine inhibited brain MMPs. We showed that carnosine inhibited both MMP-2 and MMP-9 activity by chelating zinc. Carnosine also reduced the ischemia-mediated degradation of the tight junction proteins that comprise the BBB. In summary, our findings show that carnosine inhibits MMP activity by chelating zinc, an essential MMP co-factor, resulting in the reduction of edema and brain injury. We believe that our findings shed new light on the neuroprotective mechanism of carnosine against ischemic brain damage.

scholarly journals Extracellular vesicles-transmitted miR-21a-5p altered microglia polarization after hypoxia-ischemic injury in neonatal mice via STAT3 pathways

2021 ◽  
Author(s):  
Danqing Xin ◽  
Yijing Zhao ◽  
Tingting Li ◽  
Hongfei Ke ◽  
Chengcheng Gai ◽  
...  
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Extracellular Vesicles ◽  
Luciferase Reporter ◽  
Neonatal Mice ◽  
M2 Polarization ◽  
Stat3 Phosphorylation ◽  
Microglia Polarization

Abstract Background We previously reported that mesenchymal stromal cells (MSCs)-derived extracellular vesicles (EVs) exhibit protective effects in hypoxia-ischemia (HI) brain damage. The neuroprotective action was connected with its anti-inflammatory effect. However, the mechanisms involved with this effect have not been determined. Methods A modified version of the Rice-Vannucci method was performed on postnatal day 7 mouse pups to induce neonatal HI brain injury. The model of oxygen-glucose deprivation (OGD) was established in BV-2 cells to mimic HI injury in vitro. Mice or BV-2 cells received EVs and EVs-miR-21ainhibitor at indicative time post-injury. In vivo, brain water content and TTC staining were used to evaluate the effects of EVs on HI brain injury. Immunofluorescence staining was used to observe the effect of EVs on the polarization of microglia. The effect of EVs on p-STAT3 was assessed by Western blot. In vitro, the effect of EVs on cell survival was evaluated by CCK8. Expression of miR-21a-5p and inflammatory factors was measured using qRT-PCR. Dual-Luciferase Reporter Assay was performed to illustrate the link between miR-21a-5p and STAT3. The role of miR-21a-5p in EVs on HI injury and ODG injury was further investigated by using EVs-miR-21ainhibitor.Results By using OGD mimicking HI injury in vitro, we found that MSCs-EVs treatment elevated cell viability following OGD exposure in BV-2 cells. MSCs-EVs treatment impeded microglia-mediated neuroinflammation, shifted microglia toward M2 polarization, and suppressed the phosphorylation of selective signal transducer and activator of transcription 3 (STAT3) in microglia after HI exposure in vitro and in vivo. In light of miR-21a-5p being the most highly expressed miRNA in MSCs-EVs interacting with the STAT3 pathway, further work focused on this pathway. Notably, MSCs-EVs treatment increased HI-reduced miR-21a-5p levels in BV-2 cells. Diminishing miR-21a-5p in MSCs-EVs partially attenuated its effect on microglia polarization and STAT3 phosphorylation following HI exposure in vitro and in vivo. Conclusions Our study suggested that MSCs-EVs attenuated HI brain damage in neonatal mice via shuttling miR-21a-5p, which induced microglia M2 polarization by targeting STAT3.

scholarly journals Adult mice are unresponsive to AAV8-Gremlin1 gene therapy targeting the liver

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247300
Author(s):  
Roxana Khatib Shahidi ◽  
Jenny M. Hoffmann ◽  
Shahram Hedjazifar ◽  
Laurianne Bonnet ◽  
Ritesh K. Baboota ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Insulin Signalling ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Liver Cells ◽  
Adult Mice ◽  
Gremlin 1

Objective Gremlin 1 (GREM1) is a secreted BMP2/4 inhibitor which regulates commitment and differentiation of human adipose precursor cells and prevents the browning effect of BMP4. GREM1 is an insulin antagonist and serum levels are high in type 2 diabetes (T2D). We here examined in vivo effects of AAV8 (Adeno-Associated Viral vectors of serotype eight) GREM 1 targeting the liver in mature mice to increase its systemic secretion and also, in a separate study, injected recombinant GREM 1 intraperitoneally. The objective was to characterize systemic effects of GREM 1 on insulin sensitivity, glucose tolerance, body weight, adipose cell browning and other local tissue effects. Methods Adult mice were injected with AAV8 vectors expressing GREM1 in the liver or receiving regular intra-peritoneal injections of recombinant GREM1 protein. The mice were fed with a low fat or high fat diet (HFD) and followed over time. Results Liver-targeted AAV8-GREM1 did not alter body weight, whole-body glucose and insulin tolerance, or adipose tissue gene expression. Although GREM1 protein accumulated in liver cells, GREM1 serum levels were not increased suggesting that it may not have been normally processed for secretion. Hepatic lipid accumulation, inflammation and fibrosis were also not changed. Repeated intraperitoneal rec-GREM1 injections for 5 weeks were also without effects on body weight and insulin sensitivity. UCP1 was slightly but significantly reduced in both white and brown adipose tissue but this was not of sufficient magnitude to alter body weight. We validated that recombinant GREM1 inhibited BMP4-induced pSMAD1/5/9 in murine cells in vitro, but saw no direct inhibitory effect on insulin signalling and pAkt (ser 473 and thr 308) activation. Conclusion GREM1 accumulates intracellularly when overexpressed in the liver cells of mature mice and is apparently not normally processed/secreted. However, also repeated intraperitoneal injections were without effects on body weight and insulin sensitivity and adipose tissue UCP1 levels were only marginally reduced. These results suggest that mature mice do not readily respond to GREMLIN 1 but treatment of murine cells with GREMLIN 1 protein in vitro validated its inhibitory effect on BMP4 signalling while insulin signalling was not altered.

scholarly journals The anti-adipogenic effect of angiotensin II on human preadipose cells involves ERK1,2 activation and PPARG phosphorylation

2010 ◽  
Vol 206 (1) ◽  
pp. 75-83 ◽  
Author(s):  
Paula Fuentes ◽  
María José Acuña ◽  
Mariana Cifuentes ◽  
Cecilia V Rojas
Keyword(s):  
Adipose Tissue ◽  
Angiotensin Ii ◽  
Current Knowledge ◽  
Adipogenic Differentiation ◽  
Mitogen Activated Protein Kinase ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Fat Depots ◽  
Adipogenic Effect

Despite the importance of adipocyte formation for adipose tissue physiology, current knowledge about the mechanisms that regulate the recruitment of progenitor cells to undergo adipogenic differentiation is limited. A role for locally generated angiotensin II emerged from studies with human and murine cells. Preadipose cells from different human fat depots show reduced response to adipogenic stimuli when exposed to angiotensin II. This investigation sought to gain an insight into the intracellular mechanisms involved in the anti-adipogenic response of human preadipose cells from omental fat to angiotensin II. Its effect was evaluated on cells stimulated to adipogenic differentiation in vitro, by assessment of glycerol-3-phosphate dehydrogenase activity and expression of early markers of adipogenesis. Extracellular signal-regulated kinase1,2 (ERK1,2) pathway activation was inferred from the phosphorylated to total ERK1,2 ratio determined by western blot. Exposure to angiotensin II throughout the 10-day differentiation period resulted in a reduced adipogenic response. A similar anti-adipogenic effect was observed when this hormone was present during the first 48 h of induction to differentiation. Angiotensin II treatment had no consequences on CCAAT/enhancer-binding protein β and peroxisome proliferator-activated receptor γ (PPARG) induction, but increased the phosphorylated form of the key adipogenic regulator PPARG. Upon angiotensin II exposure, a raise of phosphorylated ERK1,2 was determined, which was more prominent 8–20 h after induction of adipogenesis (when controls reached negligible values). Chemical inhibition of ERK1,2 phosphorylation prevented angiotensin II-dependent reduction in adipogenesis. These results support the participation of the mitogen-activated protein kinase/ERK1,2 pathway in the anti-adipogenic effect of angiotensin II on preadipose cells from human omental adipose tissue.

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