“…The observed predictive value of low IGFBP-3 levels on outcome were also independent of IGF-1 levels, which have been connected to neurological outcome elsewhere [17,19,25]. Thus, it remains plausible to consider IGFBP-3 to be more than just a simple binding protein; it has autonomous neuroprotective effects [20]. IGFBP-3 might exert a key function on vasculogenesis and microvascular remodeling after hypoxic injury, similarly to effects of vascular endothelial growth factor, which has been demonstrated to optimize cerebral blood flow, decrease infarction size and preserve the metabolic penumbra after ischemic tissue damage [12,13,26].…”
Section: Discussionmentioning
confidence: 97%
“…Denti et al found no association between IGFBP-3 and outcome [19]. In contrast, murine and preliminary human studies point at a potential role of IGFBP-3 in acute ischemic stroke [18,20].…”
Reports on neuroprotective effects of Insulin-like growth factor-1 (IGF-1) and Insulin-like growth factor binding protein-3 (IGFBP-3) in ischemic brain tissue are inconsistent. The aim of this study was to determine if plasma levels of IGF-1 and IGFBP-3 in acute stroke patients are indicative of 3 months functional outcome. Plasma levels were measured via chemiluminescence immunoassay in heparin blood samples of patients included in the EARLY trial (NCT00562588). Plasma samples were drawn on admission and 8 days post-stroke. Neurological deficits were assessed via modified Rankin Scale (mRS) 3 months post-stroke, resulting in favorable (mRS=0-2) or unfavorable (mRS=3-6) outcome. A multiple binary logistic regression including IGF-1 and IGFBP-3 levels and confounders was conducted. Out of 404 included patients, 89 patients had an unfavorable outcome. Mean mRS on admission as well as 3 months post-stroke was 2 (±1). Low IGF-1 levels (day 8) were independently associated with a decreased risk of an unfavorable outcome (OR 0.61; 95%CI 0.37-0.99; p=0.044). Low IGFBP-3 levels (day 8) were independently associated with an unfavorable outcome (OR 2.75; 95%CI 1.56-4.84; p<0.001). Low IGFBP-3 levels and high IGF-1 levels in the subacute phase are predictive of unfavorable outcome 3 months after stroke.
“…The observed predictive value of low IGFBP-3 levels on outcome were also independent of IGF-1 levels, which have been connected to neurological outcome elsewhere [17,19,25]. Thus, it remains plausible to consider IGFBP-3 to be more than just a simple binding protein; it has autonomous neuroprotective effects [20]. IGFBP-3 might exert a key function on vasculogenesis and microvascular remodeling after hypoxic injury, similarly to effects of vascular endothelial growth factor, which has been demonstrated to optimize cerebral blood flow, decrease infarction size and preserve the metabolic penumbra after ischemic tissue damage [12,13,26].…”
Section: Discussionmentioning
confidence: 97%
“…Denti et al found no association between IGFBP-3 and outcome [19]. In contrast, murine and preliminary human studies point at a potential role of IGFBP-3 in acute ischemic stroke [18,20].…”
Reports on neuroprotective effects of Insulin-like growth factor-1 (IGF-1) and Insulin-like growth factor binding protein-3 (IGFBP-3) in ischemic brain tissue are inconsistent. The aim of this study was to determine if plasma levels of IGF-1 and IGFBP-3 in acute stroke patients are indicative of 3 months functional outcome. Plasma levels were measured via chemiluminescence immunoassay in heparin blood samples of patients included in the EARLY trial (NCT00562588). Plasma samples were drawn on admission and 8 days post-stroke. Neurological deficits were assessed via modified Rankin Scale (mRS) 3 months post-stroke, resulting in favorable (mRS=0-2) or unfavorable (mRS=3-6) outcome. A multiple binary logistic regression including IGF-1 and IGFBP-3 levels and confounders was conducted. Out of 404 included patients, 89 patients had an unfavorable outcome. Mean mRS on admission as well as 3 months post-stroke was 2 (±1). Low IGF-1 levels (day 8) were independently associated with a decreased risk of an unfavorable outcome (OR 0.61; 95%CI 0.37-0.99; p=0.044). Low IGFBP-3 levels (day 8) were independently associated with an unfavorable outcome (OR 2.75; 95%CI 1.56-4.84; p<0.001). Low IGFBP-3 levels and high IGF-1 levels in the subacute phase are predictive of unfavorable outcome 3 months after stroke.
“…Further factors related to IGFs have been recently associated with stroke and may suggest emerging biomarkers in this pathology. A recent study showed that not only low levels of IGF-1 were associated with an unfavourable functional outcome of stroke but also the level of insulin-like growth factor binding protein-3 (IGFBP-3) [35]. More favourable outcomes should be yet associated with the evaluation of the decrease in the IGF-1 ratio and with IGFBP-3, rather than with serum levels of IGF-1 [150].…”
Section: Bone-skeletal Muscle Biomarkers In Strokementioning
Since the increasing update of the biomolecular scientific literature, biomarkers in stroke have reached an outstanding and remarkable revision in the very recent years. Besides the diagnostic and prognostic role of some inflammatory markers, many further molecules and biological factors have been added to the list, including tissue derived cytokines, growth factor-like molecules, hormones, and microRNAs. The literatures on brain derived growth factor and other neuroimmune mediators, bone-skeletal muscle biomarkers, cellular and immunity biomarkers, and the role of microRNAs in stroke recovery were reviewed. To date, biomarkers represent a possible challenge in the diagnostic and prognostic evaluation of stroke onset, pathogenesis, and recovery. Many molecules are still under investigation and may become promising and encouraging biomarkers. Experimental and clinical research should increase this list and promote new discoveries in this field, to improve stroke diagnosis and treatment.
“…There have been a number of studies that demonstrate the beneficial neuroprotective and neuroreparative effects of M2 switching [68][69][70][71]. These studies have focused on the importance of various M2 markers such as IL-4 [72,73], IL-10 [72,74,75], IL-1RA [76], TGF-β [77,78], CD206 [72,79], arginase 1 [79,80], granulocyte macrophage colony-stimulating factor [72], insulin-like growth factor 1 [81,82], and peroxisome proliferator-activated receptor-γ [70,71,83]. Even though our understanding of the role of these individual factors have become more insightful, it is very difficult to achieve beneficial neuroprotective effects by modulating just one of these factors.…”
Section: Targeting Microglia As a Therapeutic Strategymentioning
Inflammation within the brain and in peripheral tissues contributes to brain injury following ischemic stroke. Therapeutic modulation of the inflammatory response has been actively pursued as a novel stroke treatment approach for decades, without success. In recent years, extensive studies support the high potential for cell-based therapies to become a new treatment modality for stroke and other neurological disorders. In this review, we explore different types of cellular therapies and discuss how they modulate central and peripheral inflammatory processes after stroke. Apart from identifying potential targets for cell therapy, we also discuss paracrine and immunomodulatory mechanisms of cell therapy.
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