- TIMP-1 Promotes Oligodendrocyte Differentiation Through Receptor-Mediated Signaling. [Journal Article]
- MNMol Neurobiol 2018 Aug 18
- The extracellular protein tissue inhibitor of metalloproteinase (TIMP)-1 is both a matrix metalloproteinase (MMP) inhibitor and a trophic factor. Mice lacking TIMP-1 exhibit delayed central nervous s...
The extracellular protein tissue inhibitor of metalloproteinase (TIMP)-1 is both a matrix metalloproteinase (MMP) inhibitor and a trophic factor. Mice lacking TIMP-1 exhibit delayed central nervous system myelination during postnatal development and impaired remyelination following immune-mediated injury in adulthood. We have previously determined that the trophic action of TIMP-1 on oligodendrocyte progenitor cells (OPCs) to mature into oligodendrocytes is independent of its MMP inhibitory function. However, the mechanism by which TIMP-1 promotes OPC differentiation is not known. To address this gap in our understanding, herein, we report that TIMP-1 signals via a CD63/β1-integrin receptor complex to activate Akt (protein kinase B) to promote β-catenin signaling in OPCs. The regulation of β-catenin by TIMP-1 to promote OPC differentiation was counteracted, but not abrogated, by canonical signaling evoked by Wnt7a. These data provide a previously uncharacterized trophic action of TIMP-1 to regulate oligodendrocyte maturation via a CD63/β1-integrin/Akt pathway mechanism. These findings contribute to our emerging understanding on the role of TIMP-1 as a growth factor expressed to promote CNS myelination during development and induced in the adult to promote myelin repair.
- Acute Blood Pressure Management in Acute Ischemic Stroke and Spontaneous Cerebral Hemorrhage. [Review]
- CTCurr Treat Options Neurol 2018 Aug 18; 20(9):39
- We discuss the evidence and guidelines for acute blood pressure (BP) management for patients presenting with acute ischemic stroke or spontaneous cerebral hemorrhage.
We discuss the evidence and guidelines for acute blood pressure (BP) management for patients presenting with acute ischemic stroke or spontaneous cerebral hemorrhage.
- Correction: Patent foramen ovale closure, antiplatelet therapy or anticoagulation in patients with patent foramen ovale and cryptogenic stroke: a systematic review and network meta-analysis incorporating complementary external evidence. [Journal Article]
- BOBMJ Open 2018 Aug 17; 8(8):e023761corr1
- Does perturbation-based balance training prevent falls among individuals with chronic stroke? A randomised controlled trial. [Journal Article]
- BOBMJ Open 2018 Aug 17; 8(8):e021510
- CONCLUSIONS: The results are inconclusive. PBT may help to prevent falls in daily life poststroke, but ongoing training may be required to maintain the benefits.
- Leptomeningeal Enhancement is Associated with Transient Neurological Deficits after Flow Diversion of Intracranial Aneurysms. [Journal Article]
- WNWorld Neurosurg 2018 Aug 16
- CONCLUSIONS: This study challenges conventional dogma that TNDs are ischemic in etiology and suggests BBB impairment may be a potential alternative mechanism. These findings are applicable to stroke and other reversible neurological diseases.
- High-Density Lipoprotein (HDL) is associated with progression of intracranial aneurysms. [Journal Article]
- WNWorld Neurosurg 2018 Aug 16
- CONCLUSIONS: These data support the hypothesis that HDL was inversely associated with intracranial aneurysm growth, especially in male patients. Higher HDL levels and small size of aneurysm contributed to high risk of aneurysmal rupture. HDLsizeR greater than 0.31 was considered as a valuable predictor of intracranial rupture.
- Clinical outcome after mechanical thrombectomy in diabetic patients with major ischemic stroke of the anterior cerebral circulation. [Journal Article]
- WNWorld Neurosurg 2018 Aug 16
- CONCLUSIONS: The main factors for an unfavorable outcome of diabetic patients after MT are admission hyperglycemia, age, NIHSS.
- The membrane mesenchymal stem cell derived conditioned medium exerts neuroprotection against focal cerebral ischemia by targeting apoptosis. [Journal Article]
- JCJ Chem Neuroanat 2018 Aug 16
- CONCLUSIONS: The results of this study indicate that treatment with AMSC-CM improves the pathological effects in the acute phase of cerebral ischemia. These findings establish a substantial foundation for stroke therapy and future research.
- The Effect of Post-Dilatation on Outcomes in the PARTNER 2 SAPIEN 3 Registry. [Journal Article]
- JCJACC Cardiovasc Interv 2018 Aug 07
- CONCLUSIONS: BPD is performed more frequently in patients with lower % oversizing and greater calcium burden. BPD is not associated with procedural complications or an increase in 1-year adverse events of death, rehospitalization, or stroke.
New Search Next
- DNA Methylation and the YAP/WWTR1 Pathway Prevent Pathological Remodeling during Bladder Obstruction by Limiting Expression of BDNF. [Journal Article]
- AJAm J Pathol 2018 Aug 16
- Chronic bladder obstruction and bladder smooth muscle cell (BSMC) stretch provide fibrotic and mechanical environments that can induce epigenetic change. Therefore, we examined the role of DNA methyl...
Chronic bladder obstruction and bladder smooth muscle cell (BSMC) stretch provide fibrotic and mechanical environments that can induce epigenetic change. Therefore, we examined the role of DNA methylation in bladder pathology and transcriptional control. Sprague-Dawley female rats underwent partial bladder obstruction by ligation of a silk suture around the proximal urethra next to a 0.9 mm steel rod. Sham operation comprised passing the suture around the urethra. After two weeks, rats were randomized to normal saline or DNA methyltransferase inhibitor, 5-aza-2-deoxycytidine (DAC) at 1 mg/kg, 3 times/week intraperitoneally. After six weeks, bladders were weighed and divided for histology and RNA analysis by high throughput qPCR (HT-qPCR) arrays. DAC treatment during obstruction in vivo profoundly augmented BDNF expression compared to the obstruction with vehicle group, which was statistically correlated with pathophysiologic parameters. BDNF, CCN1 (official name CCNA2), and CCN2 (official name CTGF) expression clustered tightly together using Pearson's correlation analysis. Their promoters were associated with the TEAD1 and YAP/WWTR1 pathways. Interestingly, DAC treatment increased BDNF expression in BSMCs (P < 0.0002). Stretch-induced BDNF was inhibited by the YAP/WWTR1 inhibitor Verteporfin. Verteporfin improved SMC phenotype (proliferative markers, SMC marker expression) in part modulated by reducing BDNF. Expression of BDNF is limited by DNA methylation and associated with pathophysiologic changes during partial bladder outlet obstruction and SMC phenotype in vitro.