scholarly journals Downregulation of EphB2 by RNA interference attenuates glial/fibrotic scar formation and promotes axon growth

2022 ◽  
Vol 17 (2) ◽  
pp. 362
Author(s):  
Yi Li ◽  
Jian Wu ◽  
Zhen-Yu Zhu ◽  
Zhi-Wei Fan ◽  
Ying Chen ◽  
...  
Keyword(s):  
Rna Interference ◽  
Axon Growth ◽  
Scar Formation ◽  
Fibrotic Scar

scholarly journals RNAi-mediated ephrin-B2 silencing attenuates astroglial-fibrotic scar formation and improves spinal cord axon growth

2017 ◽  
Vol 23 (10) ◽  
pp. 779-789 ◽  
Author(s):  
Yi Li ◽  
Ying Chen ◽  
Ling Tan ◽  
Jing-Ying Pan ◽  
Wei-Wei Lin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Axon Growth ◽  
Scar Formation ◽  
Fibrotic Scar

scholarly journals Combined Treatment with Fasudil and Menthol Improves Functional Recovery in Rat Spinal Cord Injury Model

Biomedicines ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 258
Author(s):  
JeongHoon Kim ◽  
Hari Prasad Joshi ◽  
Kyoung-Tae Kim ◽  
Yi Young Kim ◽  
Keundong Yeo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Combined Treatment ◽  
Scar Formation ◽  
Sprague Dawley ◽  
Static Compression ◽  
Cord Injury ◽  
Fibrotic Scar ◽  
Spinal Cord Dysfunction

Neuroprotective measures by preventing secondary spinal cord injury (SCI) are one of the main strategies for repairing an injured spinal cord. Fasudil and menthol may be potent neuroprotective agents, which act by inhibiting a rho-associated protein kinase (ROCK) and suppressing the inflammatory response, respectively. We hypothesized that combined treatment of fasudil and menthol could improve functional recovery by decreasing inflammation, apoptosis, and glial scar formation. We tested our hypothesis by administering fasudil and menthol intraperitoneally (i.p.) to female Sprague Dawley rats after moderate static compression (35 g of impounder for 5 min) of T10 spinal cord. The rats were randomly divided into five experimental groups: (i) sham animals received laminectomy alone, (ii) injured (SCI) and untreated (saline 0.2 mL/day, i.p.) rats, (iii) injured (SCI) rats treated with fasudil (10 mg/kg/day, i.p.) for two weeks, (iv) injured (SCI) rats treated with menthol (10 mg/kg/day, i.p.) for twoweeks, (v) injured (SCI) rats treated with fasudil (5 mg/kg/day, i.p.) and menthol (10 mg/kg/day, i.p.) for two weeks. Compared to single treatment groups, combined treatment of fasudil and menthol demonstrated significant functional recovery and pain amelioration, which, thereby, significantly reduced inflammation, apoptosis, and glial/fibrotic scar formation. Therefore, combined treatment of fasudil and menthol may provide effective amelioration of spinal cord dysfunction by a synergistic effect of fasudil and menthol.

Possible target for preventing fibrotic scar formation following acute myocardial infarction

2014 ◽  
Vol 83 (6) ◽  
pp. 656-658 ◽  
Author(s):  
Bruno Cvjeticanin ◽  
Maja Prutki ◽  
Ivo Dumic-Cule ◽  
Zoran Veir ◽  
Lovorka Grgurevic ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Scar Formation ◽  
Fibrotic Scar

scholarly journals Proliferating NG2-Cell-Dependent Angiogenesis and Scar Formation Alter Axon Growth and Functional Recovery After Spinal Cord Injury in Mice

2017 ◽  
Vol 38 (6) ◽  
pp. 1366-1382 ◽  
Author(s):  
Zoe C. Hesp ◽  
Rim Y. Yoseph ◽  
Ryusuke Suzuki ◽  
Peter Jukkola ◽  
Claire Wilson ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Axon Growth ◽  
Scar Formation ◽  
Cord Injury

scholarly journals Spatiotemporal expression of periostin during skin development and incisional wound healing: lessons for human fibrotic scar formation

2010 ◽  
Vol 4 (2) ◽  
pp. 99-107 ◽  
Author(s):  
Hong-Ming Zhou ◽  
Jian Wang ◽  
Christopher Elliott ◽  
Weiyan Wen ◽  
Douglas W. Hamilton ◽  
...  
Keyword(s):  
Wound Healing ◽  
Scar Formation ◽  
Skin Development ◽  
Spatiotemporal Expression ◽  
Fibrotic Scar

scholarly journals Normalization of glucose metabolism by Exendin-4 in the chronic phase after stroke promotes functional recovery in diabetes

2021 ◽  
Author(s):  
Ingrid Augestad ◽  
Doortje Dekens ◽  
Dimitra Karampatsi ◽  
Osama Elabi ◽  
Alexander Zabala ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Grip Strength ◽  
Functional Recovery ◽  
Vascular Remodeling ◽  
Neuronal Cell ◽  
Chronic Phase ◽  
Scar Formation ◽  
Parvalbumin Interneurons ◽  
Fibrotic Scar

Abstract Background Glucagon-like peptide-1 receptor (GLP-1R) activation can decrease stroke risk in people with type 2 diabetes (T2D). Moreover, animal studies have shown the efficacy of GLP-1R agonists to counteract stroke-induced acute brain damage. Whether GLP-1R activation can also improve stroke recovery during the post-acute, chronic phase after stroke, however, remains to be determined. We investigated whether post-acute, chronic administration of the GLP-1R agonist Exendin-4 improves poststroke recovery and examined possible underlying mechanisms in T2D and non-T2D mice. Methods We induced stroke via transient middle cerebral artery occlusion (tMCAO) in T2D/obese mice (8 months of high-fat diet) and age-matched controls. Exendin-4 was administered daily for 8 weeks from day 3 after tMCAO. We assessed functional recovery by weekly upper-limb grip strength tests, while insulin sensitivity and glycemia were evaluated at 4 and 8 weeks after tMCAO. Neuronal cell death, stroke-induced neurogenesis, neuroinflammation, potential atrophy of GABAergic, parvalbumin + interneurons, poststroke vascular remodeling and fibrotic scar formation were investigated by immunohistochemistry. Results Exendin-4 entirely normalized the T2D-induced impairment of forepaw grip strength recovery. The recovery correlated with the normalization of glycemia and insulin sensitivity. We also show that Exendin-4 counteracted the T2D-induced atrophy of parvalbumin + interneurons and decreased microglia activation. In addition, Exendin-4 normalized density and pericyte coverage of microvessels and restored fibrotic scar formation in T2D mice. In non-T2D mice the recovery effect of Exendin-4 was minor. Conclusion This study demonstrates that post-acute, chronic GLP-1R activation mediates neurological recovery after stroke in T2D mice likely through the normalization of glucose metabolism and neuroplasticity mechanisms as well as improved vascular remodeling in the recovery phase. The results promote launching clinical trials investigating whether GLP-1R agonists improve the efficacy of rehabilitation after stroke in people with T2D.

Ethamsylate attenuates mutilated secondary pathogenesis and exhibits a neuroprotective role in experimental model of spinal cord injury

2021 ◽  
Author(s):  
Sonam Dolma ◽  
Kirti Adhikari ◽  
Teena Mamidi ◽  
Abhishek Roy ◽  
Zarna Pathak ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Neurons ◽  
Proteolytic Enzymes ◽  
Motor Impairment ◽  
Scar Formation ◽  
Secondary Damage ◽  
Cord Injury ◽  
Fibrotic Scar ◽  
Blood Spinal Cord Barrier

Abstract Deficits in the neuronal connection that succumbs to the impairment of sensory and motor neurons are the hallmarks of spinal cord injury (SCI). Secondary pathogenesis, which initiates after the primary mechanical insult to the spinal cord, depicts a pivotal role in producing inflammation, lesion formation and ultimately causes fibrotic scar formation in the chronic period. This fibrotic scar formed acts as a major hindrance in facilitating axonal regeneration and is one of the root causes of motor impairment. Cascade of secondary events in SCI begins with injury-induced blood spinal cord barrier rupture that promotes increased migration of neutrophils, macrophages, and other inflammatory cells at the injury site to initiate the secondary damages. This phenomenon leads to the release of matrix metalloproteinase, cytokines and chemokines, reactive oxygen species, and other proteolytic enzymes at the lesion site. These factors assist in the activation of TGF-β1 signalling pathway, which further leads to excessive proliferation of perivascular fibroblast, followed by deposition of collagen and fibronectin matrix, which are the main components of the fibrotic scar. Subsequently, this scar formed inhibits the propagation of action potential from one neuron to adjacent neurons. Ethamsylate, an anti-hemorrhagic drug, has the potential to maintain early hemostasis as well as restores capillary resistance. Therefore, we hypothesized that ethamsylate, by virtue of its anti-hemorrhagic activity, reduces hemorrhagic ischemia-induced neuronal apoptosis, maintains the blood spinal cord barrier integrity, and decreases secondary damage severity, thereby reduce the extent of fibrotic scar formation, and demonstrates a neuroprotective role in SCI.

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