Caveolin-1 and MLRs: A potential target for neuronal growth and neuroplasticity after ischemic stroke

Wang, Zhong; Huang, Qiangru; Zeng, Lei; Hu, Zhiping; Tang, Xiangqi

doi:10.7150/ijms.35158

Cited by 19 publications

(11 citation statements)

References 173 publications

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“…Caveolin-1 is a cholesterol binding protein important for neuronal survival and growth [ 170 ]. In this connection, drugs that upregulate caveolin-1 have been reported to promote neuronal plasticity and growth via PI3K and GSK3β signaling [ 171 ]. In recent times, the role of fatty acid binding protein 4 isoform (FABP 4 ] has also been envisaged in ischemic stroke.…”

Section: Novel Exploratory Targets In Ischemic Strokementioning

confidence: 99%

A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies

Singh

Kharwar

Dandekar

2022

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Background: Stroke is a serious neurovascular problem and the leading cause of disability and death worldwide. The disrupted demand to supply ratio of blood and glucose during cerebral ischemia develops hypoxic shock, and subsequently necrotic neuronal death in the affected regions. Multiple causal factors like age, sex, race, genetics, diet, and lifestyle play an important role in the occurrence as well as progression of post-stroke deleterious events. These biological and environmental factors may be contributed to vasculature variable architecture and abnormal neuronal activity. Since recombinant tissue plasminogen activator is the only clinically effective clot bursting drug, there is a huge unmet medical need for newer therapies for the treatment of stroke. Innumerous therapeutic interventions have shown promise in the experimental models of stroke but failed to translate it into clinical counterparts. Methods: Original publications regarding pathophysiology, preclinical experimental models, new targets and therapies targeting ischemic stroke have been reviewed since the 1970s. Results: We highlighted the critical underlying pathophysiological mechanisms of cerebral stroke and preclinical stroke models. We discuss the strengths and caveats of widely used ischemic stroke models, and commented on the potential translational problems. We also describe the new emerging treatment strategies, including stem cell therapy, neurotrophic factors and gut microbiome-based therapy for the management of post-stroke consequences. Results : We highlighted the critical underlying pathophysiological mechanisms of cerebral stroke and preclinical stroke models. We discuss the strengths and caveats of widely used ischemic stroke models, and commented on the potential translational problems. We also describe the new emerging treatment strategies, including stem cell therapy, neurotrophic factors and gut microbiome-based therapy for the management of post-stroke consequences. Conclusion: There are still many inter-linked pathophysiological alterations with regards to stroke, animal models need not necessarily mimic the same conditions of stroke pathology and newer targets and therapies are the need of the hour in stroke research.

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Section: Novel Exploratory Targets In Ischemic Strokementioning

confidence: 99%

A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies

Singh

Kharwar

Dandekar

2022

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“…Also involved in neurogenesis, lncRNA Gm15577 was identified in the Nbs1-deficient mouse model. Yue et al [ 80 ] demonstrated that Gm15577 regulates the RNA expression of Shh, Nerg1, and β-catenin, and has important functions in neuronal growth and neuroplasticity [ 81 ].…”

Section: Lncrnas and Pathways Involved In Non-syndromic Intellectumentioning

confidence: 99%

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

Barros

Leão

Santis

et al. 2021

ncRNA

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Non-syndromic intellectual disability (NS-ID or idiopathic) is a complex neurodevelopmental disorder that represents a global health issue. Although many efforts have been made to characterize it and distinguish it from syndromic intellectual disability (S-ID), the highly heterogeneous aspect of this disorder makes it difficult to understand its etiology. Long noncoding RNAs (lncRNAs) comprise a large group of transcripts that can act through various mechanisms and be involved in important neurodevelopmental processes. In this sense, comprehending the roles they play in this intricate context is a valuable way of getting new insights about how NS-ID can arise and develop. In this review, we attempt to bring together knowledge available in the literature about lncRNAs involved with molecular and cellular pathways already described in intellectual disability and neural function, to better understand their relevance in NS-ID and the regulatory complexity of this disorder.

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“…Cav1 regulates neuronal signaling [ 27 ]. When upregulated or overexpressed in the brain, Cav1 enhances receptor function and neuronal plasticity [ 28 , 29 , 30 ]. For example, enhancing Cav1 in the brain is indicated to be a potential therapy for enhancing neuroplasticity after neurodegeneration, cerebral ischemia and stroke [ 29 , 31 ].…”

Section: Introductionmentioning

confidence: 99%

“…When upregulated or overexpressed in the brain, Cav1 enhances receptor function and neuronal plasticity [ 28 , 29 , 30 ]. For example, enhancing Cav1 in the brain is indicated to be a potential therapy for enhancing neuroplasticity after neurodegeneration, cerebral ischemia and stroke [ 29 , 31 ]. Conversely, Cav1 overexpression in non-neuronal cells has been shown to mediate tumorigenesis and enhance oxidative stress in cancer [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

Caveolin-1 Expression in the Dorsal Striatum Drives Methamphetamine Addiction-Like Behavior

Avchalumov

Kreisler

Trenet

et al. 2021

IJMS

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Dopamine D1 receptor (D1R) function is regulated by membrane/lipid raft-resident protein caveolin-1 (Cav1). We examined whether altered expression of Cav1 in the dorsal striatum would affect self-administration of methamphetamine, an indirect agonist at the D1Rs. A lentiviral construct expressing Cav1 (LV-Cav1) or containing a short hairpin RNA against Cav1 (LV-shCav1) was used to overexpress or knock down Cav1 expression respectively, in the dorsal striatum. Under a fixed-ratio schedule, LV-Cav1 enhanced and LV-shCav1 reduced responding for methamphetamine in an extended access paradigm compared to LV-GFP controls. LV-Cav1 and LV-shCav1 also produced an upward and downward shift in a dose–response paradigm, generating a drug vulnerable/resistant phenotype. LV-Cav1 and LV-shCav1 did not alter responding for sucrose. Under a progressive-ratio schedule, LV-shCav1 generally reduced positive-reinforcing effects of methamphetamine and sucrose as seen by reduced breakpoints. Western blotting confirmed enhanced Cav1 expression in LV-Cav1 rats and reduced Cav1 expression in LV-shCav1 rats. Electrophysiological findings in LV-GFP rats demonstrated an absence of high-frequency stimulation (HFS)-induced long-term potentiation (LTP) in the dorsal striatum after extended access methamphetamine self-administration, indicating methamphetamine-induced occlusion of plasticity. LV-Cav1 prevented methamphetamine-induced plasticity via increasing phosphorylation of calcium calmodulin kinase II, suggesting a mechanism for addiction vulnerability. LV-shCav1 produced a marked deficit in the ability of HFS to produce LTP and, therefore, extended access methamphetamine was unable to alter striatal plasticity, indicating a mechanism for resistance to addiction-like behavior. Our results demonstrate that Cav1 expression and knockdown driven striatal plasticity assist with modulating addiction to drug and nondrug rewards, and inspire new strategies to reduce psychostimulant addiction.

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Caveolin-1 and MLRs: A potential target for neuronal growth and neuroplasticity after ischemic stroke

Cited by 19 publications

References 173 publications

A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies

A Review on Preclinical Models of Ischemic Stroke: Insights Into the Pathomechanisms and New Treatment Strategies

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

Caveolin-1 Expression in the Dorsal Striatum Drives Methamphetamine Addiction-Like Behavior

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