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Biomolecules
Special Issues
Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II)
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Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II)

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 10139

Special Issue Editor

Dr. Yuchuan Ding

E-Mail Website
Guest Editor
Department of Neurosurgery, Wayne State University School of Medicine, Detroit, MI 48201, USA
Interests: stroke; neuroprotection; brain circulation; conditioning medicine; exercise; ischemia and reperfusion injury; stress; vascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Following a successful first run, we are pleased to announce the launch of a new edition of a Special Issue on protection, plasticity, and physical rehabilitation in ischemic injury.

This issue will cover, but will not be limited to, experimental, technical and clinical studies related to health, ethical and social issues of the following: (1) cerebro- or cardiovascular disease, as well as its cause and pathology; (2) innovative treatment in stroke and ischemia/reperfusion injury, including thrombolysis and all non-drug treatments, such as oxygen, hypothermia, and remote pre-, per- or post-ischemic preconditioning. Articles with clinical interest and implications will be given preference.

As we are aware of your interest in the fields of neuroscience, neurology and neurotherapy, we would like to cordially invite you to submit your manuscripts for review and publication in Biomolecules.

Dr. Yuchuan Ding
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • stroke
  • ischemia and reperfusion
  • stress and vascular injury
  • circulation
  • conditioning medicine
  • exercise

Published Papers (4 papers)

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Research

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13 pages, 2843 KiB  
Article
Use of Botulinum Toxin for Limb Immobilization for Rehabilitation in Rats with Experimental Stroke
by Hongxia Zhang, Jialing Liu, Deborah Bingham, Adrienne Orr, Masahito Kawabori, Jong Youl Kim, Zhen Zheng, Tina I. Lam, Stephen M. Massa, Raymond A. Swanson and Midori A. Yenari
Biomolecules 2023, 13(3), 512; https://doi.org/10.3390/biom13030512 - 10 Mar 2023
Cited by 1 | Viewed by 1466
Abstract
Motor rehabilitation strategies after unilateral stroke suggest that the immobilization of the healthy, unimpaired limb can promote the functional recovery of a paretic limb. In rodents, this has been modeled using casts, harnesses, and other means of restricting the use of the non-paretic [...] Read more.
Motor rehabilitation strategies after unilateral stroke suggest that the immobilization of the healthy, unimpaired limb can promote the functional recovery of a paretic limb. In rodents, this has been modeled using casts, harnesses, and other means of restricting the use of the non-paretic forelimb in models of experimental stroke. Here, we evaluated an alternative approach, using botulinum toxin injections to limit the function of the non-paretic forelimb. Adult male rats were subjected to permanent ligation of the left distal middle cerebral artery, resulting in right forelimb paresis. The rats were then subjected to: (1) no treatment; (2) botulinum toxin injections 1 day post stroke; or (3) cast placement 5 days post stroke. Casts were removed after 5 weeks, while the botulinum toxin injection effectively immobilized subjects for approximately the same duration. Rats with bilateral forelimb impairment due to the stroke plus casting or botulinum injections were still able to feed and groom normally. Both immobilization groups showed modest recovery following the stroke compared to those that did not receive immobilization, but the casting approach led to unacceptable levels of animal stress. The botulinum toxin approach to limb immobilization had both advantages and disadvantages over traditional physical limb immobilization. The major advantage was that it was far less stress-inducing to the subject animals and appeared to be well tolerated. A disadvantage was that the paresis took roughly 10 weeks to fully resolve, and any degree of residual paresis could confound the interpretation of the behavioral assessments. Full article
(This article belongs to the Special Issue Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II))
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15 pages, 2590 KiB  
Article
Limb Remote Ischemic Conditioning Promotes Neurogenesis after Cerebral Ischemia by Modulating miR-449b/Notch1 Pathway in Mice
by Sijie Li, Yong Yang, Ning Li, Haiyan Li, Jiali Xu, Wenbo Zhao, Xiaojie Wang, Linqing Ma, Chen Gao, Yuchuan Ding, Xunming Ji and Changhong Ren
Biomolecules 2022, 12(8), 1137; https://doi.org/10.3390/biom12081137 - 18 Aug 2022
Cited by 3 | Viewed by 1867
Abstract
Neurogenesis plays an important role in the prognosis of stroke patients and is known to be promoted by the activation of the Notch1 signaling pathway. Studies on the airway epithelium have shown that miR-449b represses the Notch pathway. The study aimed to investigate [...] Read more.
Neurogenesis plays an important role in the prognosis of stroke patients and is known to be promoted by the activation of the Notch1 signaling pathway. Studies on the airway epithelium have shown that miR-449b represses the Notch pathway. The study aimed to investigate whether limb remote ischemic conditioning (LRIC) was able to promote neurogenesis in cerebral ischemic mice, and to investigate the role of the miR-449b/Notch1 pathway in LRIC-induced neuroprotection. Male C57BL/6 mice (22–25 g) were subjected to transient middle cerebral artery occlusion (MCAO), and LRIC was performed in the bilateral lower limbs immediately after MCA occlusion. Immunofluorescence staining was performed to assess neurogenesis. The cell line NE-4C was used to elucidate the proliferation of neuronal stem cells in 8% O2. After LRIC treatment on day 28, mice recovered neurological function. Neuronal precursor proliferation was enhanced in the SVZ, and neuronal precursor migration was enhanced in the basal ganglia on day 7. LRIC promoted the improvement of neurological function in mice on day 28, promoted neuronal precursor proliferation in the SVZ, and enhanced neuronal precursor migration in the basal ganglia on day 7. The neurological function score was negatively correlated with the number of BrdU-positive/DCX-positive cells in the SVZ and striatum. LRIC promoted activated Notch1 protein expression in the SVZ and substantially downregulated miR-449b levels in the SVZ and plasma. In vitro, miR-449b was found to target Notch1. Lentivirus-mediated miR-449b knockdown increased Notch1 levels in NE-4C cells and increased proliferation in the cells. The effects of miR-449b inhibition on neurogenesis were ablated by the application of Notch1 shRNA. Our study showed that LRIC promoted the proliferation and migration of neural stem cells after MCAO, and these effects were modulated by the miR-449b/Notch1 pathway. Full article
(This article belongs to the Special Issue Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II))
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14 pages, 5388 KiB  
Article
Neuroprotective Effects of Chlorogenic Acid in a Mouse Model of Intracerebral Hemorrhage Associated with Reduced Extracellular Matrix Metalloproteinase Inducer
by Yang Liu, Fei Wang, Zhe Li, Yanling Mu, Voon Wee Yong and Mengzhou Xue
Biomolecules 2022, 12(8), 1020; https://doi.org/10.3390/biom12081020 - 22 Jul 2022
Cited by 9 | Viewed by 1959
Abstract
Chlorogenic acid (CGA) has been reported to have various biological activities, such as anti-inflammatory, anti-oxidant and anti-apoptosis effects. However, the role of CGA in intracerebral hemorrhage (ICH) and the underlying mechanisms remain undiscovered. The current study aims to investigate the effect of CGA [...] Read more.
Chlorogenic acid (CGA) has been reported to have various biological activities, such as anti-inflammatory, anti-oxidant and anti-apoptosis effects. However, the role of CGA in intracerebral hemorrhage (ICH) and the underlying mechanisms remain undiscovered. The current study aims to investigate the effect of CGA on neuroinflammation and neuronal apoptosis after inhibition of EMMPRIN in a collagenase-induced ICH mouse model. Dose optimization data showed that intraperitoneal administration of CGA (30 mg/kg) significantly attenuated neurological impairments and reduced brain water content at 24 h and 72 h compared with ICH mice given vehicle. Western blot and immunofluorescence analyses revealed that CGA remarkably decreased the expression of extracellular matrix metalloproteinase inducer (EMMPRIN) in perihematomal areas at 72 h after ICH. CGA also reduced the expression of matrix metalloproteinases-2/9 (MMP-2/9) at 72 h after ICH. CGA diminished Evans blue dye extravasation and reduced the loss of zonula occludens-1 (ZO-1) and occludin. CGA-treated mice had fewer activated Iba-1-positive microglia and MPO-positive neutrophils. Finally, CGA suppressed cell death around the hematoma and reduced overall brain injury. These outcomes highlight that CGA treatment confers neuroprotection in ICH likely by inhibiting expression of EMMPRIN and MMP-2/9, and alleviating neuroinflammation, blood–brain barrier (BBB) disruption, cell death and brain injury. Full article
(This article belongs to the Special Issue Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II))
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Review

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38 pages, 2361 KiB  
Review
The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery
by Chenye Qiao, Zongjian Liu and Shuyan Qie
Biomolecules 2023, 13(3), 571; https://doi.org/10.3390/biom13030571 - 21 Mar 2023
Cited by 4 | Viewed by 4310
Abstract
Stroke causes varying degrees of neurological deficits, leading to corresponding dysfunctions. There are different therapeutic principles for each stage of pathological development. Neuroprotection is the main treatment in the acute phase, and functional recovery becomes primary in the subacute and chronic phases. Neuroplasticity [...] Read more.
Stroke causes varying degrees of neurological deficits, leading to corresponding dysfunctions. There are different therapeutic principles for each stage of pathological development. Neuroprotection is the main treatment in the acute phase, and functional recovery becomes primary in the subacute and chronic phases. Neuroplasticity is considered the basis of functional restoration and neurological rehabilitation after stroke, including the remodeling of dendrites and dendritic spines, axonal sprouting, myelin regeneration, synapse shaping, and neurogenesis. Spatiotemporal development affects the spontaneous rewiring of neural circuits and brain networks. Microglia are resident immune cells in the brain that contribute to homeostasis under physiological conditions. Microglia are activated immediately after stroke, and phenotypic polarization changes and phagocytic function are crucial for regulating focal and global brain inflammation and neurological recovery. We have previously shown that the development of neuroplasticity is spatiotemporally consistent with microglial activation, suggesting that microglia may have a profound impact on neuroplasticity after stroke and may be a key therapeutic target for post-stroke rehabilitation. In this review, we explore the impact of neuroplasticity on post-stroke restoration as well as the functions and mechanisms of microglial activation, polarization, and phagocytosis. This is followed by a summary of microglia-targeted rehabilitative interventions that influence neuroplasticity and promote stroke recovery. Full article
(This article belongs to the Special Issue Protection, Plasticity, and Physical Rehabilitation in Ischemic Injury (Volume II))
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