Shervin Banitalebi

ORCID: 0000-0001-5180-2407
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About
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Research Areas
  • Ion Transport and Channel Regulation
  • Barrier Structure and Function Studies
  • Neonatal Respiratory Health Research
  • Mesenchymal stem cell research
  • Connexins and lens biology
  • Electrolyte and hormonal disorders
  • Cerebrospinal fluid and hydrocephalus
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroinflammation and Neurodegeneration Mechanisms
  • ATP Synthase and ATPases Research
  • Cancer Cells and Metastasis
  • Ion channel regulation and function

University of Oslo
2020-2024

Abstract Fibrotic scar tissue limits central nervous system regeneration in adult mammals. The extent of fibrotic generation and distribution stromal cells across different lesions the brain spinal cord has not been systematically investigated mice humans. Furthermore, it is unknown whether scar-forming have same origin throughout types lesions. In current study, we compared scarring human pathological corresponding mouse models penetrating non-penetrating injury, traumatic ischemic stroke,...

10.1038/s41467-021-25585-5 article EN cc-by Nature Communications 2021-09-17

Abstract Fibrotic scar tissue formation occurs in humans and mice. The fibrotic impairs regeneration functional recovery. However, the origin of scar-forming fibroblasts is unclear. Here, we show that stromal forming derive from two populations perivascular cells after spinal cord injury (SCI) adult mice both sexes. We anatomically transcriptionally identify cell as pericytes fibroblasts. Fibroblasts are enriched white gray matter regions cord, respectively. Both recruited response to SCI...

10.1038/s41593-024-01678-4 article EN cc-by Nature Neuroscience 2024-06-07

Abstract Astrocyte endfeet are endowed with aquaporin‐4 (AQP4)‐based assemblies called orthogonal arrays of particles (OAPs) whose function is still unclear. To investigate the OAPs and AQP4 tetramers, we have generated a novel “OAP‐null” mouse model selectively lacking OAP forming M23‐AQP4 isoform. We demonstrated that transcript levels were not reduced by using qPCR. Blue native (BN)/SDS‐PAGE Western blot performed on OAP‐null brain primary astrocyte cultures showed complete depletion...

10.1002/glia.23909 article EN Glia 2020-09-18

Aquaporin-4 (AQP4) is the main water channel in brain and enriched perivascular astrocyte processes abutting microvessels. There a rich literature on role of AQP4 experimental stroke. While its oedema formation following middle cerebral artery occlusion (MCAO) has been studied extensively, specific impact infarct volume remains unclear. This study investigated effects total partial deletion mice subjected to distal medial (dMCAO) occlusion. Compared MCAO, this model induces smaller infarcts...

10.1113/jp284099 article EN cc-by The Journal of Physiology 2024-06-24

Translational readthrough (TRT) of aquaporin-4 (AQP4) has remarkably expanded the importance this new post-transcriptional mechanism, as well regulation potential AQP4. The TRT isoform AQP4, named AQP4ex, is central for both AQP4 polarization and water channel activity in nervous system (CNS). Here we evaluate relevance mechanism by analyzing whether AQP4ex also expressed peripheral tissues expression necessary its polarized it occurs perivascular astrocyte processes. To purpose, null mice...

10.3390/ijms21041531 article EN International Journal of Molecular Sciences 2020-02-24

There is an urgent need to better understand the mechanisms involved in scar formation brain. It well known that astrocytes are critically engaged this process. Here, we analyze incipient one week after a discrete ischemic insult cerebral cortex. We show infarct border zone characterized by pronounced changes organization and subcellular localization of major astrocytic protein AQP4. Specifically, there loss AQP4 from endfoot membranes anchor pericapillary basal laminae disassembly...

10.3390/ijms23031117 article EN International Journal of Molecular Sciences 2022-01-20

There is an urgent need to better understand the mechanisms involved in scar formation brain. It well known that astrocytes are critically engaged this process. Here we analyze in-cipient one week after a discrete ischemic insult cerebral cortex. We show infarct border zone characterized by pronounced changes organization and subcellular localization of major astrocytic protein AQP4. Specifically there loss AQP4 from endfoot membranes anchor pericapillary basal laminae disassembly...

10.20944/preprints202201.0065.v1 preprint EN 2022-01-06
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